Report of the
Secretary's Task
Force on
Black &
Minority
Health
U.S. Department of Health and
Human Services
U.S. NATIONAL
LIBRARY
OF
MEDICINE
Volume IV:
Cardiovascular
and
Cerebrovascular
Disease
Part 2
Report of the
Secretary's Task
Force on
Black &
Minority
Health
U.S. Department of Health and
Human Services
January 1986
Cxjfl
3(bCb
SUBCOMMITTEE ON CARDIOVASCULAR AND CEREBROVASCULAR DISEASES
TABLE OF CONTENTS
PART 2
Supporting Papers
1. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart
Disease Risk Factors in Black Americans ......... 229
2. Lucile L. Adams, Laurence 0. Watkins, Lewis H. Kuller,
Daniel D. Savage, Richard Donahue, Ronald E. LaPorte:
Relationship of Social Class to Coronary Disease Risk
Factors in Blacks: Implications of Social Mobility for
Risk Factor Change................285
3. Hector F. Myers: Coronary Heart Disease in Black Populations:
Current Research, Treatment, and Prevention Needs ...... 303
4. Melford J. Henderson, Daniel D. Savage: Prevalence and
Incidence of Ischemic Heart Disease in United States'
Black and White Populations.............347
5. Helen P. Hazuda: Differences in Socioeconomic Status
and Acculturation among Mexican Americans and Risk of
Cardiovascular Disease ............... 367
6. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart
Disease Risk Factors in Hispanic Americans ........ 393
7. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart
Disease Risk Factors in Asian/Pacific Islander Americans .... 415
8. Shiriki K. Kumanyika, Daniel D. Savage: Ischemic Heart
Disease Risk Factors in American Indians and Alaska
Natives....................44 5
9.
Lewis H. Kuller: Stroke Report
477
Ischemic Heart Disease
Risk Factors in Black
Americans
Shiriki K. Kumanyika, Ph.D., M.P.H.
Assistant Professor
Department of Epidemiology
Johns Hopkins School of Hygiene and Public Health
Baltimore, Maryland
Daniel D. Savage, M.D., Ph.D.
Medical Advisor
National Center for Health Statistics
Hyattsville, Maryland
TABLE OF CONTENTS
1.0 CIGARETTE SMOKING ............... 232
1.1 Prevalence.................232
1.1.1 Data Sources
1.1.2 Black/white differences in prevalence of current and
heavy smoking: 1965-1982
1.1.2.1 Current Smoking: Men
1.1.2.2 Heavy Smoking: Men
1.1.2.3 Current Smoking: Women
1.1.2.4 Heavy Smoking: Women
1.2 Impact..................239
1.2.1 Data Sources
1.2.2 Findings
1.3 Implications................2^4
1.4 Recommendations...............2^5
1.5 References ................2^6
2.0 CHOLESTEROL................248
2.1 Data Sources................248
2.2 Findings.................250
2.2.1 Total and lipoprotein cholesterol comparisons among
black and white men
2.2.1.1 Total cholesterol: men
2.2.1.2 Lipoprotein cholesterol: men
2.2.2 Total and lipoprotein cholesterol comparisons among
black and white women
2.2.2.1 Total cholesterol: women
2.2.2.2 Lipoprotein cholesterol: women
2.2.3 Basis of lipoprotein cholesterol differences in blacks
and whites
2.2.4 Impact of cholesterol-associated risk on CHD
disparities between blacks and whites
2.2.5 Intervention studies
229
2.3 Recommendation ................ °
2.4 References.................263
3.0 ELEVATED BLOOD PRESSURE AND HYPERTENSION ....... 267
3.1 Prevalence.................2"'
3.1.1 Data Sources
3.1.2 Findings
3.1.2.1 Elevated Blood Pressure and Hypertension in Black and
White Men, 1960-1980
3.1.2.2 Demographic Patterns : Men
3.1.2.3 Prevalence of Elevated Blood Pressure and Hypertension
in Black and White Women, 1960-1980.
3.1.2.4 Demographic Patterns : Women
3.2 Left Ventricular Hypertrophy ........... 275
3.3 References.................279
4.0 CONCLUSION ...............282
230
INTRODUCTION
The Task Force on Black and Minority Health Subcommittee on
Cardiovascular and Cerebrovascular Diseases is attempting to understand and
document the extent and determinants of racial disparities in
cardiovascular and cerebrovascular diseases. This paper focuses on black
Americans and on the ischemic heart disease (IHD) component of
cardiovascular morbidity and mortality. IHD prevalence and incidence are
addressed in a separate paper (Henderson and Savage). Data and issues
relating to standard and other IHD risk factors are considered here. The
specific objectives of this paper are to summarize and evaluate the
available information on IHD risk factors in black men and women and to
discuss implications of the data for the DHHS Task Force on Black and
Minority Health.
The scope of this paper is broad due to the need to cover several
different risk factors in both black men and women and the need to scan a
large literature on cardiovascular disease in whites for the relatively
limited information on minority populations. For practical purposes
related to the division of responsibilities among consultants to the Task
Force, subjects which would be coherently considered together have been
separated. Thus, IHD outcomes are discussed in relative isolation from
cerebrovascular disease and diabetes. Also, an attempt is made to examine
separately risk factors which occur in clusters and which interact. Some
important factors such as obesity have already been incorportated into the
subcommittee report by Dr. Watkins and, to avoid duplication of effort,
have not been discussed here at length. The assumption is that a complete
multivariate picture will emerge from a synthesis of several papers, by the
Subcommittee and Task Force members.
Based on the impression of Henderson and Savage from their review of
prevalence and incidence of IHD in black Americans, the context for
consideration of IHD risk among blacks has been as follows:
* In black men, up to between ages 55 and 65, the prevalence-
incidence of IHD appears to be similar to that in white men.
* After about age 60-65 (the range of the average life span of
black men), black men have a substantially lower prevalence/
incidence of IHD than white men (average life span 65 to 71
years).
* IHD prevalence/incidence in black women is similar to or
greater than that of white women, with no crossover.
Cigarette smoking, cholesterol, hypertension, and diabetes are the
standard risk factors for IHD. References describing prevalence, impact,
and intervention aspects of three of these determinants have been selected
and evaluated for implications related to the Task Force Mission.
Diabetes' risks have been addressed by the Diabetes Subcommittee of the
231
Task Force. Left ventricular hypertrophy (LVH) (which is highly prevalent
in blacks relative to whites) is discussed as a putative independent IHD
risk factor. Emphasis has been given to recent references (1980 to
present), with attention to time trends, in order to make the scope
manageable and also to provide sufficiently timely perspectives for action.
1.0 CIGARETTE SMOKING AMONG BLACK AMERICANS
1.1 PREVALENCE
1.1.1 Data Sources
National probability estimates of the prevalence of cigarette smoking
among black adult men and women during and between 1965-1983 are available
from the National Health Interview Survey (NHIS), the National Health
Examination Surveys (NHANES), and the Centers for Disease Control
Behavioral Risk Factor Survey (CDC-BRFS)(1-9). NHIS and NHANES data are
from in-person interviews. CDC data are from a telephone survey. All of
these sources provide estimates of rates of current smoking for the years
covered. In addition, NHIS sources provide data on number of cigarettes
smoked per day for current smokers (mean or categorical distribution),
percentages of former smokers, smokers who have attempted to stop smoking,
length of time since stopping, and tar and nicotine levels. NHANES
provides percentages of heavy smokers, defined as 25 cigarettes or more per
day. All sources provide comparison data for whites. However, NHIS and
NHANES include Mexican-Americans in the white category.
The treatment of age in published tables varies. NHIS reports use
20-24, 25-34, and 35-44 years, with 45-54 and 55-64 years either separate
or combined as 45-64. NHANES data are reported for decades between 25 and
74 years. Only age-adjusted data were available for some black-white
comparisons in both NHIS and NHANES. CDC data are reported for the
categories 25-44, 45-64 and 65+ years. Time trends can be examined within
NHIS and NHANES data, but only on a cross-sectional basis. No direct
comparisons across data bases are appropriate due to the different sampling
and data collection protocols. All smoking data in these surveys are
self-reported (i.e., they have not been validated by biochemical tests).
In addition, estimates of smoking status of black and white men and
women in several large, widely-based samples were identified:
* American Cancer Society data on smoking status of 1 million men and
women (black n=25,000) over age 40, screened in 25 states in 1959 for
prospective follow-up (10).
" American Health Foundation data on smoking status by education and
black or white race among 23,953 (black n=3628) men and women in nine U.S.
cities (major east, west, north, south population centers), 1970-75 and
1976-80 (cross-sectional). Seventy percent or more of this population was
over 45 years of age (range 20-80). The population consisted of
hospitalized men and women diagnosed with nontobacco-related conditions
and selected to be age-matched controls of adult cancer cases. Data for
232
the four race-sex groups are presented for each of the two time
periods within two educational categories (high school or less and college
or more) (11).
* Multiple Risk Factor Intervention Trial (MRFIT) data on smoking status
of 348,874 (black n=23,490) men ages 35-57 screened at 22 clinical centers
in 18 U.S. cities during 1973-75 (12).
* MRFIT data on smoking status of 12,866 (black n=931) men ages 35-57
with risk scores in the upper 10-15% of the Framingham distribution who
were screened during 1973-75 and randomized to a specialized intervention
or to control. Smoking status at screening and after intervention
(thiocyanate adjusted) are presented (13).
* Hypertension Detection and Follow-Up Program (HDFP) data on smoking
status by systolic and diastolic blood pressure levels for 59,610 (black
n=18,127) men and women ages 30-69 years screened during 1973-74 in 14 U.S.
communities. Data for each sex-race group are presented for several blood
pressure categories and by medication use with four age categories and
age-adjustment (14).
1.1.2 Black/White Differences in Prevalence of Current and Heavy
Smoking: 1965 - 1982
1.1.2.1 Current Smoking: Men
Age-adjusted national estimates of prevalence of current smokers
indicated an 8-9% higher prevalence of smoking in black compared to white
men (age >=20 years) in 1965, 1976, and 1980--although rates for both black
and white men had declined by approximately 14% (4). The direction of the
difference in smoking rates between black and white men was the same in all
data sources reviewed, i.e., rates for black men were higher than those for
white men. However, the size of the difference varied from 2% in the
American Cancer Society study (10) to 17-18% in college-educated
hospitalized cancer controls (11) and in the HDFP screenees (14).
In the NHIS and NHANES reports (6,7), the size of the black-white
differential in male smoking rates remained relatively constant between
1970 and 1980 (less than 1% change in the difference between the two rates)
(Table S-l). In the hospitalized cancer control population (11) with a
high school education or less, the difference in black and white male
smoking rates increased by 5% (black rates dropped less than white rates).
In contrast, smoking rates in college educated men in this population
showed a 6.5% narrowing of the black/white difference: rates among
college-educated black men dropped more than those of the white men.
Longitudinal data on the MRFIT Usual Care group showed a slight increase in
the black/white difference (from 5.7% to 7.4%) between the time of
screening 1973-75 and follow-up six years later.
233
Table S-l. Selected comparisons of self-reported smoking rates
for black and white men, 1965-1980 (% current smokers in
population subgroup).
REF/ AGE
SOURCE RANGE
1965 | 1971-75 | 1976 | 1976-80 | 1980 |CHANGE
(6) >=20 BM 59.6
NHIS years WM 51.3
50.1
41.0
44.9
37.1
-14.7
-14.2
(7) 25-74 BM
NHANES WM
55
43
50.7
39.6
-4.7
-4.0
(11) 20-80
hospitalized BM
<=high sch WM
>=college BM
WM
59,
47
54
35
55.1
37.8
36.5
25.3
-4.3
-9.7
-15.7
-10.2
(12) 35-57 BM
MRFIT WM
screenees
50.0
35.9
(14) 30-69 BM
HDFP meds WM
49.2
30.6
no meds BM
WM
57.1
39.2
Age-specific
rates in men show
45-65, and higher
to be the highest
higher prevalence
group in data for
difference for 35
changing pattern
tabulations of national probability estimates of smoking
the lowest rates in men over 65, next lowest among men
rates among men 20-44. Rates in 25-34 year-old men tend
Comparison of black and white rates indicate that the
of smoking in black vs. white men is seen in every age
1965, 1976, and 1980. A relatively small black/white
-44 year-old men in 1980 (44.2% vs. 42.2%) may indicate a
for this birth cohort (6).
Age-specific data for blacks but not whites are given in one of the
available NHANES reports (7). Race-specific data from the CDC-BRFS for the
25-44, 45-64, and 65+ age-groups are included in Carter Center Report (8)
as the basis for calculating attributable risks associated with smoking.
These data (see below) do not fit the overall picture indicated by NHIS and
234
NHANES regarding smoking prevalence differences between black and
white men--in either the size of the black/white difference or the
prevalence of smoking in black men over 65 (NHIS 27.9% in 1980 (6) and
NHANES II 26.9 in 1976-80 (7) as compared to 39.2 in the CDC data for 65+
black men.
Table S-2. Percent of current smokers in the NHIS (1980) and
CDC-BRFS (1982) U.S. population samples,
black and white men ages 25 years and over
NHIS CDC
25-34 35-44 45-64 65+ 25-44 45-64 65+
BM 52.0 44.2 48.8 27.9 39.4 38.3 39.2
WM 42.0 42.4 40.6 16.6 37.8 36.5 16.4
At the present writing, two important aspects of the CDC data are
unclear: 1) the socioeconomic distribution of the sample (given that all
respondents were contacted by telephone; and 2) the upper age limit of the
sample compared to NHIS (actually the upper limit of NHIS is unclear; only
NHANES data clearly designate the upper age limit). The definition of
"current smoking" is not likely to differ greatly between surveys.
If the CDC data are comparable to that from NHANES or NHIS, then the
CDC prevalence rates can be interpreted as the more current data as
compared to the pre-1981 estimates from the other two sources. As
indicated above, with the exception of black males over 65 years, the CDC
rates are lower than those reported for men of similar ages in 1980. Thus,
the CDC rates are plausible as evidence of a continued decline in smoking
rates in both races and a narrowing of the gap between black and white men
under age 65. The high rate of smoking in black men over age 65 in the CDC
data is difficult to interpret. The possible limitations of the CDC data
should be kept in mind when evaluating the attributable risk calculations,
presented later in this section, which are based on these smoking
prevalence rates.
1.1.2.2 Heavy Smoking : Men
NHIS age-adjusted estimates of the percent of adult smokers (age >=20
years) who smoke 25 or more cigarettes per day show an increase between
1965 and 1980 in both black and white males. The prevalence of heavy
smoking is substantially higher among white men compared to black men and
the increase in heavy smoking rates between 1965 and 1980 is steeper for
white men (Table S-3).
235
Table S-3. Percentages of smokers or population sub-group
smoking 25 or more cigarettes per day, black and
white men, 1965-1980.
REF/ AGE | 1965 | 1971-75 | 1976 | 1976-80 | 1980 |CHANGE
SOURCE RANGE | | | I
(6) >=20 BM 8, .6 10, .8 13.8 +5.8
NHIS * WM 26 .0 33, .3 37.3 +11.3
(7) 25-74 BM 7.5 8.5 +1.0
NHANES # WM 16.9 16.6 -0.3
(7a) 35-74 BM 5.6 9.6 +4.0
NHANES// (12) 35-57 WM BM 17.1 18.5 17.5 +0.4
MRFIT WM 26.9
screenees
% of current smokers
# % of population subgroup
NHANES estimates of heavy smoking in the 25-74 year-old population
--expressed per 100 population (% of population subgroup rather than as a
proportion of smokers only)--indicate no appreciable change in the
proportion of heavy smokers in the population. Thus, the increase in the
percent of heavy smoking in men appears to be relative to the overall
decline in the number of smokers. The decline in smoking among men has
been among light (<15 cigarettes per day) and moderate (15-24 cigarettes
per day) smokers. The NHANES estimates of heavy smoking in the 35-74 year
old segment of the population do suggest an increase in the number of black
men who are heavy smokers. Smoking rates in this age-group of men declined
only slightly (48.7% to 46.5% from 1971-75 to 1976-80) (7a).
Age-specific data indicate that 35-64 year-old smokers are more likely
to be heavy smokers than the other age-groups among both black and white
men (6). Among white men, all age-groups of smokers showed a consistent
increase in the percent of heavy smokers between 1965 and 1980, with the
steepest rise in the 35-44 year-old age-group. Among black male smokers,
although no age-groups show a decline in rates, the age-specific picture of
changes in heavy smoking among black men is much less consistent than for
whites and is complicated by inadequate cell sizes for stable estimates in
the 20-24 and 65+ year age-groups in 1965 and 1976. The age-adjusted
236
cross-sectional data are probably misleading as to trends in heavy
smoking for any age-group or birth cohort of black men. In the NHANES data
which do give estimates for all decades between 25 and 74, 25-34 year-olds
show a 7% decrease while 35-44 and 55-64 year-olds show 8 and 7% increases.
1.1.2.3 Current Smoking: Women
With the exception of MRFIT, all of the data sources described include
data for women. Smoking patterns for women are very different from those
of men. Rates are lower, time trends are different, and consistent
black-white differentials are not observed.
Data collected before 1970 (6,10) and after 1976 indicate an equivalent
or slightly lower prevalence of smoking in black vs. white women (6,7,11)
(Table S-4). Between 1971 and 1976 the prevalence of smoking in black
women was higher in all samples examined (6,7,11,14). Smoking rates of
black women have decreased to a greater extent than those of white women
since 1976 in the NHIS and NHANES samples and in both the lower and higher
educated segments of the American Health Foundation population of
hospitalized cancer controls (11).
Table S-4. Selected comparisons of self-reported smoking rates
for black and white women, 1965-1980 (% current
smokers in population subgroup).
REF/
SOURCE
AGE
RANGE
| 1965 | 1971-75 | 1976 | 1976-80 | 1980 |CHANGE
(6) >=20 BF 32.7
NHIS WF 34.5
34.7
32.4
30.6 -2.1
30.0 -4.5
(7) 25-74 BF
NHANES WF
46.2
34.0
31.6
33.0
-14.6
- 1.0
(11) 20-80
hospitalized BF
<=high sch WF
>=college BF
WF
39.3
33.1
42.3
34.1
25.0 -14.3
28.0 - 5.1
26.5 -15.8
28.9 - 5.2
(14)
HDFP
30-69 BF
meds WF
29.8
23.8
no meds BF
WF
38.6
33.8
237
The age-specific data for women indicate substantially lower prevalence
of smoking in women age 65 years and older compared with younger women (6).
The percent of current smokers among white women (but not for black women)
age 65 years and over increased sharply between 1965 and 1980. NHANES
data, which separate 45-54 and 55-64 year-old women, show a substantial
.break towards lower smoking prevalence rates in black women over age 55
years.
CDC and NHIS age-specific data on smoking prevalence in women are shown
in Table S-5. As seen in the data for men, CDC rates are lower and may be
evidence of a continuing downward trend. No striking black/white
differences in prevalence are evident in either data set. If the data sets
are comparable, then smoking trends in black and white women age 65 years
and over are changing: rates in black women in this age-group may be
increasing and those in this age-group of whites decreasing.
Table S-5. Percent of current smokers in the NHIS (1980) and
CDC-BRFS (1982) national probability samples,
black and white women ages 25 and over
NHIS CDC
25-34 35-44 45-64 65+ 25-44 45-64 65+
BF 34.2 36.5 34.3 9.4 30.8 24.4 13.6
WF 31.6 35.6 30.6 17.4 33.4 31.3 11.2
1.1.2.4 Heavy Smoking: Women
Black/white differences in the prevalence of heavy smoking are
evident among women and are of the same nature as those observed for men.
Substantially more white than black women smokers report use of 25 or more
cigarettes per day. The percentage of heavy smokers among white women
smokers increased to the same extent as for white men in the NHIS data for
1965-80. A much lesser increase was observed in black women over these
three surveys. NHANES estimates of the percentage of heavy smokers among
25-74 year-old women do not show an appreciable change for either black or
white women (see Table S-6).
238
Table S-6. Percentages of smokers or population sub-group
smoking 25 or more cigarettes per day, black and
white women, 1965-1980.
REF/ AGE | 1965 | 1971-75 | 1976 | 1976-80 | 1980 |CHANGE
SOURCE RANGE | | | | | I
(6) >=20 BF 4, ,6 5, .6 8.6 + 4.0
NHIS * WF 13, .9 20 .9 25.2 +11.3
(7) 25-74 BF 3.0 3.9 +0.9
NHANES # WF 7.4 8.6 +1.2
(7a) 35-74 BF 1.1 3.5 +2.4
NHANES# WF 6.0 8.2 +2.2
* % of current smokers # % of population subgroup
Age-specific data for heavy smoking among women indicate that women
smokers age 20 or less or over age 65 are least likely to fall into the
heavy smoking category (6). The increase in percent of white women smokers
who are heavy smokers between 1965 and 1980 is seen consistently in each
age-group of white women (6). Trends across surveys cannot be evaluated in
the NHIS data for black women heavy smokers due to inadequate numbers in
several categories. NHANES age-group-specific percentages of heavy smokers
are available for black women ages 25-54 for 1971-75 and ages 25-74 for
1976-80 (7). Apparent differences in smoking trends of different birth
cohorts render general statements about time trends in heavy smoking among
black women misleading—a situation similar to that observed in the heavy
smoking data for black men.
1.2 Impact
1.2.1 Data Sources
Four sources for estimates of the impact of smoking on coronary heart
disease in nationally-based samples were identified:
* The American Cancer Society prospective study (10) presents CHD
mortality ratios for black men and women. Mortality ratios for blacks were
calculated using deaths for whites in the comparable sex-age-group (5 year
age-group at entry) as the denominator of "expected" deaths and deaths
observed in blacks as the numerator. Actual death rates are not presented.
Dose-response effects of smoking were examined by calculating the ratio of
deaths for each of three smoking categories to deaths among nonsmokers,
within race. Mortality ratios of black smokers with and without a history
239
of disease were also presented, using rates for white nonsmokers
with no major disease history as the expected rates. The analysis is based
on 642 and 487 CHD deaths in 22,000 black males and females 40 years and
older during a 12 year period of follow-up between 1960 and 1972. Smoking
categories were: never smoked, 1-9, 10-13, and 20+ cigarettes per day.
CHD was defined by ICD-7 420.0, 420.1 and 420.2.
* Kleinman, Feldman, and Monk (National Center for Health Statistics)
estimated the extent to which the 20% decline in smoking between 1965 and
1976 could account for the decrease in CHD mortality for men and women
35-64 years old during the same time period (3). NHIS population
percentages in 4 smoking categories were used to estimate expected percent
change in CHD death rates by each of four dose-response models and for each
of four risk models. Smoking categories were: 0, <15, 15-24, and >=25
cigarettes per day--recognizing that the larger percentage of former
smokers in the nonsmoking category in 1976 vs. 1965 would lead to some
degree of overestimation of effects. The dose-response models were:
constant risk at any dose; logarithmic (risk increases rapidly in the lower
dose range and then levels off); linear (similar increase in risk with each
additional cigarette); and exponential (higher risk associated with each
additional cigarette). Risk models were derived from the Veterans',
American Cancer Society, British Physicians, and Framingham studies. CHD
was defined by ICD-8 codes 410-413 (1968) extrapolating backwards to cover
1965, 1966, and 1967.
" Five year cerebrovascular, CHD, CVD and all-cause mortality (6018
deaths) among 23,940 black and 325,384 white male MRFIT screenees (12) was
subjected to logistic regression analyses to determine associations with
several risk factors, including cigarette smoking. CVD was defined by
ICD-9 codes 390-459; CHD by codes 410 to 414; cerebrovascular disease by
codes 430-438. Smoking categories were: nonsmokers, 1-15, 16-25, 26-35 or
>35 cigarettes per day at the time of screening.
* The Carter Center Report includes estimates of the CHD deaths, years
of life lost due to CHD death, and CHD cases attributable to smoking in the
U.S. population and the proportion of CHD deaths and cases in persons 25
years or older that could be prevented if cigarette smoking were eliminated
(8). Cigarette smoking is defined by the CDC 1982 data on percent of
current smokers, described earlier. Population attributable risk estimates
were derived from the Risk Factor Update Project logistic regression
equation (Breslow et al., cited in 8). This equation is similar to the
Framingham equation but is based on pooled equations for several major CVD
studies and permits estimates for blacks and whites. CHD death was defined
by ICDA codes 410-414 using 1980 death rates.
Each of these analyses carries several assumptions and can only be
interpreted in light of the risk model, morbidity and mortality data, and
risk factor patterns which apply. For example, the MRFIT and Carter Center
analyses of smoking effects hold several competing risk factors, and some
risk factor interactions constant. The American Cancer Society and NCHS
analyses do not. The ACS and MRFIT populations are volunteers for health
risk-related studies and are prospective. Both the NCHS (3) and Carter
240
Center (8) reports provide smoking risk estimates for the U.S.
population but they use smoking prevalence data from two different and not
necessarily comparable data bases.
1.2.2 Findings
The American Cancer Society study (10) demonstrates a significantly
higher risk of 12-year CHD mortality among black men and women smokers
under age 65, compared to white men and women nonsmokers in the same age
range at entry. Higher CHD mortality associated with smoking was seen in
black men and women both with and without a major disease history. The
prevalence of smoking was somewhat higher in white men than black men,
consistent with the higher CHD mortality among the white men (i.e., the
black-white CHD mortality ratio was less than one for men in all age
groups). However, certain characteristics of the study sample suggest that
it was not representative of blacks in the general population. For
example, the prevalence of smoking was lower among black men compared to
white men in this sample and the prevalence of major disease was not
substantially greater in the black men, as might have been expected. The
sample was geographically broad, but consisted of friends, relatives, and
neighbors of ACS volunteers. The authors point out that educational levels
in the sample are higher than those reported in census figures and that
inner city persons are underrepresented.
CHD mortality among black women was greater than for white women for
women ages 40 through 59 at entry. Somewhat more white women than black
women smoked and were heavy smokers. The prevalence of major disease, as
defined in this study, was 12% higher among the black women (32% vs. 20%).
More of the black women were 30% or more overweight (17% vs. 4%).
The MRFIT screenee population (12) is probably healthier than average
due both to the use of employment sites for screening and to the fact that
the highest risk men have been excluded due to enrollment in the randomized
trial. Individual effects of smoking are considered, i.e., after
adjustment for other risk categories (age, serum cholesterol concentration,
diastolic blood pressure level). Smoking is more prevalent in the black
men, but they are less heavy smokers. Smoking was associated with a
significant, similar excess risk of CHD in black and white men in this
population. This association was not dependent on the presence of heart
attack or diabetes; removal of such men from the analysis did not alter the
result.
Dose response effects of smoking on CHD mortality were positive and
generally similar in blacks and whites, allowing for some instability of
cause-specific mortality rates among the relatively small numbers
contributing to rates for black men in the heavy smoking categories. CHD
mortality was higher in smokers than nonsmokers among black men with and
without hypertension and with and without elevated serum cholesterol.
Kleinman et al. (3) determined the percentage decline in CHD deaths
for 35-64 year-olds in the U.S. population between 1965 and 1976 which
could be attributed to a decline in smoking over the same period.
241
Estimates are only presented for men, since smoking rates for women did not
decline significantly in the time period addressed.
Although four models are used to calculate expected decline in deaths
associated with changes in smoking patterns, estimates based on the
"constant risk" model lend themselves to the most straightforward
interpretation. Estimates with this model are based simply on the
percentage of current smokers, without regard to average number of
cigarettes smoked. In black males, changes in smoking prevalence could
account for 23, 23, and 21 percent of the CHD mortality decline for the
35-44, 45-54 and 55-64 year-old age-groups, respectively. Comparison
percentages for white males were 40, 50, and 16%. Thus, changes in smoking
had less of an impact on the decline in CHD mortality in black as compared
to white men 35-54 and slightly more of an impact in black men 55-64 years
old. Results based on the other risk models, which take the number of
cigarettes smoked into account, show similar results. The factors other
than smoking which contributed differentially to the decline in CHD
mortality among black and white men are uncertain.
The Carter Center Report (8) provides estimates of the number and
percent of CHD deaths and cases which would theoretically be eliminated if
smoking prevalence were reduced to zero. These estimates are conservative
in that they assume that no other risk factors would change in a favorable
direction. The CDC-based smoking prevalence data used in these
calculations are in Tables S-2 and S-5. In general, the population
attributable risk estimates (8, Table 17) closely parallel the prevalence
data and to that extent show a high black-white ratio only among men over
age 65, for whom the CDC data show a questionably high prevalence rate.
For both white and black men between 25 and 65, smoking-related preventable
CHD deaths are estimated at 33 to 37% of total CHD deaths. For CHD cases,
percentages of preventable events are approximately 10% lower. A higher
proportion of preventable black compared to white male CHD cases is
suggested in the 45-64 year age-group as well as in men 65 years and over.
(Note, the picture for smoking-related preventable cerebrovascular disease
deaths is quite similar to that for CHD in this analysis, except that
estimates of preventable cases among 45-64 men are the same for blacks and
whites.)
Other "CHD impact" variables analyzed were proportional number of cases
and deaths attributable to smoking, years of life lost, number of hospital
and restricted activity days and medical costs which can be attributed to
smoking. These estimates are summarized in Table S-7 for men.
242
Table S-7 Population attributable risk fractions for smoking
for several CHD variables in non-white and white
men: estimates for the U.S. population (8)
Table No Variable Non-white White
(percent of cases)
23 CHD deaths 33 21
24 CHD-related lost yrs. of life 35 34
25 CHD cases 28 17
26 CHD-related hospital days 27 16
27 CHD-related days of rest, activ. 28 17
28 CHD-related medical expend. 27 16
All of these estimates show a proportionately greater impact on CHD of
smoking in non-white compared to white men, with the exception of years of
life lost.
Estimates of the percent of CHD deaths in women that would be
prevented if smoking in women were eliminated show a much lesser impact
than in men, but very similar within-age percentages in black and white
women: BW - 8.2, 6.7, and 3.7 % in the 25-44, 45-64 and 65+ age-groups,
respectively; 8.8, 8.3, and 3.1% in white women. Referring back to the CDC
prevalence data in Table S-5, the impact of smoking elimination in women is
about a third of the prevalence of smoking, whereas in men the impact was
approximately equal to the smoking prevalence. Data for women for the
other CHD variables are summarized in Table S-8. Smoking attributable CHD
risks in women are much lower than those for men and there are no racial
differences. As pointed out in the Carter Center report, the impact is
least for deaths and higher for variables which reflect the relatively
young age of occurrence of smoking related CHD deaths and cases.
Table S-8. Population attributable risk fractions for smoking
for several CHD variables in non-white and white
women: estimates for the U.S. population (8)
Table No Variable Non-white White
(percent of cases)
23 CHD deaths 4 4
24 CHD-related lost yrs. of life 7 8
25 CHD cases 12 10
26 CHD-related hospital days 10 9
27 CHD-related days of rest, activ. 12 10
28 CHD-related medical expend. 10 10
243
Confidence in the estimates for the 65+ age male population is limited
by the departure of smoking prevalence figures in black men from the
pattern usually seen in the 65+ age-group. In men 25-64, based on data
indicating roughly equivalent smoking prevalence in black and white men,
the theoretical benefits of eliminating smoking in blacks are substantial.
The population impact of smoking on CHD morbidity and mortality in black
men may be slightly greater than for white men in the 45-64 age-group.
Smoking has a lesser impact on CHD in women compared to men. When
risks associated with smoking alone are considered, CHD impact is not
different in black compared to white women. However, smoking enhances a
more unfavorable multivariate risk picture for blacks than for whites.
1.3 Implications
That the basic association between smoking and CHD holds for blacks as
well as whites is apparent from the studies available, although the degree
of risk appears to be somewhat less in black compared to white men, and
similar in black and white women.
The dynamic state of population smoking behaviors over time and the
substantial changes in IHD risk that occur with smoking cessation severely
limit the utility of cross-sectional data. In addition, the sampling
approach once appropriate to descriptions of the U.S. population is
outdated. Since race has been recognized as an important proxy health
variable, sampling approaches should be designed to permit racial subgroup
comparisons as well as descriptions of U.S. population parameters in the
aggregate. Such sampling should include awareness of the need to partition
race and socioeconomic status effects.
For example, the extent of socioeconomic differences among blacks is
demonstrated in the hospitalized cancer control data from the American
Health Foundation (11): both high school and college educated black men
smoked more than white men, in both time periods studied (see Table S-l).
However, the decrease in smoking prevalence among college educated black
men was more than three times that in high school educated black men and
nearly 60% greater than that in college educated white. Data aggregated on
either educational level or race would not convey this difference, but the
difference has important implications for intervention and provides
important clues to patterns which might be hidden in longitudinal data
which classify blacks and whites only on smoking status at entry.
The longitudinal data available are outdated in terms of the current
smoking prevalence and, as implied above, in terms of the actual smoking
status of persons initially classified as smokers during the year or months
immediately prior to fatal or morbid events.
Consideration of potential benefits of intervening on smoking in black
men and women should include the relative likelihood of success per unit of
effort compared to the other risk reduction possibilities. Only minimal
literature was identified relating to perspectives for intervention on
smoking in the black population. NCHS data indicate that in 1978, black
244
men and women, although lighter smokers, are more likely to smoke
cigarettes with high tar and nicotine content, that fewer blacks are
successful when they attempt to stop smoking although more blacks had tried
to quit at some time (2). Sex difference in attempts to stop smoking were
more pronounced in blacks than whites. Similar percentages of men and
women had stopped smoking or attempting to in the year prior to interview
(28.5 and 31.5%). Among black men and women, substantially more women than
men had attempted to quit (44.2% vs. 34.1%).
In the MRFIT randomized trial, thiocyanate-adjusted percentages of
black and white men in the special intervention group who had stopped
smoking at each annual visit were quite similar (13, Table 8). It is
interesting to note that the unadjusted percentages among the black men
were 6 to 15% higher than those of whites before adjustment, implying that
reporting bias may have been greater in the black men. However, the
success at smoking cessation in the special intervention group of black men
was equal to that of whites (35.9 and 35.5 of white and black special
intervention men stopped smoking). Both blacks and whites in the usual
care group were less successful in smoking cessation, and whites did
somewhat better than blacks (22.2 vs. 18.9% stopped smoking).
A study of factors influencing trial and adoption of smoking among
children and adolescents (ages 8-17) in Bogalusa, Louisiana reported
significant race and sex differences in the social learning which leads to
eventual smoking (15). The number of "smoking models" in the child's
environment was found to predict whether a child would try smoking, but the
pattern of influence was different in black compared to white children.
1.4 Recommendation
A broader base of short-range prevalence and trend data on smoking
behaviors in blacks is needed, followed by specialized interventions to
accomplish permanent smoking cessation in blacks. Although smoking
cessation may be associated with some weight gain, there will still be a
net benefit of the smoking cessation. Smoking differentials between blacks
and whites do not parallel morbidity-mortality patterns. However, smoking
is a risk factor for both CHD and for cancer. The need to reduce smoking
prevalence among blacks should not be neglected.
245
1.5
References
1. Bonham, GS. Use habits of cigarettes, coffee, aspirin,
and sleeping pills, United States, 1976. Vital and health
statistics. Series 10. Data from the National Health Survey;
No. 131. DHEW Publication No. (PHS) 80-1559). October
1979.
2. Moss AJ. Changes in cigarette smoking and current smoking
practices among adults. United States, 1978. National
Center for Health Statistics. Advancedata. No. 52. September
19, 1979.
3. Kleinman JC, Feldman JJ, Monk MA. The effects of changes
in smoking habits on coronary heart disease mortality.
Am J Pub Health 1979;69:795-800.
4. Schoenborn CA, Danchik KM. Health practices among adults,
United States, 1977. National Center for Health Statistics.
Advancedata No. 64. November 4, 1980.
5. National Center for Health Statistics. Health United States
1980, Tables 27 (pp 162-63) and 28 (pp 164-65). DHHS Pub. No.
(PHS) 81-1232. Public Health Service. Washington.
U.S. Government Printing Office, Dec. 1980.
6. National Center for Health Statistics. Health United States,
1983, Tables 30 (pp. 129-130) and 31 (pp. 131-132). DHHS
Pub. No. (PHS) 84-1232. Public Health Service. Washington.
U.S. Government Printing Office, Dec. 1983.
7. Rowland MB, Fullwood R. Coronary heart disease risk
factor trends in blacks between the first and second National
Health and Nutrition Examination Surveys, United States,
1971-1980. Am Heart J 1984;108:771-778.
7a. Rowland M, Fulwood R, Kleinman JC. Changes in heart disease
risk factors, in reference 7, pp. 13-17.
8. Haynes SG, White CC, Tolsma D, Newman JM, McGee D. Closing
the gap for cardiovascular disease. Carter Center Report
August 27, 1984 (unpublished manuscript courtesy of Dr. Haynes)
Table 16.
9. Bradstock MK, Marks JS, Forman M, Gentry EM, Hagelin GC,
Trowbridge FL. Behavioral risk factor surveillance. 1981-83.
MMWR 1984;33:lss-4ss. (reference on methodology of CDC Survey)
10. Garfinkel L. Cigarette smoking and coronary heart disease
in blacks. Comparison to whites in a prospective study.
Am Heart J 1984;108:802-806.
246
11. Covey LS, Mushinski MH, Wynder EL. Smoking habits in a
hospitalized population. Am J Pub Health 1983;73:1293-1297.
12. Neaton JD, Kuller LH, Wentworth D, Borhani NO. Total and
cardiovascular mortality in relation to cigarette smoking,
serum cholesterol concentration, and diastolic blood pressure
among black and white males followed up for five years.
Am Heart J;1984;108:759-770.
13. Connett JE, Stamler J. Responses of black and white men
to the special intervention program of the Multiple Risk
Factor Intervention Trial (MRFIT) Am Heart J 1984;108:
839-850.
14. Hypertension Detection and Follow-up Program. Baseline
characteristics of the enumerated, screened, and hypertensive
participants. The Hypertension Detection and Follow-Up
Program Cooperative Group. Hypertension 1983;5:IV-1 - IV-295.
15. Hunter SM, Baugh JG, Webber LS, Sklov MC, Berenson GS.
Social learning effects on trial and adoption of cigarette
smoking in children. The Bogalusa Heart Study. Prev. Med.
1982;11:29-42.
247
2.0 CHOLESTEROL
2.1 Data sources
The adequacy of the available data on cholesterol levels in black men
and women is markedly influenced by the increasing interest in lipoprotein
cholesterol components rather than total cholesterol. In particular,
high-density lipoprotein cholesterol has been the focus of considerable
recent interest both as a possible protective factor against IHD and as one
for which black persons may have an advantage relative to their white
age-sex peers (1-4).
For total cholesterol, the Health Examination Survey (NHES, 1960-62)
and National Health and Nutrition Examination Survey (NHANES I 1971-74 and
NHANES II 1976-80) provide national probability estimates of distributions
and means by age, sex, and race for black and white children and adults
(5-7,9). Analyses of 1971-74 serum cholesterol levels by socioeconomic
characteristics have also been published (8). The NHES and NHANES data
provide representative estimates of mean serum cholesterol levels and the
prevalence of elevated cholesterol (using arbitrary cut points) for the
time periods they cover and can, to some extent, be used to evaluate
changes in the cholesterol levels of blacks and whites over time.
Cycle II of the National Health and Nutrition Examination Survey will
provide data on 1976-80 levels of high-density lipoprotein cholesterol
(HDL) for a national probability sample of U.S. black and white men and
women ages 20-74. Estimates of mean HDL levels for race-sex groups in 6
age categories have been made. However, release of these data has been
delayed due to a need to resolve methodological issues which influence
interpretation of NHANES HDL values relative to published values from other
large studies. These issues are currently being evaluated by the National
Center for Health Statistics and the National Heart, Lung, and Blood
Institute.
For the purposes of this report to the Task Force on Black and Minority
Health, Robert Murphy, Director of the NCHS Division of Health Examination
Statistics, has authorized inclusion of certain provisional statements on
black-white differences in mean HDL levels. These statements, included
under "Findings" (section 2.2), were provided by Robinson Fulwood, Health
Statistician (communication to Shiriki Kumanyika), with certain caveats.
Sample sizes for the NHANES II HDL values in blacks are small. Numbers of
intended and actual HDL values in each age-group of black men and women are
given in Table C-l.
248
Table C-l. Sample sizes for estimates of HDL values in black
men and women ages 20-74, United States 1976-80.
Black Men Black Women
Age Group Intended" Actual// Intended* Actual//
20-24 79 65 94 77
25-34 139 110 145 116
35-44 70 53 103 81
45-54 62 45 100 79
55-64 129 91 135 98
65-74 128 92 152 115
Total 607 456 729 566
* Intended = number of respondents for whom total cholesterol was determined
# Actual = number of respondents for whom an adequate quantity of blood
remained after determinations of total cholesterol and trigylcerides to
permit determination of HDL-cholesterol as well
For whites, HDL values are available for approximately 3800 men and 4300
women. The smallest sample in any age-group for white men is 472 (581
intended); for white women 506 (624 intended).
The sample sizes for blacks are adequate for stable estimation of mean
HDL cholesterol levels in each sex-age-group according to the criteria
applied by the Division of Health Examination Statistics. However, most of
the age-sex samples of HDL values for blacks do not meet optimum criteria
for estimation of standard errors. Thus tests of statistical significance
of black-white differences must be interpreted cautiously. All of the
sample sizes meet the criterion of a minimum of 25 for standard error
estimation. However, only two of the groups (25-34 year-old black men and
65-74 year-old black women) in the total cholesterol data (i.e., the
numbers shown in Table C-l as "intended") met a second criterion of having
observations in both of the paired probability sampling units for at least
12 of the 32 pseudostrata. Since the first criterion is met in the HDL
data, standard errors will be published, but with asterisks indicating that
full confidence can not necessarily be placed in the starred standard error
values or in related statistical tests.
In this summary for the Task Force, emphasis has been given to
published studies which present data comparing lipoprotein rather than only
total cholesterol levels in blacks and whites, and primarily in the adult
population at IHD risk. (If needed for reference, HDL comparisons in black
and white neonates, preschool, school-age and adolescent children are
summarized in a 1984 review by Glueck et al.(2)). Studies associating
either total or HDL cholesterol with IHD risk have also been reviewed.
249
Data sources identified in addition to the NCHS population estimates
can be categorized according to the relevant issues, as follows:
a) comparisons of lipoprotein cholesterol levels in black
and white men, women, or families (4,11-18);
b) cholesterol comparisons between blacks and whites where
the socioeconomic status of the black and white subjects
is considered (4,11,13,14,17,19,33);
c) studies related to possible explanations for HDL differences
in blacks and whites, including data on lipoprotein cholesterol
in Caribbean and African blacks (4,20-27);
d) data comparing the effectiveness of dietary intervention
on cholesterol levels in blacks and whites (28,29);
e) estimates of the relative impact of. elevated serum cholesterol
on IHD risk in blacks compared to whites (30-32).
The ascertainment of cholesterol levels is not equivalent across
studies. Methodological differences include whether or not subjects had
fasted before blood was drawn, whether cholesterol was measured in plasma
or serum, whether samples were frozen before analysis and, if so, the time
and conditions of storage, and analytic procedures. Although the effect of
these factors on cholesterol determinations is not large, the small
differences introduced complicate the interpretation of small differences
in group means which, if real, may have important risk implications. Thus,
comparisons across studies are made here only with reference to the
relative consistency of racial differences observed in different data sets.
2.2. Findings
2.2.1 Total and lipoprotein cholesterol comparison among
black and white men
2.2.1.1 Total cholesterol: men
Representative national data permitting comparisons of total
cholesterol levels between black and white men within the three time
periods of the NCHS examination surveys are shown in Table C-2. Data from
the NHES are not strictly comparable with the NHANES data(6). However,
comparison of cholesterol distributions in NHANES I and II is appropriate
for estimation of time trends.
250
Table C-2. Age-specific comparisons of mean serum cholesterol
in national probability samples of U.S. black and
white men in three time periods between 1960 and
1980.
NHES NHANES I NHANES II
1960-62* 1971-75// 1976-80!
( mgms per deciliter )
AGE BM WM BM WM BM WM
25-34 195.0 207.1 214.2 209.9
35-44 217.2 228.1 224.7 231.5 207.1 206.8
45-54 226.6 231.4 237.1 239.9
55-64 229.5 233.6 243.8 239.9 227.8 228.4
65-74 224.0 229.9 237.3 236.4 217.5 221.8
age 210.5 218.8** 225.7 217.5!! 215.4 216.7!!
adjusted
* Ref 5, Table 6
** for ages 18-74; age-adjusted estimates not published for
25-74 year-old adults
// age-specific data for 1971-74, from ref 6, table 4
! ref 30, table 15a; data for ages <65 grouped by 20 year spans
!! age-adjusted data for 25-74 year-olds taken from ref 9, table VI
In 1960-62, age-specific and overall serum cholesterol levels of black
men were consistently less than those of white men. Age-specific data for
1971-75 and 1976-80 do not show consistent black-white differences. The
data in Table C-3 indicate a decrease in the prevalence of elevated serum
cholesterol in black men between 1971-75 and 1976-80 but this decrease was
not statistically significant. The prevalence of elevated serum cholesterol
was eight percent higher in black than white men in 1971-75, decreased to
3% higher in 1976-80. The largest decrease in cholesterol levels among
black men was among men 55 or older.
251
Table C-3. Prevalence of Serum Cholesterol >260 mg/dl in
black and white men, 1971-75 and 1976-80: age
specific rates for black men ages 25-74; age-
adjusted rates for black and white men ages 25-74.
NHANES I 1971-75 NHANES II 1976-80
rate per 100 population
AGE Black Men
25-34* 10.9 9.3
35-44 24.3 23.6
45-54 28.7 25.3
55-64 32.3 24.2
65-74 28.0 18.7
25-74// BM:23.2 WM:15.3 BM: 19.3 WM:16.3
* Ref 9, Table IV // Ref 9, Table V
A consistent socioeconomic influence on cholesterol in black men has
not been reported. • An NCHS analysis of cholesterol levels in 1971-74 (8)
suggests that the impression of socioeconomic effects is related to the SES
variable used. Cholesterol levels in men tended to increase with
increasing levels of annual family income. An inverse effect of education
on serum cholesterol levels was observed in white but not black men.
A discrepancy in SES effects on cholesterol in black and white men was
observed in a MRFIT screenee population in California (33). The prevalence
of elevated cholesterol (defined as >= 260 mg/dl) among white men was lower
at higher SES levels, using categories of a 77 point education-occupation
scale as the SES measure. Cholesterol levels of the black screenees were
different at different SES levels, but the direction of these differences
was not consistent (33). There were noteworthy black-white differences in
the prevalence of elevated serum cholesterol in two of the six SES
categories (lowest and second highest categories; prevalence higher in
whites in both groups). Prevalence rates in the other categories were
similar (33, Table 3). The pattern seen may have been somewhat affected by
differing distributions of the black and white men within the 35-57 year
age range (52% of black men vs. 61% of white men were 45-57 years old).
Total cholesterol levels of the black men in the Framingham Minority
Study population were lower than those of the white men in every age-group
studied (age range 20-69) and the age-adjusted means in black and white men
were significantly different (11). In this sample, 56% of black compared
to 44% of white men under age 50 were college-educated. Sixty-four percent
of black compared to 22% of white men over age 50 were college-educated.
252
2.2.1.2 Lipoprotein cholesterol: men
HDL levels are consistently higher in black men than in white men in the
20-74 year-old cross-section of NHANES II respondents. The size of the
differences is relatively similar in the age-groups between 20 and 54
(7,6,8,and 6 mg/dl in each successive age-group). Levels in white men are
the same at ages 55-64 and 65-74, but levels in black men are higher in the
55-64 year-olds than in younger or older black men. Thus the black-white
difference is highest in the 55-64 year age-group (10 mg per dl). The
difference in 65-74 year-old men is 6 mg/dl, similar to that seen before
age 55. The statistical significance of these differences has not yet been
tested. The relationship of the HDL distributions to the respective total
cholesterol distributions should be considered in interpreting these HDL
data.
As summarized by Glueck et al. (2), studies in black and white male
children and adults suggest that HDL levels in black males are higher than
those of whites from early childhood on and that the size of the difference
increases after maturation. Maturational changes in lipid profiles occur
in males of both races (decline in HDL, increases in low-density
lipoprotein (LDL) cholesterol and triglycerides) but appear to follow a
less atherogenic course in black vs. white males.
The Evans County Heart Study investigators compared HDL and LDL
cholesterol levels of 110 randomly-selected black men with those of white
men individually matched on age and total cholesterol level (17). Men with
evidence of CHD were excluded. With total cholesterol levels held constant
(by matching) mean HDL cholesterol levels were significantly higher in the
black men (by 11 mg/dl) and LDL cholesterol levels significantly lower (by
6 mg/dl). The differences were not statistically explained by occupation,
education, social class, or smoking habits but were to some extent
explained by body mass differences between the black and white men.
Consistency of these differences across age cannot be determined due to the
age-matching analytical approach. HDL and LDL cholesterol levels of black
and white men in the upper fertile of the Quetelet index were not different
(17, Figure 8).
More recent studies in the Evans County population further specify
apolipoprotein differences between black and white men (4). Apo A-I levels
were significantly higher and Apo C-II significantly lower in black than
in white men, suggesting that black men in Evans County have a greater
proportion of the (lighter, cholesterol-rich) HDL-2 subfraction. Alcohol
consumption rather than race was a significant variable in levels of Apo
A-II. The differences in levels of Apo C-II but not Apo A-I were still
statistically significant after adjustment for age, Quetelet index,
smoking, and alcohol consumption.
The Lipid Research Clinics (LRC) Program has contributed several studies
which consistently indicate a more favorable lipid profile in black
compared to white men (the LRC protocol excludes men using antidiabetic,
antiuricemic, antihypertensive, or lipid lowering medications). The
Cincinnati LRC Population Study compared lipoprotein cholesterol levels of
253
43 pairs of black and white men, ages 20 to 60, matched on age and total
plasma cholesterol. HDL levels were significantly higher and LDL/HDL
ratios significantly lower in black men (15). A substudy in 9 pairs of
hypercholesterolemic men (total plasma cholesterol >250 mg/dl) yielded the
same results (15).
The Princeton School District Study of the Cincinnati LRC compared HDL
and LDL levels in black and white men ages 20-59. This study also
indicated significant racial differences (higher HDL and lower LDL in black
men) (12). Age-group (20-39 or 40-59) did not affect relative HDL and LDL
levels, although total plasma cholesterol was higher in the older men. A
study of socioeconomic factors and CHD risk in the same population
indicated that HDL and LDL differences between blacks and whites remain
after adjustment for education and occupation (13).
Black-white differences in cholesterol in men age 20-44 years were
analyzed in pooled screening data from five LRC centers (14). Higher HDL
and lower LDL were observed for black men when the distributions of these
variables were compared by pooling across age with covariance adjustment
for age, total cholesterol, and Quetelet Index. Similar differences were
observed when comparisons were made between pairs of black and white men
matched for age and total cholesterol. Stepwise covariance adjustment for
possible confounding factors indicated that with age and total cholesterol
effects statistically removed, Quetelet index had a small negative
confounding effect on black-white differences in HDL-cholesterol levels
(i.e., the difference increased from 8.3 to 9.5 mg/dl when Quetelet index
was added as a covariate). Triglycerides had a positive confounding effect
(the difference decreased from 9.5 to 7.9 mg/dl with the further addition
of triglycerides to the equation).
In a collaborative LRC report combining data on men ages 20-79 from
ten study centers, a greater proportion (17% vs. 3%) of black men than
white men with high total cholesterol were of the hyperalpha type (16).
This was found using either of two definitions of hypercholesterolemia
(race-age-sex specific 95th percentile or an age-specific cut point).
Although the reported black-white differences in HDL and LDL levels
were not statistically explained by socioeconomic status variables in the
above studies, the limited range of socioeconomic status among black
subjects may give an incomplete picture on this point. Black men in the
Evans County cohort were of low socioeconomic status whereas the white
subjects include both low and high SES persons (32). In the Cincinnati
Princeton School District Study (13), some black households were in the
highest education and income categories but the numbers of these were too
small to permit stratum specific comparisons. Thus, although an overall
black-white difference may still remain after differences in the
black-white SES distribution have been accounted for, it is not certain
that the high SES black men have the advantageous lipid profiles relative
to their white counterparts.
254
The Framingham Minority Study (11) is unique in having compared blacks
and whites in a sample which included a high proportion of college-educated
black men. HDL-cholesterol levels of black men in this study were not
higher than those of the white men. In fact, the mean HDL levels of the
black men were significantly lower than those of the white men, although
the ratio of mean HDL cholesterol to mean total cholesterol (which was also
significantly lower in black men) was similar.
The Framinghman Minority Study finding is supported by a report from
the Bogalusa study. Hunter and coworkers reported that although
alpha-lipoprotein levels of black children were higher and beta-lipoprotein
levels lower than those of white children in most parental-education
categories, an opposite pattern was observed among children whose parents
had a post-graduate education (19). When the parental SES variable was
blue vs. white collar occupation, black children but not white children had
SES-related differences in mean alpha-lipoprotein levels. Racial
differences in alpha-lipoprotein levels decreased from 64 mg/dl (black
children higher) among children of blue collar workers to only 6.9 mg/dl
(black children higher) among children of white collar workers. The
relative difference in alpha-lipoprotein levels between children of blue
vs. white collar parents was much larger than that for total cholesterol,
beta- or pre-beta-lipoprotein levels.
In summary, when one assesses differences in total cholesterol between
blacks and whites, HDL-cholesterol levels should be considered. The total
cholesterol/HDL cholesterol ratio is needed for useful HDL comparisons in
data where subjects have not been matched on cholesterol levels or HDL
levels. Significant declines in the prevalence of elevated serum
cholesterol levels are not evident in the NHANES data for either black or
white men. Socioeconomic aspects of cholesterol-related risk may vary
with the indicator used, are probably different for black and white men,
and are not monotonic in black men. More data are needed on this point.
With the exception of a study which included a large percentage of high SES
black men, higher HDL cholesterol levels in black compared to white men are
a consistent finding, across several studies and at several ages.
Apparently, the protection theoretically afforded by HDL cholesterol does
not effectively counter other risk factors in black men under age 60 years,
since prevalence/incidence of IHD appears similar in younger black and
white men.
2.2.2. Total and lipoprotein cholesterol comparisons among
black and white women.
2.2.2.1 Total cholesterol: women
National probability estimates of mean serum cholesterol and
elevated serum cholesterol in black and white women in the United
States are shown in Tables C-4 and C-5. In 1960-62, overall mean
cholesterol levels of black women were lower than those of white
women. Levels of black and white women tended to diverge with
increasing age, with the largest difference in women 55-64. For
NHANES I, the age-specific data indicate slightly higher cholesterol
255
levels in black vs. white women under age 65, although the overall
age-adjusted means for the two racial groups are identical.
Cholesterol levels of black and white women changed only slightly
between 1971-75 and 1976-80. Black women aged 45-64 years had
slightly lower mean levels than white women.
Table C-4. Age-specific comparisons of mean serum cholesterol
in national probability samples of U.S. black and
white women in three time periods between 1960 and
1980.
NHES NHANES I NHANES II
1960-62* 1971-75// 1976-80!
milligrams per deciliter
AGE BF WF
25-34 197, ,9 198, .0
35-44 213, .1 214, .2
45-54 232, ,2 237, ,6
55-64 239, .0 264, .9
65-74 258 .2 267, .4
age 217, .8 224, , 1*
adjusted
BF WF BF WF
207.3 202.8
216.9 216.4 198.3 198, .3
244.7 242.5
260.8 256.4 237.8 239 ,7
259.7 261.8 242.6 246, .3
221.2 221.4!! 219.2 219 .9! !
* Ref 5, Table 6
** for ages 18-74; age-adjusted estimates not published for
25-74 year-old adults
// age-specific data for 1971-74, from Ref 6, Table 5
! Ref 30, Table 15b; data for ages <65 grouped by 20 year spans
!! age-adjusted data for 25-74 year-olds taken from Ref 9, Table VI
Table C-5 indicates inconsistent trends in the prevalence of
elevated serum cholesterol (using a 260 mg/dl cut point) among
different age-groups of black women between NHANES I and NHANES II.
The largest change was a decrease among the oldest group of women;
however, prevalence rates for women age 35-64 years increased
slightly. The similarity of age-adjusted rates for black women in
NHANES I and NHANES II may be misleading because age adjustment
obscures age-specific trends.
256
Table C-5. Prevalence of Serum Cholesterol >260 mg/dl in
black and white women, 1971-75 and 1976-80: age
specific rates for black women aged 25-74; age-
adjusted rates for black and white women aged
25-74.
NHANES I 1971-75
NHANES II 1976-80
AGE
rate per 100 population
Black Women
25-34*
35-44
45-54
55-64
65-74
8.7
7.7
23.5
29.3
43.5
6.0
13.3
25.0
32.2
29.9
25-74//
BF:19.6 WF:20.2
*Ref 9, Table IV
BF: 19.0 WM:19.5
// Ref 9, Table V
The NCHS analysis of socioeconomic influences on serum cholesterol
levels of NHANES I adult female respondents indicated an inverse effect of
both education and income (8). This inverse effect in women was in
contrast to the weakly positive effect observed in men. The income effect
was significant in white but not black women. In the Framingham Minority
Study (11), total cholesterol levels of the black women were lower than
those for white women for all age-groups studied (range 20-69) except women
aged 50 to 59 years. Sixty-five percent of the black vs. 32% of the white
women under age 50 years in the Framingham Minority Study sample were
college-educated. Among the women over age 50, 27% of the black vs. 14% of
the white women were college-educated.
2.2.2.2 Lipoprotein cholesterol: women
In the NHANES II data, high-density lipoprotein cholesterol levels are
consistently higher in black women than in white women although the
differences are smaller than those seen in men. As in men, the largest
black-white difference in HDL levels among women is in the 55-64 year age
group. Differences between ages 20 and 54 are 4, 2, 3, and 1 mg/dl in
successive age-groups. In the 55-64 year-old women, HDL levels are 6 mg/dl
higher in black women than white women, due primarily to an increase in the
black women. HDL levels are somewhat lower for both black and white women
in the 65-74 year-old age-group, but the black-white difference decreases
to 4 mg/dl due to a larger drop in the HDL levels of the black women.
Thus, black-white differences in lipoprotein cholesterol for women
parallel'those for men but are of a lesser magnitude. This parallel
picture of slightly, but not substantially higher HDL and lower LDL levels
among black compared to white women is reported in several studies
257
described earlier for men (12,14-17). In the Cincinnati LRC Princeton
School Study, HDL differences in black compared to white women were larger
in women not using exogenous sex steroid hormones than in women who were
using them and were statistically significant in the nonhormone using
group (12). In the collaborative LRC Prevalence Study, the increase in
age- total cholesterol-adjusted HDL differences in black and white women
when the Quetelet index was added to the equation was greater than the
increase in men. When the Quetelet index was in the model, the higher mean
HDL cholesterol levels in black women were statistically significant
(further addition of trigylcerides decreased the difference to
nonsignificant levels) (14).
HDL-cholesterol differences in women in the Framingham Minority Study
also parallel those in men, i.e., HDL and total cholesterol levels in black
women were significantly lower than in white women (with the exception of
higher total cholesterol levels in black than in white women age 50-59).
However, HDL/total cholesterol ratios were similar in black and white
women. The mean Quetelet index of black and white women in this sample was
not different.
In summary, distributions of serum cholesterol and lipoprotein cholesterol
are similar in black and white women. Data regarding socioeconomic
influences on cholesterol in women are limited. NHANES I data suggest that
levels of cholesterol increase as SES decreases. If so, then the larger
proportion of black than white women who are of low SES are at risk for
elevated cholesterol. Black-white differences in levels of HDL cholesterol
which would be expected on the basis of findings in men are suggested in
the data for women but are usually very small and not significant. When
the entire adult age spectrum is considered, serum cholesterol levels
appear to have remained stable in both black and white women between
1971-75 and 1976-80. However, a higher prevalence of elevated cholesterol
in 35-64 year-old black women in NHANES II compared to NHANES I is
suggested by the data. This may be a noteworthy finding, if valid. Any
trends towards increased risk in black women should be targeted for
intervention, due to the excess of other risk factors and IHD prevalence in
this group.
2.2.3 Basis of lipoprotein cholesterol differences in blacks
and whites
Gartside et al. (22) examined the extent and direction of black-white
differences in several factors associated with HDL-levels including:
intakes of protein, fat, carbohydrate, saturated fat, oleic acid, lineoleic
acid and cholesterol (total and per kilogram of body weight); Quetelet
index, self-reported maximum and minimum weight and weight at age 25;
alcohol intake; cigarette smoking,; leisure time exercise and habitual
physical activity; self-reported prevalence of diabetes; and hypertension.
Of the factors found to differ between blacks and whites in NHANES II,
the substantially higher relative weight of black compared to white women
appeared to be the most likely explanation for the loss of the HDL
advantage for black women. Substantial differences in obesity between
258
black and white men were not evident in the national population data and
most of the studies reviewed. The greater prevalence of diabetes and the
greater tendency to be treated with HDL-lowering antihypertensive
medications among blacks than whites would work in the same direction for
women. Higher levels of habitual activity in black than in white men at
some ages would tend to enhance differences (22).
As noted above, adjustment for the Quetelet index has been more often
reported to alter the observed black-white differences in HDL-cholesterol
than does controlling for other possible confounders (14,17). The
environmental influence on lipoprotein patterns is also suggested by the
absence of significant black-white differences at birth (2) and by a
possible disappearance of racial differences among high SES groups.
It might be said that a genetic basis for lipoprotein profile
differences between blacks and whites is suggested by studies of blacks in
other countries. For example, in a study of men from 13 countries, the
highest HDL to total cholesterol ratios were observed among African men
(21). In his review of CHD in developing countries, Watkins cites several
studies indicating that lipoprotein profiles among African and Caribbean
men are favorable to low CHD risk (20). These findings clearly do not
separate genetic from environmental influences on differential lipid
patterns.
Gartside et al. postulate that genetic selection has favored blacks
with relatively higher HDL related to the protective role of
HDL-cholesterol against sleeping sickness (22). In this respect, it is
also interesting to note a recent report by Dai et al. of a possible direct
or indirect positive association between HDL levels and plasma testosterone
in a sample of 255 MRFIT participants (23). Studies by Ross et al. have
postulated that higher testosterone levels in black men might explain their
higher prevalence of prostatic cancer compared to white men (24).
2.2.4 Impact of cholesterol-associated risk on CHD disparities
between blacks and whites
The importance of black-white differences in lipoprotein profiles
may be much more in the utility of racial contrasts for etiologic analyses
than in the potential for reducing racial disparities in CHD incidence and
prevalence. The Cincinnati LRC group concluded (based on familial
aggregation studies) that the relative contribution of genetic compared to
environmental factors to HDL levels may be greater in blacks than whites
(2). This line of reasoning is compatible with the lesser consistency and
strength of association between lipid levels and measures of obesity in
black compared to white children (25) and adults (26) and with lesser
effects of cigarette smoking and oral contraceptives on HDL in black
compared to white children and adolescents (27). This might suggest that
interventions directed specifically at the HDL component of cholesterol
would yield a relatively lesser benefit for blacks. This is a testable
hypothesis.
259
Berenson and coworkers have pointed out that the proneness of blacks
to other CHD risk factors may override the degree of "subtle protection
afforded by high alpha-lipoprotein levels (25). Considering that the
overall lipid picture is better for black men and no worse for black women
compared to their age-sex peers, the similar rates of CHD in black men
compared to white men before age 55 or 60 and in black women at all ages
indirectly supports this conclusion. Analyses in the Cooperative
Lipoprotein Phenotyping Study indicate that HDL levels were lower in CHD
cases compared to control in black, white and Japanese men (18). However,
a tabulation of CHD prevalence rates by HDL cholesterol level implied a
threshold effect rather than a gradient. Prevalence rates did not differ
markedly among men with HDL-cholesterol levels between 45 and 75 mg/dl.
The striking prevalence differences were between men with HDL cholesterol
levels less than 35 or 25 mg/dl (18). The HDL levels in most of the
studies of black-white differences report mean cholesterols in the
intermediate rather than low range, possibly because persons at highest
risk have been excluded by the study protocols.
However, this does not advise against efforts to prevent or reverse
trends toward elevated total cholesterol in the black population. The
NHANES data suggest that the prevalence of elevated serum cholesterol in
black men may be higher than that of white men (Table C-3) using 260 mg/dl
as a cut point. The impression from multivariate analyses is that, with
other factors held constant, the impact of elevated serum cholesterol on
CHD in blacks is not substantially different from that in whites (31,32).
In addition, when higher prevalence of hypertension and smoking (black men)
are factored in, any added risk factor multiplies the risk of IHD.
The Carter Center findings on the potential benefits of reducing serum
cholesterol levels in the population can be summarized as follows (see
section 1.2.1 (data sources on the impact of smoking on IHD risk) for a
description of the Carter Center analytic approach).
In men, the proportion of CHD deaths that could be prevented if
borderline (240-259 mg/dl) and elevated (>= 260 mg/dl) cholesterol levels
were decreased to 219 mg/dl (considered to be normal) is slightly greater
for black than white men (14.1 vs. 9.0 percent) in the 25-44 year age
range. The comparable proportions for black and white men ages 45-64 and
65 plus are approximately eight and three percent, respectively, in both
racial groups. Proportionate reductions in CHD cases are 11 and 7% for
black and white men ages 25-44, 12 and 10 percent for 45-64 year-old men
and 8% in black and white men ages 65 and over (30).
In women, the greatest reductions in CHD mortality associated with
reduction of borderline and elevated cholesterol levels to below 220 mg/dl
would be among women over age 45, approximately 18% in both black and white
women. Below age 45, reduction in CHD deaths among women is a third of
that after age 45 and is the same (6%) for black and white women. The
potential benefits of such cholesterol reductions on CHD cases among women
is more striking: 18% among women under age 45 and 38-39% among women over
age 45, again, with the same level of benefit in women of both races (30)
260
The Carter Center report (30) also presents estimates for the
theoretical possibility of reducing cholesterol levels above 260 mg/dl to
below that level. Percentage reductions follow similar patterns as those
described above, but are much lower. For example, reductions in CHD cases
among women over age 45 would be 18-22 percent compared to the 38-39
percent which would occur if "normal" were defined as below 220 mg/dl.
Carter Center population attributable risk fractions for cholesterol
on CHD are summarized in Table C-6 for non-white and white men and women.
The earlier stated pattern of greater potential benefits in women but with
no substantial racial difference is also reflected in these estimates.
Table C-6. Population attributable risk fractions for cholesterol
on several CHD variables in non-white and white men and women:
estimates for the U.S. population (30)
Table CHD MEN WOMEN
No* Variable Non-white White Non-white White
(percent 1 of cases)
23 deaths 5 1 5 1 17 19
24 yrs.lost life 10 8 I 15 16
25 cases 11 9 1 35 38
26 hospital days 10 9 1 37 38
27 restrict, act. 11 9 1 35 38
28 medical expend. 11 9 1 38 38
in Reference 30
2.2.5 Intervention Studies
The limited evidence identified on the effectiveness of dietary
intervention on cholesterol levels of hyperlipidemic black women and men is
quite encouraging. A report from the Chicago Heart Association (29)
indicated that an educational intervention was more successful with black
men and women than with whites. Most of the participants in this study
were black, primarily from the inner city. Six to nine months after entry
into the program, the black participants, who had higher cholesterol levels
at baseline, had made slightly greater changes in fat consumption and had
achieved greater reductions in cholesterol levels (8.1 vs. 4.5%, p<0.05)
than white participants. The majority of participants (60%) were women;
dietary adherence among women was better than among men. Nutritional
knowledge scores of blacks were lower at baseline but were equivalent to
those of whites after one, six, and nine months of intervention. In the
MRFIT study, plasma cholesterol levels of black and white men decreased to
a similar extent. Improvements of special intervention compared to usual
care black men were slightly greater than for whites (28).
261
2.3 Recommendat ion
The evidence of equivalent or better lipoprotein profiles in blacks
does not justify inattention to cholesterol levels in blacks. Efforts
targeted to blacks should be included in the general effort to shift the
distribution of cholesterol levels in the population downward. This should
not, however, take priority over targeted interventions on hypertension,
obesity, LVH, and smoking in blacks.
262
2.4 References
1. Gillum RF, Grant CT. Coronary heart disease in black
populations. II. Risk factors. Am Heart J;1982:104:852-864.
2. Glueck CJ, Gartside P, Laskarzewski PM, Khoury P, Tyroler
HA. High-density lipoprotein cholesterol in blacks and
whites. Potential ramifications for coronary heart disease.
Am Heart J. 1984;108:815-826.
3. Curry CL, Oliver J, Mumtaz FB. Coronary artery disease
in blacks. Risk factors. Am Heart J 1984;108:653-657.
4. Heiss G, Schonfeld G, Johnson JL, Heyden S, Hames CG,
Tyroler HA. Black-white differences in plasma levels of
apolipoproteins. The Evans County Heart Study. Am Heart
J 1984;108:807-814.
5. National Center for Health Statistics. Serum cholesterol
levels of adults. United States 1960-62. Vital and Health
Statistics. PHS Publication No. 1000. Series 11. No.22
March 1967. Washington, D.C.
6. National Center for Health Statistics. Total serum cholesterol
levels of adults 18-74 years. United States 1971-74, by
Sidney Abraham, Clifford Johnson, and Margaret Carroll.
Vital and Health Statistics. Series 11, Data from the
National Health Survey; No 205. DHEW Publication No. (PHS)
78-1652. April 1978.
7. National Center for Health Statistics. Total serum cholesterol
levels of children 4-17 years, United States, 1971-74,
by Sidney Abraham, Clifford Johnson, and Margaret Carroll.
Vital and Health Statistics. Series 11. No. 207. DHEW
Pub No. (PHS) 78-1655. 1978
8. National Center for Health Statistics. Serum cholesterol
levels of persons 4-74 years of age by socioeconomic charac-
teristics, United States 1971-74, by Robinson Fulwood,
Sidney Abraham, and Clifford Johnson. Vital and Health
Statistics Series 11, No. 217. DHEW Publication No. (PHS)
80-1667.
9. Rowland ML, Fulwood R. Coronary heart disease risk factor
trends in blacks between the first and second National
Health and Nutrition Examination Surveys, United States,
1971-1980. Am Heart J 1984;108:771-779.
10. Namboodiri KK, Green PP, Kaplan EB, Tyroler HA, Morrison
JA, Chase GA, Elston RC, Rifkind BM, Glueck CJ. Familial
aggregation of high density lipoprotein cholesterol.
The Collaborative Lipid Research Clinics Program Family
Study. Arteriosclerosis 1983;3:616-626.
263
11. Wilson PWF, Savage DD, Castelli WP, Garrison RJ, Donahue
RP, Feinleib M. HDL-cholesterol in a sample of black adults.
The Framingham Minority Study. Metabolism 1983;32:328-332.
12. Morrison JA, Khoury P, Mellies M, Kelly K, Horvitz R, Glueck
CJ. Lipid and lipoprotein distributions in black adults.
The Cincinnati Lipid Research Clinics Princeton School
Study. JAMA 1981;245:939-942.
13. Khoury P, Morrison JA, Laskarzewski P, Kelly K, Mellies
MJ, King P, Larsen R, Glueck CJ. Relationships of education
and occupation to coronary heart disease risk factors in
schoolchildren and adults. The Princeton School District
Study. Am J Epidemiol 1981;113:378-395.
14. Tyroler HA, Glueck CJ, Christensen B, Kwiterovich PO.
Plasma high-density lipoprotein cholesterol comparisons
in black and white populations. Circ 1980;62:IV-99 -
IV-107.
15. Morrison JA, de Groot I, Kelly KA, Mellies MJ, Khoury P,
Edwards BK, Lewis D, Lewis A, Fiorelli M, Heiss G, Tyroler
HA, Gleuck CJ. Black-white differences in plasma lipids
and lipoproteins in adults. The Cincinnati Lipid Research
Clinic Population Study. Prev Med 1979;8:34-39.
16. Morrison JA, Khoury P, Laskarzewski P, Gartside P, Moore
M, Heiss G, Glueck CJ. Hyperalphalipoproteinemia in hyper-
cholesterolemic adults and children. Trans Assoc Am Phys
1980;93:230-243.
17. Tyroler HA, Hames CG, Krishan I, Heyden S, Cooper C, Cassell
JC. Black-white differences in serum lipids and lipop-
rotein in Evans County. Prev Med 1975;4:541-549.
18. Castelli WP, Doyle JT, Gordon T, Hames CG, Hjortland MC,
Hulley SB, Kagan A, Zukel WJ. HDL cholesterol and other
lipids in coronary heart disease. The Cooperative Lipoprotein
phenotyping study. Circ 1977;55:767-772.
19. Hunter SM, Frerichs RR, Webber LS, Berenson GS. Social
status and cardiovascular disease risk factor variables
in children. The Bogalusa Heart Study. J Chron Dis 1979;
32:441-449.
20. Watkins LO. Coronary heart disease and coronary disease
risk factors in black populations in underdeveloped countries.
The case for primordial prevention. Am Heart J 1984;108:
850-862.
264
21. Knuiman JT, West CE, Burema J. Serum total and high density
lipoprotein cholesterol concentration and body mass index
in adult men from 13 countries. Am J Epidemiol 1982;116:
631-642.
22. Gartside PS, Khoury P, Glueck CJ. Determinants of high-density
lipoprotein cholesterol in blacks and whites. The second
National Health and Nutrition Examination Survey. Am Heart
J 1984;108:641-653
23. Dai WS, Gutai JP, Kuller LH, Laporte RE, Falvo-Gerrard
L, Caggiula A. Relation between plasma high-density lipoprotein
cholesteroland sex hormone concentrations in men. Am J
Cardiol 1984;53:1259-1263.
24. Ross RK, Paganini-Hill A, Henderson BE. The etiology of
prostate cancer. What does the epidemiology suggest?
The Prostate 1983;4:333-343.
25. Berenson GS, Webber LS, Srinivasan SR, Cresanta JL, Frank
GC, Farris RP. Black-white contrasts as determinants
of cardiovascular risk in childhood. Precursors of coronary
artery and primary hypertensive disease. Am Heart J
1984;108:672-683.
26. Khoury P, Morrison JA, Mellies MJ, Gleuck CJ. Weight change
since age 18 in 30-to-55-year-old whites and blacks. Assoc-
iations with lipid values, lipoprotein levels, and blood
pressure. JAMA 1983;250:3179-3187.
27. Webber LS, Hunter SM, Baugh JG, Srinivasan Sr, Sklov
MC, Berenson GS. The interaction of cigarette smoking,
oral contraceptive use, and cardiovascular risk factor
variables in children. The Bogalusa Heart Study. Am J
Pub Health 1982;72:266-274.
28. Connett JE, Stamler J. Responses of black and white males
to the special intervention program of the Multiple Risk
Factor Intervention Trial. Am Heart J 1984;108:839-849.
29. Mojonnier ML, Hall Y, Berkson DM, Robinson E, Wethers B,
Pannbacker B, Moss D, Pardo E, Stamler J, Shekelle RB,
Raynor W. Experience in changing food habits of hyperlipidemic
men and women. J Am Dietet A 1980;77:140-148.
30. Haynes SG, White CC, Tolsma D, Newman JM, McGee D. Closing
the gap for cardiovascular disease. Carter Center Report.
August 27, 1984.
265
31. Neaton JD, Kuller LH, Wentworth D, Borhani NO. Total
and cardiovascular mortality in relation to cigarette
smoking, serum cholesterol concentration, and diastolic
blood pressure among black and white males followed up
for five years. Am Heart J 1984;108:759-770.
32. Tyroler HA, Knowles MG, Wing SB, Logue EE, Davis CE, Heiss G, Heyden
S, Hames CG. Ischemic heart disease risk factors and twenty-
year mortality in middle age Evans County black males.
Am Heart J 1984;108:738-746.
33. Kraus JF, Borhani NO, Franti CE. Socioeconomic status,
ethnicity, and risk of coronary heart disease Am J Epidemiol
1980;111:407-414.
266
3.0 ELEVATED BLOOD PRESSURE AND HYPERTENSION
3.1 Prevalence
3.1.1 Data Sources
The NCHS Health Examination and Health and Nutrition Examination
Surveys (NHES and NHANES) provide probability estimates for several blood
pressure variables for black and white adults in the U.S. population for
three time periods (1960-62, 1971-75, and 1976-80). Measurements and
definitions in NHES and NHANES I and II are sufficiently comparable to
permit valid estimates of trends in hypertension prevalence among blacks
and whites over the 1960-1980 period. Several NCHS reports (1-4) have
served as the basis for the following discussion of prevalence of elevated
blood pressure and hypertension for race-sex groups in the age range 25-74
years. When considering the black-white comparisons which follow, the
larger standard errors of the estimates for blacks should be kept in mind.
In addition, for 1971-75, published tables are available for estimates
of blood pressure variables by geographic region, urban/rural residence and
socioeconomic status. These data are of interest because of possible
variation in hypertension patterns in blacks and whites in demographic
sub-categories in the U.S.
Emphasis has been given to variables for which tabulations for all
three surveys are available by race and sex. These variables are as
follows: elevated blood pressure, (defined by NCHS as systolic blood
pressure (SBP) of at least 160 and/or diastolic blood pressure (DBP) of at
least 95), hypertension (elevated blood pressure and/or on medication),
previously undiagnosed hypertension, treated hypertension, and controlled
hypertension. Although the cut points for designation of elevated blood
pressure are somewhat arbitrary, the ones used by NCHS are useful for
comparing NHES and NHANES data. There is no indication that different
conclusions about black-white disparities would be drawn if variables
reflecting the entire blood pressure distributions were to be used.
NCHS blood pressure estimates reported here are based on three readings
taken at specified points in the examination protocols (the NHANES I and
NHANES II measurements each include one reading with the respondent supine;
other readings were with respondents sitting). Data for the different time
periods have been age-adjusted (by NCHS) to the U.S. population at the
midpoint of NHANES II (1978) for comparison purposes.
Now that substantial progress in blood pressure treatment and control
among both blacks and whites has been documented, the changes in patterns
of hypertension in blacks, compared to whites, over time deserve special
attention (i.e., have there been decreases in the black-white disparities
on hypertension variables?). Also, trends in the prevalences of target
organ damage and hypertension-related end points deserve careful
assessment.
267
Prevalence is a function of incidence and duration. That is, the
percentage of people in the population who will be found to have
hypertension at a given point in time is influenced both by the percentage
of new cases of hypertension at that point (incidence) and by the
percentage of people with hypertension who are surviving (duration). If
the rate at which new cases of hypertension develop remains constant, the
proportion of hypertensives in the population will increase if
hypertensives are effectively treated and thereby live for longer time
periods. Effective treatment of hypertension should be reflected in a
decrease in the prevalence of elevated blood pressure. However, the
survival of hypertensives is not only a function of blood pressure level
but also of the degree of end organ damage and comorbidity. These may
differ among controlled hypertensives with similar blood pressures. For
example, among hypertensive men in the Hypertension Detection and Follow-up
Program randomized trial, black men had substantially higher mortality than
white men (black-white ratios of 5-year-life table all-cause mortality were
1.8 and 1.9 in stepped and referred care groups)(6). The variable which
most differentiated the black and white men at baseline was prevalence of
ECG-LVH. In addition, more of the black men were on antihypertensive
medication at baseline and more had a history of diabetes or stroke (6).
The incidence of hypertension is difficult to ascertain. Long-term
follow-up of large populations, with careful attention to the initial
definitions of who is normotensive at the outset, are needed. Attempts to
ascertain hypertension incidence among blacks have been summarized in a
recent review by Oni (5). In cross-sectional data used for time trend
analyses, incident and prevalent cases among the newly-identified
hypertensives are difficult to separate on the basis of blood pressure
measurement alone. Newly identified cases of elevated blood pressure may
have been of longstanding duration. Patterns of hypertension incidence
over time are essentialy unknown.
At present, there is no basis for assuming that the incidence of
hypertension has decreased, since the major efforts have been at the level
of secondary, rather than primary prevention. These secondary prevention
efforts are expected to prolong the lives of people with hypertension,
i.e., to increase the duration of hypertension, and might be expected to
result in increased prevalence over time. If similar or decreased
prevalence is seen, then the possibility that treated hypertensives are
dying at similar or greater rates should be considered. This could be due
to increased case-fatality among hypertensives (perhaps associated with a
particular type of treatment), or to coincidental increases in overall
mortality of persons with hypertension due to other causes. Another likely
possibility is that hypertensives, especially mild hypertensives, may go
off of medication after a long period of control and not have increases in
blood pressure for several months. In a cross-sectional survey, such
individuals would not be classified as hypertensive by either the elevated
blood pressure or the "on medication" criteria.
268
3.1.2 Findings
3.1.2.1 Elevated Blood Pressure and Hypertension in Black and
White Men, 1960-1980
Prevalence rates of elevated blood pressure for black and white men in
1976-80 (the most current national probability sample estimates available)
are compared in Table H-1. In general, elevated blood pressure is observed
with greater frequency in older age-groups. Elevated blood pressure was
more common in black than in white men surveyed in 1976-80 in all age
groups. However, the slope of increased prevalence with age is different
for black and white men.
Large racial differences in rates of elevated blood pressure were
observed among the 35-44 and 55-64 year-old men (but only at these ages).
The black-white prevalence differences among the 35-44 year-olds probably
reflect the younger age of onset of hypertension among blacks compared to
whites; white rates have "caught up" in the 45-54 year-old group. The
disparity among the older men (55-64 years of age) may reflect somewhat
lower proportions of effectively treated hypertensives in black compared to
white men at these ages (see Table H-3). The inconsistency in the pattern
of race difference by age suggests that comparisons based on age-adjusted
data may be inadequate for some purposes.
Table H-1. Age-specific and overall prevalence of elevated
blood pressure in black and white men ages 25-74,
United States, 1976-1980.*
rate per 100 population with elevated
blood pressure**
Age-group 25-34 35-44 45-54 55-64 65-74 Total
Black Men 11.7 22.3 23.0 39.2 27.5 22.4
White Men 8.4 10.6 21.2 22.3 24.5 15.9
Black minus
White 3.3 11.7 1.8 16.9 3.0 6.5
* from Reference 1, Table 5
** defined as SBP >=160 mmHg and/or DBP> >=95 mmHg
As shown in Table H-2, the overall prevalence of elevated blood pressure
has declined substantially in both black and white men ages 25-74. The
decline among black men (35.3%) was larger than for white men (11.8%),
lowering the black-white ratio from 2.0 in 1971-75 to 1.45 in 1976-80. The
highest prevalence of elevated blood pressure among black men was in the
55-64 year age-group in both surveys. The percent decrease in prevalence
269
was relatively consistent across age-groups among black men--slightly lower
than the overall 35.3% in the 25-34 year-old men and slightly higher among
the 35-44 year-old men.
Table H-2. Percent decline in prevalence of elevated blood
pressure between 1971-75 and 1976-80, black men
in age-groups between 25 and 75 and age-adjusted
for black and white men, U.S.
rates per 100 population
1971-75 1976-80 % change*
25-34 16.4 11.7 - 28.7
35-44 37.7 22.3 - 40.8
45-54 34.7 23.0 - 33.7
55-64 59.9 39.2 - 34.5
65-74 43.7 27.5 - 37.1
25-74 Black 35.7 23.1 - 35.3
25-74 White// 18.0 15.9 - 11.7
* calculated from rates in reference 4, table II; elevated blood
pressure defined as SBP >=160 and/or DBP >=95 mmHg.
// from Reference 4, Table V
On the surface at least, the data in Table H-2 indicate progress in
hypertension detection and control between 1971 and 1980 which benefitted
black men to a relatively greater extent than white men. However, the data
on hypertension prevalence are only partially helpful in confirming this
impression of progress in reducing the black-white hypertension disparities
(Table H-3). As noted earlier, better coverage of black hypertensives
theoretically implies improved survival and increased prevalence (assuming
no decrease in incidence). The proportion of hypertensives among black men
ages 25-74 increased between NHES and the NHANES I augmentation survey
(1974-75) (NHANES la), but then decreased such that prevalence in 1976-80
was lower than that observed in 1960-62. Although this difference was
apparently not statistically significant, it is in contrast to what the
NCHS report identifies as a significant increase in hypertension prevalence
among white men over the 20 year period (1). The meaning of this trend in
prevalence is unclear.
Trends in hypertension awareness, treatment, and control among black
and white men are also summarized in Table H-3. The interpretation of
these variables is relatively straightforward and shows considerable
improvement for men of both races, particularly for black men, in awareness
and use of medication. The percent of black hypertensive men who had not
been diagnosed previously dropped sharply between NHES and NHANES la and
declined further between NHANES la and NHANES II. Improvements in
270
awareness among white men were similar, but of a lesser degree. The
proportion of unaware hypertensives was nearly 15% greater for black than
for white men in 1960-62 and nearly 5% less in 1976-80.
A similar cross-over was observed for the percentage of black
compared to white hypertensives on medication between NHES and NHANES II:
a slightly smaller percentage of hypertensive black than white men were on
medication in 1960-62; a slightly higher percentage of black compared to
white men were on medication in 1976-80. Levels of awareness were 60% or
greater among both black and white men; medication use was lower--around
40%. However, although the extent of control tripled for black men and
nearly doubled for white men during this period, hypertensive black men on
medication were less likely than white men to have adequately controlled
blood pressure in all three survey periods. Overall levels of control were
still quite low in men (on medication) of both races in 1976-80.
Table H-3. Rates of hypertension prevalence, awareness, treatment,
and control, black and white men, ages 25-74, U.S.,
1960-62, 1974-75, and 1976-80*
percent of
hypertensives
in population//
percent of
hypertens ives
not previously
diagnosed
percent of
hypertensives
on medication
percent of
hypertensives
on medication
whose blood
pressure was
controlled////
1960-62 1974-75 1976-80
BM 31.8 37.1 28.3
WM 16.3 21.4 21.2
BM 70.5 41.0 35.7
WM 56.7 42.3 40.6
BM 18.5 24.0 40.9
WM 22.4 25.9 38.3
BM 5.0 12.7 16.1
WM 11.8 15.1 20.9
* Reference 1, Table 7; data are age adjusted to the U.S. population
at the midpoint of NHANES II (1976-80).
// defined as either SBP >=160, DBP >=95, or taking antihypertensive
medication
//// hypertensives on medication and with blood pressures below
the levels considered as elevated range (below the cut points
for elevated blood pressure)
271
3.1.2.2. Demographic Patterns : Men
Mean blood pressure levels of black men in 1971-75 were consistently
higher than those of white men in all four regions of the country. Mean
blood pressure levels among black men are highest in the Northeast and
lowest in the West (3, Table 17; age-adjusted rates). Similarly, black men
had higher mean blood pressure levels than white men in both urban and
rural areas. The mean blood pressures of black men in rural areas were
higher than for black men in urban areas (3, Table 18; age-adjusted rates).
Tabulations by annual family income and level of education indicated higher
blood pressures among the black compared to white men at each level of
these variables (3, Tables 19 and 20; age-adjusted rates), with the
exception that black men with less than 5 years of education had mean blood
pressures considerably below the rest of the distribution. (Note that
these are trends in the data and not necessarily statistically significant
differences.)
3.1.2.3 Prevalence of Elevated Blood Pressure and Hypertension
in Black and White Women, 1960-1980.
Age-specific and overall prevalence rates of elevated blood pressure in
black and white women in 1976-80 are shown in Table H-4. Prevalence
increased with age in women of both races and was 1.7 to 3 times higher in
black than white women in every age-group. Black-white differentials are
larger in women over 45 years of age than among younger women (this is also
the age-group when blood pressure levels of women catch up with and then
exceed those of men).
Table H-4. Age-specific and overall prevalence of elevated
blood pressure in black and white women ages 25-74,
United States, 1976-1980.*
rate per 100 women with elevated
blood pressure**
Age Group 25-34 35-44 45-1 54 55-64 65-74 Total
Black Women 4.3 17.6 37, ,3 36.4 43.4 23.2
White Women 2.3 6.5 12, ,1 18.3 26.3 11.4
Black minus
White 2.0 11.0 25, .2 18.1 17.1 11.8
from Reference 1, Table 5
defined as SBP >=160 mmHg and/or DBP >=95 mmHg
Table H-5 indicates decreases in the prevalence of elevated blood
pressure among black women in each age-group, but with a considerable
age-time interaction (i.e., very different levels of decrease in different
272
age-groups). The decrease among black women 25-74 years is approximately
representative of the level of decrease among 35-44 and 55-64 year-old
women. A very large decrease (65%) was observed among the youngest group
of women. Minimal decreases were observed in the other two age-groups.
Unlike black men, who showed proportionately larger overall decreases than
white men in 1971-1980, the overall decreases in black and white women were
of the same order. Thus, the ratio of elevated blood pressure prevalence
in black and white women was constant at 2.2.
Table H-5. Percent decline in prevalence of elevated blood
pressure between 1971-75 and 1976-80, black women
in age-groups between 25 and 75 and age-adjusted
for black and white women, U.S.
rates per 100 population
1971-75 1976-80 % change
25-34 12.4 4.3 - 65. 3*
35-44 23.9 17.6 - 26.3
45-54 39.4 37.6 - 4.6
55-64 46.0 36.4 - 20.9
65-74 46.7 43.4 - 7.1
25-74 Black 30.5 24.4 - 20.0
25-74 White// 14.2 11.1 - 21.8
* calculated from rates in Reference 2, Table II; elevated blood
pressure defined as SBP >=160 and/or DBP >=95 mmHg.
// from Reference 4, Table 5
Data on hypertension prevalence (Table H-6) show higher prevalence in
black compared to white women, with essentially no changes in either group
over the three survey periods. The 20% decline in the
prevalence of elevated blood pressure is not accompanied by a change in
hypertension prevalence (at least not in the overall age-adjusted data).
Thus, as discussed earlier, no conclusion is possible regarding changes in
the survival of women with hypertension over time. Awareness of
hypertension increased in women of both races and to approximately the same
degree. More black than white women with hypertension had been previously
informed of their condition in NHES and NHANES II. In 1976-80 less than
15% of hypertensive black women and 25% of white women were previously
unaware of their condition. Approximately 60% of both black and white
women hypertensives were on medication in the 1976-80 survey. There was no
racial difference in the proprortion of the women on medication whose blood
pressures were adequately controlled in either NHES or NHANES II. However,
the proportion of control approximately doubled over this time period. The
273
proportion of hypertensive women whose medications were adequately control-
ling their blood pressure levels was approximately twice that for men.
Table H-6. Rates of hypertension prevalence, awareness, treatment,
and control, black and white women, ages 25-74,
U.S.,1960-62, 1974-75, and 1976-80*
percent of
hypertensives
in population//
percent of
hypertensives
not previously
diagnosed
percent of
hypertensives
on medication
percent of
hypertens ives
on medication
whose blood
pressure was
controlled////
1960-62 1974-75 1976-80
BW 39.8 35.5 39.8
WW 20.4 19.6 20.0
BW 35.1 28.9 14.5
WW 43.9 29.7 25.2
BW 48.1 36.4 60.6
WW 38.2 48.5 58.6
BW 20.2 22.3 38.3
WM 21.9 28.1 40.3
* Reference 1, Table 7; data are age adjusted to the U.S. population
at the midpoint of NHANES II (1976-80).
// defined as either SBP >=160, DBP >=95, or taking antihypertensive
medication
//// hypertensives on medication and with blood pressures below
the levels considered as elevated range below the cut points
for elevated blood pressure
3.1.2.4 Demographic Patterns : Women
As described for men, blood pressures of black women in 1971-75 were
higher than those of white women in all four regions, in all types of
residential areas and at all income and education levels (3, Table 17-20;
age-adjusted rates). Regional patterns of blood pressure are different in
black men and women. Whereas blood pressures among black men in the
Northeast were highest, the highest levels among black women were in the
South and West. Rural black women had higher blood pressures than those in
urban areas. In tabulation by educational levels, black women with less
than 5 years of education were noticeably different from the rest of the
blood pressure distribution, but blood pressure levels were higher in this
group of women--not lower, as observed in men (note that these are trends
from tables and not necessarily significant).
274
3.2 Left Ventricular Hypertrophy (LVH)
Left ventricular hypertrophy (LVH), a putative independent risk factor
for IHD, is a lethal marker (7,8). LVH in the general adult population is
primarily due to prolonged blood pressure elevations (7). It was an
antecedent finding in 45% of all cardiovascular deaths in the Framingham
Study (9). The five-year mortality rate in Framingham men who developed
ECG-LVH was 35% compared to approximately 10 to 15% or less expected
otherwise (9). For women, 20% of those who developed ECG-LVH were dead
within five years. For those aged 65 years and older these mortality rates
were 50% and 35%, respectively. Kannel has suggested that the excess
mortality associated with ECG-LVH may not be attributable to associated
hypertension since ECG-LVH carried three times the risk of hypertension
without the ECG finding (9). On the other hand, the degree of hypertension
may not have been comparable in those with and without ECG-LVH since the
clinic blood pressures used to define hypertension in the Framingham study
may not have adequately reflected degree of hypertension (e.g. by not
adequately reflecting variations in 24-hour blood pressure or duration of
hypertension). The mortality rate associated with possible LVH was
one-half that of definite ECG-LVH. Chest x-ray LVH was associated with
one-third the cardiovascular mortality rate of ECG-LVH (9).
Risk of cardiovascular morbidity is also markedly increased in those
with ECG-LVH. In age 40 year-old Framingham men with systolic blood pressures
of 195 and positive status on glucose intolerance and cigarette smoking,
ECG-LVH raises the eight-year probability of cardiovascular disease from 459
per 1000 to 708 per 1000 (10). ECG-LVH confers a 2 to 9-fold increased risk
of stroke, cardiac failure, coronary disease and peripheral arterial
disease (9).
In the HDFP, age-adjusted five-year total mortality in the stratum with
mild hypertension at baseline (stratum I) was approximately double in white
and black Referred Care males who were LVH positive compared to LVH
negative by ECG (11).
The prevalence of ECG-LVH is greater in blacks than whites for both
sexes (8). These prevalence differences are clearly demonstrated in
baseline data for 10,940 HDFP participants, as shown below (Table P-l).
These baseline prevalence patterns were evident after adjustment for age
and blood pressure level (12). The prevalence of ECG-LVH was progressively
higher in HDFP Strata II and III (baseline diastolic blood pressure 105-114
and 115+ mmHg) vs. stratum I (baseline DBP 90-104 mm Hg) (13). Percentages
in stratum III were more than 3 times those in stratum I, suggesting a dose
response relationship. Race-sex specific baseline ECG-LVH prevalence data
by blood pressure strata have also been published (13,14).
275
White men 1892 2 .4
Black men 1064 8 .5
White women 1185 1. .8
Black women 1344 7. .9
Table P-l. Baseline prevalence of ECG-LVH by race-sex and
randomization group for HDFP participants (ages
(30-69 years, n=10,940) *
Percent of Subgroup
n Stepped Care n Referred Care
1861 3.1
1084 9.0
1156 1.7
1354 7.8
* from Reference 13, Table 2.3--"...based on combined R-wave and
ST-T segment changes: tall R-wave (Minnesota Code 3.1) and
major ST segment depression (Minnesota code 4.1-4.3) or major
T-wave inversion (Minnesota code 5.1-5.3)"
The reasons for the black excess of ECG-LVH are unclear. Since the
differences are observed within each stratum of baseline blood pressure
among the HDFP participants, these racial differences for given levels of
blood pressure may be indicative of the inadequacy of our usual measures of
blood pressure (e.g., one to three blood pressures in a clinic
setting)(7,8). Earlier onset and longer duration of blood pressure in
blacks are likely contributors (8). Duration of blood pressure elevations
is difficult to ascertain. Assessment of a possible association with
ECG-LVH is further complicated by duration and type of antihypertensive
treatment (7,15-17). Regression of ECG-LVH with antihypertensive treatment
was observed in the HDFP (18). An additional or alternative explanation
for black-white differences in LVH prevalence is that the left ventricular
response to a given blood pressure elevation is greater in blacks than in
whites (8,19,20).
Echocardiography (echo) detects LVH earlier than either ECG or chest
x-ray (15,21). Echo has the greatest sensitivity and specificity of the
three diagnostic tools (7,15,21). Thus, the prevalence of echo-LVH is
higher than LVH by ECG in a given population (7). The proportion of
echo-LVH cases which progress to ECG-LVH and the proportion of the latter
which survive to be ascertained have not been documented. The prognostic
significance of LVH by echo rather than ECG criteria has been uncertain.
However, recent data from Framingham have documented a significant
association of echo-LVH with all-cause mortality, independent of standard
risk factors (22). In that study, approximately twice as many of the men
and women about age 70 at time of echo measurement) who died (compared to
those alive) in a two-year period after examination had echo LVH. However,
only 7% of the women who died and none of the men had LVH by ECG.
Data on the prevalence of echo-LVH are limited. Reference data for
whites have been reported from Framingham (7). There are no
population-based echo-LVH reference data for blacks. Small-scale studies
in American and African blacks have documented the presence of
276
significantly higher LV wall thickness, interventricular septal thickness,
LV mass or mass index and lower LV fractional shortening in hypertensives
vs. normotensive controls (23,25), and proportionate to the level of blood
pressure. These patterns are reportedly similar uo those observed in
whites and in Japanese (8).
Dunn et al. (20) observed higher LV mass index (LV mass per square
meter of body surface area) in 30 black hypertensives compared to
age-sex-blood pressure matched controls. Posterior wall thickness was
correlated to blood pressure and total peripheral resistance in the black
but not white subjects in that study. Hammond et al. (19) similarly found
greater echo target organ changes in blacks matched for blood pressure
levels with whites.
Savage et al. (23) found that echo findings were similar between black
and white hypertensive subjects carefully matched for several possible
confounders: age, sex, treatment status, level and known duration of
hypertension, and renin subgroup. If the origin of black-white echo-LVH
differences is related to blood pressure variables, then the matching
protocol and inadequate power (n=35 blacks and 35 whites) in this study may
have obscured these differences.
Hammond et al. (19) have reported results of echo-LVH comparisons in
an occupationally-based sample of black and white normotensive (n=75) and
hypertensive (n=132) men and women in New York City. The hypertensives in
this study included newly identified hypertensives defined as (DBP>=95
mmHg, SBP >=160 mmHg or both, sustained on three occasions over a three
week period and not previously taking antihypertensive medications.
Hypertensives also included persons receiving antihypertensive medications
before joining the study, regardless of blood pressure level at screening.
No echo variables were different between black and white normotensives,
suggesting that the echo baseline in blacks and whites was the same. Among
the hypertensives, LV mass index was similar in blacks and whites but
relative wall thickness, cardiac output and total peripheral resistance
were higher in blacks. Blood pressures of the black and white
hypertensives were similar. Differences observed may be explained in
various ways including either different durations (and/or actually
different severity of hypertension) or differential effects of blood
pressure elevations.
In the New York City study (19), progression of LVH in the newly
diagnosed, untreated hypertensives was not differentiated from possible
regression of left ventricular measurements towards normal in the
hypertensive subjects on medications at the time of screening. Differences
in echo findings in the two groups were not observed at the time of study
but may have been present at one time. Three studies (16,17,26) documenting
regression of echo-LVH in hypertensives with antihypertensive treatment
have included blacks. One of these studies (16) reported regression very
early in therapy (at one month) which was sustained during treatment over
an 18 month follow-up period. It is noteworthy, however, that methyldopa
but not hydrochlorothiazide, was associated with regression of echo-LVH.
Diuretics (e.g. hydrochlorothiazide) are often recommended as the preferred
277
treatment for blacks (27). Much more information is needed regarding the
significance of regression of echo-LVH (and other changes) in response to
various antihypertensives. If differing hypertensive regimens are
recommended for black and white hypertensives on a racial basis (27) the
potential significance of such information is obvious.
More information is also needed about how representative clinic blood
pressures are. This is suggested by the 10 year prospective study of
Perloff et al. (28), showing prognostic significance of ambulatory blood
pressure independent of clinic blood pressures.
In summary, if blood pressure elevation of long duration is
related to LVH (which is true (7)) and if LVH then becomes established as
an independent IHD risk factor (which appears to be true (22)), then the
attributable risks of LVH in blacks may be greater than in whites. As
noted above, the onset of blood pressure elevations in blacks occurs at an
earlier age than in whites. The prevalence of such elevations is also
greater in blacks. Finally, early (echo) LVH and late (ECG) LVH may be
greater in blacks than in whites with the same apparent level of blood
pressure elevation.
ACKNOWLEDGEMENTS
We gratefully acknowledge the editorial assistance of Sandra
J. Anderson and Elisabeth Pitt.
278
3.3 References
1. Rowland M, Roberts J. Blood pressure levels and hypertension
in persons ages 6-74 years. United States 1976-80. NCHS.
Vital and Health Statistics. AdvanceData No. 84, October, 1982.
2. National Center for Health Statistics. Blood pressure levels
of persons 6-74 years, 1971-1974, Roberts J., Maurer K. Vital and
Health Statistics. Series 11. No. 203. DHEW Pub. (HRA) 78-1648.
September, 1977.
3. National Center for Health Statistics. Hypertension in adults 25-74
years of age, United States 1971-75, Roberts J, Rowland, M. Vital and
Health Statistics. Series 11. No. 221. PHHS Pub. No. (PHS) 81-1671.
April, 1981.
4. Rowland ML, Fulwood R. Coronary heart disease risk factor trends in
blacks between the first and second National Health and Nutrition
Examination Surveys, United States 1971-1980. Am Heart J 1984; 108:
771-779.
5. Oni A. Intraracial factors in blood pressure variations among the black
population. J Natl Med Assoc 1984; 76:594-603.
6. Hypertension Detection and Follow-up Program Cooperative Group. Five-year
findings of the Hypertension Detection and Follow-up Program.
II. Mortality by race, sex, and age. JAMA 1979;242:2572-2577.
7. Savage DD, Abbott RD, Padgett S, Anderson SJ, Garrison RJ.
Epidemiologic features of left ventricular hypertrophy in
normotensive and hypertensive subjects. In Cardiac Left
Ventricular Hypertrophy, HEDJ ter Keurs, JJ Schipperheyn,
eds. Martinus Nijhoff. 1983, pp. 3-15.
8. Savage DD. Echocardiographic assessment of cardiac anatomy
and function in black and white hypertensive subjects.
In Textbook of Ethnic Medicine, R Williams ed (in press).
9. Kannel WB. Left ventricular hypertrophy in hypertension:
prognostic and pathogenetic implications. The Framingham
Study. In The Heart in Hypertension, Strauer BE ed. 1981,
p.123.
10. Kannel WB. An overview of the risk factors for cardiovascular
disease. In Prevention of Coronary Heart Disease. Practical
Management of the Risk Factors, Kaplan NM, Stamler J, eds.
Philadelphia: W.B. Saunders Company. 1983, Chapter 1, pp. 1-19.
11. Tyroler HA. Overview of risk factors for coronary heart
disease in black populations. Am Heart J 1984;108:658-660.
279
12. The HDFP Cooperative Group, presented by Prineas R. Sex
and race differences in end organ damage among 10,940
hypertensives. Am J Cardiol 1978:41:402(abstract).
13. Taylor JO, Borhani NO, Entwisle G, Farber M, Hawkins CM,
on behalf of the HDFP Cooperative Group. Summary of the
baseline characteristics of the hypertensive participants.
Hypertension 1983;5(part II, no.6):IV-44 - IV-50.
14. Hypertension Detection and Follow-up Program Cooperative
Group. Five-year findings of the Hypertension Detection
and Follow-up Program. Mortality by race-sex and blood
pressure level. A further analysis. J Comm Health 1984;9:
314-327.
15. Savage DD, Devereux RB. Echocardiography and hypertension.
Primary Cardiology. 1981;7:137-149.
16. Wollam GL, Hall WD, Porter VD, Douglas MB, Unger DJ, Blumstein
BA, Costonis GA, Knudtson ML, Felner JM, Schlant RC. Time
course of regression of left ventricular hypertrophy in
treated hypertensive patients. Am J Med 1984;75:100-110.
17. Schlant RC, Felner JM, Blumstein BA, Wollan GL, Hall WD,
Shulman NB, Heynsfield SB, Gilbert CA, Tuttle EB. Echo-
cardiographic documentation of regression of left ventricular
hypertrophy in patients treated for essential hypertension.
Eur Heart J 1982;3(supp A):171-175.
18. The Hypertension Detection and Follow-up Program Cooperative
Group. Regression of left ventricular hypertrophy (LVH)
with anti-hypertensive therapy. Circ 1981;64(Supp IV);
IV-322 (abstract).
19. Hammond IW, Alderman MH, Devereux RB, Lutas EM, Laragh
JH. Contrast in cardiac anatomy and function between black
and white patients with hypertension J Natl Med Assoc
1984;76:247-255.
20. Dunn FC, Chandraratna P, de Carvalho JGR, Basta LL, Frohlich
ED. Pathophysiologic assessment of hypertensive heart
disease with echocardiography. Am J Cardiol 1977;39:789-795.
21. Savage DD, Drayer JIM, Henry WL, Matthews EC Jr, Ware JH,
Gardin JM, Cohen ER, Epstein SE, Laragh JH. Echocardiographic
assessment of cardiac anatomy and function in hypertensive
subjects. Circulation, 1979;59:623-32.
280
22. Savage DD, Garrison RJ, Castelli WP, Kannel WB, Anderson
SJ, Feinleib M. Echocardiographic data from Framingham and newer
studies of echocardiography. Echocardiographic left ventricular
hypertrophy in the general population is associated with increased
2-year mortality, independent of standard coronary risk
factors. AHA Council on Epidemiology (invited paper), 1985.
23. Savage DD, Henry Wl, Mitchell JR, Taylor AA, Gardin JM,
Drayer JIM, Laragh JH. Echocardiographic comparison of
black and white hypertensive subjects. J Natl Med Assoc
1979;71:709-712.
24. Schlant RC, Felner JM, Heynsfield SB, Gilbert CA, Tuttle
EB, Blumenstein BA. Echocardiographic studies of left
ventricular anatomy and function in essential hypertension.
Cardiovas Med 1977;2:477-491.
25. Adesanya CO, Sanderson JE, Verheihen Ir PJY, Brinkman AW:
Echocardiographic assessment and systolic time interval
measurements in the evaluation of severe hypertension in
Nigerian Africans. Aust NZ J Med 1981;11:364-369.
26. Devereux RB, Savage DD, Sachs I, Laragh JH. Long-term
effects of hypertension on the heart. Clin Res 1980;28:
330A (abstract).
27. The 1984 report of the Joint National Committee on Detection,
Evaluation, and Treatment of High Blood Pressure. The Joint
National Committee on Detection, Evaluation, and Treatment
of High Blood Pressure. Arch Intern Med 1984;144:1045-1057.
28. Perloff D, Sokolow M, Cowan R. The prognostic value of
ambulatory blood pressures. JAMA 1983;249:2792-2798.
SUPPLEMENTAL REFERENCES
S-l. Folkow B, Nordlander MIL, Strauer B-E, Wikstrand J eds.
Pathophysiology and clinical implications of early structural
changes. Hypertension 1984;6:(Suppl 3)iii-l - iii-187.
S-2. Messerli RH, Schlant RC, eds, Proceedings of a Symposium:
Left Ventricular Hypertrophy in Essential Hypertension.
Am J Med 1983;75:1-120.
S-3. Panidis IP, Kotler MN, Ren J-F, Mintz GS, Ross J, Kalman P.
Development and regression of left ventricular hyertrophy.
J Am Coll Cardiol 1983;3:1309-1320.
S-4. Tarazi RC. Regression of left ventricular hypertrophy: partial
answers for persistant questions (editorial). J Am Coll Cardiol
1983;3:1349-1351.
281
4.0 CONCLUSION
Our review suggests that intensified efforts to understand and reduce
black-white differentials in hypertension (and, possibly, left ventricular
hypertrophy) and obesity (black women) offer the greatest opportunity among
the standard and putative independent cardiovascular risk factors for
reduction of cardiovascular morbidity-mortality disparities between blacks
and whites. These intensified efforts should of course be in the context
of continued vigorous efforts to reduce all of the cardiovascular risk
factors in both blacks and whites.
282
Relationship of Social Class
to Coronary Disease Risk
Factors in Blacks:
Implications of Social
Mobility for Risk Factor
Change
Lucile L. Adams, Ph.D.
Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Laurence O. Watkins, M.D., M.P.H.
Section of Cardiology
Medical College of Georgia
Augusta, Georgia
Lewis H. Kuller, M.D., Dr.P.H.
Chairman, Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Daniel D. Savage, M.D., Ph.D.
Medical Advisor
National Center for Health Statistics
Hyattsville, Maryland
Richard Donahue, Ph.D.
National Heart, Lung, and Blood Institute
Bethesda, Maryland
Ronald E. LaPorte, Ph.D.
Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
Coronary heart disease (CHD) is the leading cause of death among United
States blacks, mortality rates being similar in black and white men and
greater in black women than in white women (1). National survey data from
1962 revealed similar CHD prevalence rates for blacks and whites (2). Small
studies in two southern states have revealed lower CHD incidence in black Chan
in white men in the period 1960-1974, and greater CHD incidence in black than
in white women (3,4). Among both men and women, black rates of admission to
the hospital with the diagnosis of acute myocardial infarction are lower than
those of whites(5). These data on the CHD experience of blacks are
conflicting, but it is clear that compared to whites, blacks have a greater
prevalence of CHD risk factors including hypertension, cigarette smoking, and
among middle-aged women, obesity and diabetes mellitus (6). It is somewhat
paradoxical that black men in particular do not have higher CHD rates than
whites.
This paradox would be intensified if, as has been hypothesized, there is
an inverse relationship between social class and risk of CHD. A 1968 review
of this subject by Antonovsky (7), and a more recent one by Jenkins (8), have
discussed the conflicting data with regard to CHD in white populations. Some
studies suggest higher risk of CHD with high social status, while others
indicate a lower risk. An explanation for these diametrically opposed results
has been proposed by Morgenstern (9). Guided by Cassel, he suggested that the
association of CHD risk with social status might have been altered during the
period of rapid social change in urban populations in the U.S. in the period
1930-1950. In this formulation, among individuals and groups which came to
enjoy the benefits of rapid industrial growth, those of high socioeconomic
status (SES) initially asssumed high CHD risk status, but as they adapted more
rapidly to the new material conditions by altering lifestyles, they became at
significantly lower risk than their low SES counterparts.
Such links as exist between SES and CHD risk may be mediated by causal
links between SES and lifestyle, and between lifestyle or lifestyle changes
and biological risk factors. In this hypothetical framework, low or high SES
may be linked to CHD risk because of an association with adverse risk factor
distributions, or SES may modify the effect of the major biological risk
factors on CHD incidence. In an investigation of the data on CHD prevalence
(1960), incidence (1960-1967), and mortality (1960-1974) in the white adult
population of Evans County, Georgia, Morgenstern found evidence of a change in
the predicted direction for the association between SES and CHD in men (9)
That is, the prevalence of CHD was initially higher in white men of high SES,
but during follow-up, the incidence of CHD was lower in the cohort of 35-54
year old men of high SES. In addition, there was evidence that the changing
relation between SES and CHD risk was partly due to differential change in
certain biological risk factors, especially hypertension. That is, there was
greater adverse risk factor change among younger low SES men. In addition,
there was no evidence that SES modified the effect of the major biological
risk factors on CHD.
Because of systematic discrimination, the black population of the U.S.
has been largely of low SES (10). In the last 20 years, there have been rapid
285
socioeconomic changes in certain segments of the black population (11), and
some black families have experienced upward mobility, either within a
generation or between successive generations. In view of such changes, the
implications of Morgenstern's hypothesis and observations for the associations
betwen SES and CHD incidence and between SES and CHD risk factor distributions
in blacks are important, but no systematic examination of this subject has
been done (12-14).
This review will summarize the data on 1) the extent and characteristics
of socioeconomic change in blacks since 1960; 2) The relation between SES and
CHD incidence and mortality in blacks; 3) the cross-sectional associations
between SES and related factors and the prevalence (and incidence) of CHD risk
factors; and 4) the risk factor characteristics of black population samples
from the higher end of the socioeconomic spectrum. The latter will be
discussed as examples of black populations which may have experienced upward
mobility, either recent or remote, and which might make manifest the impact of
such mobility on CHD risk factors.
Socioeconomic Status Changes in Blacks
In the period 1960-1981, there were increases in the percentage of black
adults above age 25 years who completed high school or four years of college
(15). By 1981, the median number of years of schooling for black males and
females exceeded 12, and the black-white difference was less than one year.
During these two decades, the median duration of formal education had
increased by 4.4 years for black males, and 3.5 years for black females, but
by only 1.9 and 1.3 years for white males and females, respectively. These
changes in educational attainment were associated with changes in the
occupational profile of blacks. There has been an increase in the percentage
of blacks who are white-collar workers, and a decline in the percentage of
farm workers. Between 1972 and 1981, the percentage of blacks employed in
professional, technical, managerial or administrative jobs increased from
11.2% to 15.7% (16). However, despite the broader range of occupations now
held by blacks, especially black women, the majority of blacks, especially
men, remain blue-collar or service workers. Blacks remain more likely to be
unemployed (17). The black unemployment rate in 1982 was 17.3%, compared to
8.6% for whites. This 2:1 ratio has remained virtually unchanged since 1960.
Blacks who are unemployed are likely to remain so for longer periods of time.
Family incomes remain substantially lower among blacks than whites (15).
This is so, particularly for families headed by women. It is noteworthy that
the financial rewards of education are dissimilar for blacks and whites. Only
18.1% of white families in which the head of the household has at least four
years of college earn less than $20,000 per year. The comparable number for
black families is 34.7%. Similarly, 35.5% of white families whose heads of
household have four years or more of college earn more than $40,000 per year,
while only 18.1% of similar black families have such incomes. The disparity
is more striking, if it is noted that of all black families in which the
householder has at least four years of college, 23.7% earn less than $15,000
per year, a proportion similar to that for white families in which the
286
householder has four years of high school (26.1%). Income disparities between
blacks and whites appear to be attributable to differences in pay-rates for
black and white men holding the same types of jobs (18), and more to
restriction in the job opportunities open to blacks once they have completed
their education, than to differences in educational attainment.
These considerations serve to emphasize that a relatively small
proportion of a black population can be considered "upwardly mobile". Social
mobility refers to the movement of an individual from one social position to
another different from the one to which he/she was accustomed. For the
individual, there are different types of social mobility and the
classification depends on the reference point (14). Intergenerational
mobility takes into account the social position of offspring with respect to
that of the parents. This can be compared to intragenerational or career
mobility which takes account of changes experienced by the same individual
within his/her lifetime. As a consequence of recent social change, some
blacks have experienced intergenerational mobility, and others
intragenerational mobility, or even both. In the course of this report we
shall examine data on groups of blacks in whom upward mobility is presumed to
have occurred in current or recent generations, by virtue of their superior
educational attainment and social position compared to the general black
population.
One of the samples of blacks which shall be considered "upwardly mobile"
for the purpose of this review is constituted of college students. This
appears reasonable, since data from a national study of male college students
which examined occupational expectations according to race and socioeconomic
background reveal that among blacks, the level of education of the father is
an important determinant of career aspirations, college performance and
occupational expectations (19). Professional orientations of black college
students may reflect the orientations and experiences of high-achievement
parents.
Socioeconomic Status, Social Mobility and CHD Incidence.
As a prelude to consideration of the limited data on blacks, observations
on white U.S. populations will be reviewed. The observations in Evans County,
Georgia have been noted briefly (3). In the 1960 prevalence study, high-SES
white men had a CHD prevalence rate 2 or 3 times that of lower SES white men.
The 1960-1967 incidence study showed that high SES was associated with higher
CHD incidence for white men over age 55 years, but was inversely related to
CHD incidence in white men 35-54 years of age. In this study, SES was
assessed by use of the McGuire-White index which takes account of occupation,
education, and source of income of the head of each household.
Studies in white populations which have used education as the marker of
SES have suggested that education is associated with lower CHD incidence. For
example, Hinkle et al (20) observed that the incidence of new CHD events and
deaths was approximately 30% lower among college-educated men than among non-
college-educated men. On the other hand, the association between CHD
287
incidence and occupation may be different from that observed for education.
In a 1957 study of CHD incidence in North Dakota, Syrae et al (21) found that
the incidence of CHD was higher among white-collar workers than among blue-
collar or agricultural workers. An analysis which took account of the
occupation (agricultural or non-agricultural) of each subject's father,
indicated that the excess risk was confined to those white-collar workers from
an agricultural (i.e., rural) background (22).
Studies of career or intragenerational occupational mobility among whites
have also detected higher rates of coronary disease among the mobile than
among the nonraobile. Syrae et al (22) made such observations on coronary
incidence in North Dakota, and similar cross-sectional observations on CHD
prevalence in an urban area in California (23). In the North Dakota Study
(22), Syme et al noted significantly higher CHD incidence rates in the group
of men who had made four or more major job changes since age 18 years
(compared to those with one or no job changes), and the group of men who had
made two or more major cross-country moves since age 18 years (compared to
those who had made one or no such moves). The CHD incidence rates were
significantly higher in the "highly mobile" group (the entire group of white-
collar workers with paternal agricultural background, and all men with high
occupational or geographic mobility) than in the stable group (farmers with
paternal agricultural background) or the remaining "moderately mobile" group.
The analyses suggested that the contribution of sociocultural mobility t~ CHD
incidence was independent of cigarette smoking, blood presssure, and body-
weight. The necessity for such analyses is illustrated by a report from the
Tecumseh Community Health Study (24). In men and women, ages 35-69 years,
residential mobility and urban residence, particularly in childhood, were
related not only to the prevalence of CHD, but also to hypertension and
cigarette smoking.
Kaplan et al (25), in the initial Evans County report, noted that the
prevalence of CHD in white men was higher in upwardly mobile men from the
lower social classes than among those who were not mobile. The observation
discordant with those of Syme et al (22) was that upward mobility among the
upper social classes was associated with CHD prevalence rates lower than those
among the nonmobile. Other data on the relationship of sociocultural mobility
and CHD incidence have been obtained from a follow-up study of 13,728 male
Harvard University students. Gillum and Paffenbarger (26) observed that
individuals who exhibited intergenerational mobility (that is, their social
class was eventually higher than that of their fathers) had a 1.5 times higher
risk of fatal CHD and MI than those who did not experience such mobility.
A single study has examined the relationship between SES and CHD
incidence in blacks in and around Charleston, South Carolina, and one recent
analysis may cast some light on the relationship between SES and CHD mortality
in urban blacks in Los Angeles, California. In the Charleston Heart Study
(4), a special cohort of high-SES black men was assembled by peer nomination.
Over 14 years of follow-up (1960-1974), the incidence of CHD in this group of
men was less than half of that in the predominantly low-SES men in the random
population sample. In this study, SES was assessed on the basis of occupation
288
and income. The risk characteristics of the high-SES group have not been
specifically reported, though one publication from the Charleston Heart Study
has revealed that the incidence of hypertension was 3-4 times as high in low-
SES as in high-SES men (27). This particular observation is similar to the
Evans County finding in white men.
Frerichs and coworkers examined the association betwen income and
cardiovascular disease mortality rates in 1979-1981 in Los Angeles County
(28). In this study, they determined the median family income in each census
tract, assigned this value to the resident population and to individual
residents who died, and aggregated census tracts into five income groups. The
age-adjusted mortality rate from Diseases of the Heart (International
Classification of Disease Codes 390-398, 402, 404-429) was inversely related
to income. The contribution of ischemic heart disease (ICD 410-414) to the
age and sex-adjusted mortality rate for diseases of the heart was 62.6% for
the entire county, 53.7% for blacks, and 63.4% for whites. The age-adjusted
ischemic heart disease mortality rate of black men was 18% lower than that
recorded for white men, 223.9 compared to 274/100,000, while the rates for
women were virtually identical, 158.1 and 158.5/100,000. The inverse
association between mortality from diseases of the heart and income was common
to both blacks and non-blacks. Compared to black men in the higher income
group (_> $28,500), black men in the lowest income group (_< $13,600) had a 53%
excess risk of death from diseases of the heart. The risk differential for
women was 33%. Such analyses were not performed for deaths from ischemic
heart disease, but since they constitute the majority of the deaths in
question, a similar relationship to income is likely. No study of
intragenerational or intergenerational mobility (social, cultural,
occupational or geographic) and CHD incidence in blacks has been reported
(14).
SES and CHD Risk Factor Associations in Blacks
Hypertension
Among both blacks and whites, there is a distinct inverse association
between SES and blood pressure. For example, Syrae et al (29) assessing SES in
1968-1969 on the basis of education and occupation, detected a higher
prevalence of hypertension in blacks of low SES. Similarly, as noted earlier,
in Charleston County, South Carolina, the incidence of hypertension in 1960-
1974 in black men was inversely related to social class (27). In a black
Baltimore population (30), there was also an inverse association between
income and the incidence of hypertension in 1973-1977. Over this 3-4 year
period, the incidence of hypertension in sons of professionals was
approximately one quarter of that observed in sons of laborers.
The relationship between the prevalence of hypertension and the duration
of formal education was also striking in the screening conducted in 1973-1974
for the Hypertension Detection and Follow-Up Program (31). I~ blacks with
less than 10 years of education, the prevalence of hypertension was 43.9%,
while in those who had completed college, the prevalence was 27.7%. For
whites, the corresponding rates were 23.1% and 13.5%. Mean systolic and
289
diastolic blood pressures in adults ages 18 to 74 years examined by NHANES II
(1976-1980) were inversely related to the duration of formal education of
examinees in all race and sex groups, the association being more marked for
women than for men (32). The prevalence of definite hypertension (systolic
blood pressure 160 mmHg or greater or diastolic blood pressure 95 mmHg or
greater, or taking antihypertensive medication) showed a slight, not
statistically significant, decline between 1960 and 1980 in black adults (32),
coincident with their increased educational attainment.
In Bogalusa, Louisiana, among black children ages 5-14 years examined in
1973-1974, those whose parents had a postgraduate education had lower systolic
blood pressures than did similar white children. In addition, there were no
racial differences in systolic and diastolic blood pressure between children
of white-collar workers (33). These findings are in contrast to the
significantly higher blood pressure levels observed among black children after
statistical control for education and occupation, when the entire group of
children in the community sample was used as the basis for racial comparisons.
Elevated Serum Cholesterol
In NHANES I (1971-1975), serum cholesterol levels were significantly
higher in the lowest socioeconomic class (on the basis of education and
income) among whites, but not among blacks (34). There was no clear
relationship of cholesterol level to education among black men ages 18-74
years, but among women, serum cholesterol level was generally lower among
those of higher income. Across income levels, black women had generally lower
mean serum cholesterol levels than did white women.
Examination of the impact of parental social status on risk factor
variables in 5-14 year old children in Bogalusa, Louisiana in 1973-1974
revealed that black children had significantly higher total serum cholesterol
levels and alpha lipoprotein (HDL-cholesterol) after account was taken of
parental education and occupation (33). However, among children whose parents
had a postgraduate education, blacks tended to have lower total serum
cholesterol and HDL-cholesterol as well as higher pre-beta lipoprotein
cholesterol (VLDL) than white children. Among children of white-collar
workers, there were no statistically significant differences between the
groups for total cholesterol and HDL-cholesterol.
High Density Lipoprotein Cholesterol
There is limited information concerning the relationship of SES to HDL-
cholesterol in blacks. Most of the studies which have evaluated HDL-
cholesterol levels in blacks have examined low-SES poulations. Among U.S.
adults, black males have higher HDL-cholesterol levels than white males, while
the levels for black females are comparable to those of white females (35).
In the Lipid Research Clinics Program (1971-1976), a direct association was
detected between SES (measured by education) and HDL-cholesterol in white
subjects. The black sample in this study was too small to permit such an
evaluation.
290
The Framingham Minority Study evaluated a sample of well-educated blacks
in Framingham, Massachusetts in 1980 (36). It is remarkable that the age-
adjusted HDL-cholesterol levels observed in this population are lower than
those of whites, and lower than those reported for other U.S. black
populations (37). The educational attainment of this black population was
such that 56% had completed four years of college. Wilson et al (36)
speculated that blacks of middle-and upper-SES (a correlate of relatively high
educational attainment) might have lipoprotein profiles different from those
reported in lower-SES groups. Data on men recruited into the Multiple Risk
Factor Intervention Trial (1973-1976) are in accord with this hypothesis (38).
In this study, mean HDL-cholesterol levels of black men were significantly
higher than those of white men, but in a multiple regression analysis which
took account of age, cigarettes smoked per day, diastolic blood pressure,
number of alcoholic drinks consumed per week, and body mass index,
socioeconomic status was inversely related to HDL-cholesterol concentrations
in black men, but directly related to HDL-cholesterol concentrations in white
men. The black-white differences in HDL-cholesterol levels were largest among
those of lower SES and were smaller at higher SES levels.
Cigarette Smoking
There are relatively few data available on the association between SES
and cigarette smoking in blacks. Data from the 1970 Health Interview Survey
indicate that within industries, substantially higher percentages of
individuals in the lower occupational ranks (where blacks are overrepresented)
smoke (39). In the Princeton School District Study (40), there was an inverse
relationship between SES (assessed by education and occupation of the head of
the household) and the prevalence of cigarette smoking among both black
children and adults.
Comparison of data from two successive National Health and Nutrition
Examination Surveys (NHANES I and II, 1971-1975 and 1976-1980) (41), indicates
that the prevalence of smoking declined in black men and women between the
surveys, more among women than among men. The proportion of black adults who
were heavy smokers (25 or more cigarettes per day) did not change
significantly, indicating that the decrease in the prevalence of smoking was
due to a reduction in the ranks of light or moderate smokers. Data derived
from interviews performed between 1970 and 1980 of hospitalized black adult
patients yield some information on the prevalence of cigarette smoking in two
educational strata, high school or less, and college or more (42). They
indicate that the prevalence of cigarette smoking was lower among college-
educated black men than among black men with less education, and there was a
more marked increase in the proportion of former cigarette smokers among the
college-educated men in the second five-year period. Among black women, the
prevalence of cigarette smoking was similar in the two educational strata in
both periods, 1970-1975 and 1976-1980, though the prevalence had declined in
both groups by about 15% during the period between 1976-1980. These data
suggest that smoking cessation is more likely among those with more education.
This is consistent with data from the 1970 Health Interview Survey which
revealed that smokers in the higher occupational ranks are more likely to
291
cease smoking (39). Also, other survey data (43), indicate that black smokers
who earn more than $15,000 per year, and those who report regular medical care
are more interested in quitting smoking and report enjoying smoking less than
do those with lower income and less access to health care.
Obesity
The relation of SES and obesity in blacks is largely unexplored.
Physical Activity
There is a paucity of literature that evaluates physical activity levels
in blacks. The limited information from one available study suggests no
difference in physical activity levels between blacks and whites. In the 1977
National Health Interview Survey (44), respondents were asked to rate their
own level of physical activity relative to other persons of their age: more
active, about as active, or less active. Self-perceived levels of physical
activity were similar in blacks and whites. A race-specific analysis has not
been reported, but self-perceived level of physical activity exhibited a
positive relationship to income. The likelihood of a direct association
between nonwork-related physical activity and SES is also suggested by the
results of a statewide Massachusetts Survey (probably predominantly white) in
which reported participation in sports and exercise increased linearly with
both education and income (45).
CHD Risk Factor Characteristics of Upwardly Mobile/High SES Blacks
Two population samples examined within the last decade provide relatively
complete data on CHD risk factors in blacks at the upper end of the SES
spectrum. The Framingham Minority Study (36) examined a random sample of 45
black men and 55 black women, residing in Framingham, Massachusetts in 1980.
The educational characteristics and HDL-cholesterol data of this sample have
already been discussed. The age range of the participants was 20-69 years and
the mean age was 42 years for both sexes. A younger sample of blacks who may
be upwardly mobile is represented by University of Pittsburgh freshmen
recruited during the 1982-1983 and 1983-1984 academic years (46). This sample
included 285 black students (134 men and 151 women; mean age of 18.0 +0.6
years for each sex). Their parents were well-educated compared to the general
black population. They represented a relatively homogeneous population with a
median family income of $21,000 which is similar to $20,500 for the general
white population, and far in excess of the $11,600 median income for the
general black population.
Mean blood pressures of Framingham Minority subjects were considerably
lower than those of the general U.S. population (47). However, the small
sample size precludes definitive statements in this regard. The Pittsburgh
freshmen had lower systolic blood pressures than those observed for men and
women of comparable age in the First National Health and Nutrition Examination
Survey (NHANES I) (47). In the Framingham Minority Study, 13% of the men had
hypertension and 18% of the women. In the Pittsburgh sample, 6.0% of the men
292
and 4.0% of the women had either SBP _^ 140 mm Hg or DBP > 90 mm Hg.
Comparable figures are 15.0% for men and 3.2% for women ages 18-24 in the
general U.S. population.
The prevalence of cigarette smoking in the Framingham Minority study was
42.2% for men and 30.9% for women. Comparble data reported in the NHANES II
study were 46.5% and 29.9% for black men and women, respectively (41). This
is similar to the prevalence of smoking in the U.S. white population but lower
than that of U.S. blacks described in the NHANES I (48). Relatively few of
the Pittsburgh Freshmen were smokers, 7.5% of men and 10.7% of women.
Framingham Minority Study men had a mean body mass index similar to that
of the U.S. general population. However, the 90th and 95th percentiles of
body mass index for black Framingham women were somewhat lower than those of
U.S. black women (49) suggesting a lower prevalence of obesity in this
population and a greater similarity to the white female population.
The HDL-cholesterol levels of the Pittsburgh black men were significantly
greater than those of a white Pittsburgh freshmen comparison group (50). This
reflected primarily differences in the HDL2 fraction. However, for women
there was no difference in HDL levels between black and white Pittsburgh
freshmen. In addition, self-reported physical activity levels paralleled the
HDL-chol and HDL2~chol results. That is, black females and white females had
similar self-reported physical activity levels while black males had a
significantly higher self-reported activity level than white males (51).
Socioeconomic Status and Cardiovascular Health Knowledge
The data presented so far on associations of SES with behaviors which
affect cardiovascular risk suggest that cigarette smoking is more likely among
blacks of low-SES, and smoking cessation and high levels of regular leisure-
time physical activity are more likely among blacks of high-SES.
The few available studies of knowledge of cardiovascular risk factors
among blacks suggest relative lack of knowledge among low-SES blacks regarding
the association between certain dietary practices, including intake of salt
and saturated fat, on cardiovascular risk profiles (52,53). A 1982 telephone
survey of a national probability sample of 1000 subjects performed by the Food
and Drug Administration and the National Heart, Lung and Blood Institute
revealed that respondents who were poorly educated, of low income or resident
in the South had less than average awareness of diet-health relationships. In
particular, educational level was positively correlated with concern about
consumption of fats and cholesterol. In addition, food purchasing, food
preparation, and food consumption habits among low-SES blacks are intimately
connected with a culture of poverty (54).
The available data suggest the need for focused and behaviorally-oriented
cardiovascular health education programs in socioeconomically deprived black
populations.
293
Conclusions
There are limited data on the relationship between social class and
cardiovascular disease incidence and mortality in blacks. However, these data
suggest that the risk of coronary disease is higher among low-SES blacks than
among high-SES blacks. The data on the relationship between SES and the
prevalence of CHD risk factors in blacks also suggest an association of low-
SES with higher prevalence of hypertension, obesity, and cigarette smoking.
Since the excess prevalence of diabete.s in middle-aged black women appears to
be related to obesity (55), this may reflect some influence of SES. High-SES
appears to be associated with a lower prevalence of hypertension, a greater
likelihood of smoking cessation, and greater leisure-time physical activity.
Only in the case of HDL-cholesterol does there appear to be an association
between high-SES and a potentially adverse level of the risk factor.
No study to date has examined the impact of "upward mobility"
(operationalized as described earlier) on CHD risk factors in blacks. In the
case of HDL-cholesterol, this appears to be an important area for future
investigation. If, as has been suggested, HDL-cholesterol might account for
the lower CHD incidence in black men observed in some studies, it would be
important to take explicit account of social class and social mobility
differences among blacks in future cohort or surveillance studies.
In addition, if socioeconomic improvement is associated with a lower
incidence or prevalence of risk factors such as hypertension, obesity,
diabetes mellitus, and cigarette smoking, it is conceivable that factors which
impede such improvement among blacks might contribute to persistently higher
levels of these risk factors than in whites. However, it is probably
inappropriate to focus on economic factors to the exclusion of cultural
factors. The recent (1979-1982) evaluation by Stern et al (56) of CHD risk
factors among Mexican Americans in three San Antonio neighborhoods, (labelled
"traditional", "transitional" and "suburban") revealed an inverse relationship
between socioeconomic status and the "obesity-related" CHD risk factors,
diabetes mellitus, hypertriglyceridemia and low HDL-cholesterol levels in
women. Among men, such a relationship existed only for diabetes, and was less
marked. On the other hand, total cholesterol levels and low density
lipoprotein cholesterol levels were higher in more affluent men, but not in
women. The observation that "obesity-related" risk factors were higher in
Mexican Americans than in Anglos of similar SES in the same neighborhoods
suggested that cultural factors might be more important than socioeconomic
ones. Dietary, physical activity, cigarette smoking, and alcohol consumption
habits are among the possible culturally-based determinants of CHD risk.
The issue of socioeconomic and sociocultural change and its effect on CHD
risk factors and CHD incidence is an important one for blacks. Research
should be initiated in this area. Simultaneously, interventions should be
directed to fostering the possible beneficial effects of socioeconomic and
sociocultural change and blunting possible adverse effects.
294
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299
Coronary Heart Disease in
Black Populations: Current
Research, Treatment, and
Prevention Needs
Hector F. Myers, Ph.D.
Department of Psychology
University of California at Los Angeles
ABSTRACT
This paper summarizes the existing knowledge base contained in the
collection of papers and reports from two national meetings on coronary
heart disease (CHD) in black populations. Evidence is presented that
suggests that CHD morbidity and mortality rates are roughly comparable
between blacks and whites, but blacks appear to be at greater risk of
sudden death than whites due to the higher prevalence of hypertension,
obesity, diabetes, and greater socioeconomic disadvantage. The quality
and availability of sound epidemiologic data on CHD in blacks are
generally criticized, and specific recommendations for improvements are
offered.
An extensive review of available evidence on risk factor status and
trends in black and white populations is also provided, and speculations
about possible racial differences in operative risk factors and
function, and in protective factors are made. Arguments are provided
for the salience of socioeconomic and sociocultural factors in CHD in
blacks, and an analysis of how these factors might interact to affect
CHD risk status, risk management, and CHD morbidity and mortality
differences is offered.
Consideration of the possible role of differences in the quality,
effectiveness, and accessibility of health care between blacks and
whites as possible contributors to the observed CHD differences is
given. Provocative evidence of differential patterns of medical care of
CHD patients as a function of race and socioeconomic status is
presented.
Finally, the need to support CHD prevention activities is
discussed, and specific programmatic recommendations for future research
on coronary heart disease in black populations are offered.
303
INTRODUCTION
The American Heart Journal recently published a special supplement
issue that compiled the papers and plenary group reports from two
national meetings on coronary heart disease in black populations: a
symposium sponsored by the American Heart Association Council on
Epidemiology, and a workinq conference sponsored by the National Heart,
Lung, and Blood Institute (NHLBI) (American Heart Journal (AHJ), Sept.,
1984, Vol. 108, No. 3, Part 2). These meetings and the subsequent
publication were catalyzed by the recommendations of the Black Health
Care Providers Task Force on High Blood Pressure Education and Control
(BHCPTF) and by the recent publication of two major review papers on
coronary heart disease in blacks (Gillum, 1982; Gillum & Grant, 1982).
Both factors stimulated the interest and concern of medical and social
scientists in exploring the range of issues and questions raised about
coronary heart disease in black populations.
To this end, the papers in the special AHJ issue reviewed and
discussed the major theoretical and clinical issues regarding the
incidence and prevalence of CHD, the operative risk factors for CHD, and
the possible contributory role of current medical attitudes and
practices in CHD-related deaths among blacks. The working conference
participants also offered a series of specific recommendations for
further research needs and priorities. This report provides an
integrative summary of the state of our current knowledge about CHD in
blacks as reviewed in the AHJ proceedings, and organizes the sugqested
research priorities into coherent programmatic recommendations to guide
future research on coronary heart disease in this population.
Four major substantive questions emerge as salient concerns in the
recent reviews on CHD in black populations. First, what conclusions can
be drawn from our present epidemiologic evidence on the incidence and
prevalence of coronary heart disease in black Americans as compared to
white Americans? Included here are considerations of CHD morbidity and
mortality, and sudden death, as well as epidemiologic and other evidence
on angina pectoris, myocardial infarction (MI), and coronary
atherosclerosis as integral to the CHD spectrum.
The second major question is: What are the specific risk factors
and possible resistant or protective factors for CHD for blacks, and to
what extent do blacks and whites differ in the nature and relative
importance of these factors? Consideration is given here to whether or
not the CHD risk factors identified for whites are the same and have the
same degree of importance for blacks, and whether there may be genetic
and/or socioenvironmental factors that increase the resistance of blacks
to coronary heart disease.
The third major question is: What role do socioeconomic,
sociopsychological, and sociocultural factors play in the observed
patterns of CHD morbidity and mortality in blacks? Consideration is
given here to the range of social factors that exert detrimental
effects on the social and health status of black Americans. Particular
attention is paid to the conceptualization and measurement of these
factors, as well as to the specification of their diffprential impact on
304
CHD risk and risk management, on CHD morbidity, on medical treatment of
CHD, and, ultimately, on CHD mortality in blacks.
The fourth major question addresses the health care system.
Specifically, to what extent do physicians' attitudes and beliefs, and
clinical practices in health-care institutions in treatinq coronary
heart disease in blacks result in either differential access or
differential quality of medical care for blacks? Furthermore, to what
extent do these practices ultimately contribute to the
disproportionately higher MI case fatality rates for blacks?
CONCEPTUAL PERSPECTIVE
Underlying these major concerns about CHD in black populations is a
conception of hypothesized roles that various factors play in
determining risk for CHD, in impacting on the course of the disease, and
ultimately on the outcome of this disease in black populations.
Included are biological factors, and psychosocial and sociocultural
factors, all of which interact to differing degrees and at different
points in the coronary heart disease process.
Current conceptual models confer priority on biologic processes
(i.e., genetic and metabolic) and on health behaviors as primary
contributors to CHD risk, morbidity, and mortality. A family history of
high blood pressure or of CHD, elevated blood pressure, presence of ECG
abnormalities, obesity, diabetes, and high cholesterol levels are all
acknowledged biologic risk factors. Similarly, personal health habits
including smoking, limited physical exercise, heavy alcohol consumption,
and such psychosocial factors as disadvantaged socioeconomic status,
sustained disturbing emotions (e.g., anger), a time-oressured,
aggressive behavioral type (Type A), and high life stresses have all
been associated with increased CHD risk (Figure 1, Kasl, 1984; McDonald
et al., 1984; Gillum & Grant, 1982). Finally, a tendency to ianore,
deny, or minimize the significance of CHD symptoms (e.g., chest pains),
and to delay seeking medical care has also been associated with
increased risk for CHD-related deaths (Gillum, 1982).
These factors are viewed as interacting to affect CHD morbidity,
with the psychosocial factors operating primarily as mediators of the
biological predispositions. However, several questions have been raised
about whether some of the psychosocial factors might not operate as
independent precursors. Smoking has been identified as an accepted risk
factor for CHD and there is preliminary evidence that Type A behavior is
a potential risk factor for CHD; these are examples of factors that
operate biobehaviorally to increase CHD risk (Kleinman et al., 1979;
Coronary Prone Behavior Review Panel, 1981). Similarly, questions have
been raised about socioeconomic disadvantage which appears to be a
social system precursor of a variety of pathogenic outcomes including
CHD (James, 1984a).
In addition to their direct and indirect effect on CHD risk,
psychosocial factors also seem to affect disease course by influencing
risk behavior management and the recognition and management of symptoms.
305
This is particularly true of such factors as socioeconomic status,
cultural beliefs about health and illness, symptom tolerance, heal inn
beliefs and practices, and help-seeking behaviors (Jackson, 1981).
Individual help-seeking behavior, compliance behaviors, and attitudes
toward the sick role also contribute to the course of CHD.
Symptom recognition and management are also likely to be affected
by the prevailing beliefs and treatment practices of health care
providers. These include the knowledge and beliefs of individual
physicians about CHD in particular populations, the pattern of usual
care provided to CHD victims (e.g., diagnostic and treatment practices),
and the host of factors that affect the pattern of care likely to be
provided (e.g., financial resources of the patients, the technical
resources of the providers, etc.) (Davis et al., 1981; Yelin et al.,
1983; Brook et al., 1983). Analyses of health care system factors
should also include the availability and response times of emergency
services, and the beliefs and behaviors of these personnel when
responding to CHD crises in low-income, black communities. Although
comparatively less is known about the contribution of health care system
factors in CHD morbidity and mortality, there is preliminary evidence
suggesting that certain patient characteristics such as race, ability to
pay, gender, and age may contribute to differences in the quality of
medical care received, and to the pattern of health compliance behaviors
observed (Shapiro et al., 1970; Jackson, 1981; Yelin et al., 1983).
This interaction of differential treatment and differential pre- and
post-hospital patient behaviors probably contributes ultimately to
differential CHD mortality rates in the affected qroups.
In sum, at the core of our concerns about CHD in black populations
is the need to identify the major biologic, sociopsychologic,
sociocultural, and health care system factors that may be causally
implicated in this disease. There is a related need to specify more
carefully to what degree and at what point in the CHD process these
factors make their contributions, and whether the contributions are
direct or indirect. In the specific case of CHD in blacks, we must
actively entertain the possibility that not only is the pattern of
occurrence of CHD somewhat different, but that the factors causally
implicated and their pattern of contribution at each point in the CHD
process in blacks may differ significantly from that reported for
whites. The justification for this hypothesis rests in the suggestive
evidence reported in the most recent review on CHD risk factors (Curry
et al., 1984; Tyroler, 1984; McDonald et al., 1984).
WHAT DO WE PRESENTLY KNOW ABOUT CHD IN BLACKS?
1. Epidemiologic Evidence
There is general consensus that our present epidemiologic data on
coronary heart disease in blacks are inadequate. Specific criticisms
have been levelled at the practice of the National Center for Health
Statistics and other national health data collection agencies of
collapsing all health statistics on blacks into the "non-white"
category. This practice confounds the health trends of the various
306
ethnic minorities and, in so doing, obscures important differences
between them. The national health surveys such as the National Health
and Nutrition Examination Surveys (NHANES) I and II, and some of the
major cardiovascular disease surveillance and treatment studies, when
they have not excluded blacks from their samples (as in the Framingham
Heart Study), have used small, nonrepresentative samples -- inadequate
indicators of national black population trends. In the Multiple Risk
Factor Intervention Trial (MRFIT), for example, only 6.5% of their
randomized sample was black. In the Hypertension Detection and
Follow-up Program (HDFP), however, the investigators, recognizing the
importance of hypertension in the black population, oversampled and thus
enrolled a sample that was 26% black, in the study, as a whole. In the
hypertensive group of HDFP, 44% were black. Questions have also been
raised about how representative the largely rural, southern, black
samples in the Evans County and Charleston Heart Studies are of black
populations elsewhere in the nation.
Several investigators have also questioned the scientific basis for
our rather simplistic classification of groups by race, the tendency of
many to infer (inappropriately) that observed racial group differences
are due to biologic differences between the groups (Cooper, 1984), and
the tendency of many biomedical investigators to ignore the biologic,
socioeconomic, and psychosocial heterogeneity of blacks (Watkins, 1984a;
James, 1984a, b; Myers, 1982). Our present knowledge suggests that the
U.S. black population is neither biologically nor socioeconomically
homogeneous and, as such, failure to take adequate account of this
heterogeneity in study samples is likely to produce nongeneralizable
findings, or may result in incorrect conclusions about the contribution
and significance of race as a biologic factor in explanations of
observed differences between blacks and whites. This error of assuming
homogeneity in study cohorts is probably also committed with respect to
whites and other ethnic groups.
As a result of these conceptual and methodologic problems, there
are ongoing disagreements about what conclusions can be drawn about
coronary heart disease prevalence and mortality rates, and about the
incidence of myocardial infarction in blacks. Gillum (1982) and Watkins
(1984a) both note contradictory findings when comparing vital statistics
with mortality data from more carefully designed epidemiologic studies
that included large samples of blacks. For example, according to the
vital statistics, the age-adjusted mortality rates from CHD in blacks
exceeded those of whites, especially between the age-groups 35-44 years,
45-55 years, and 55-64 years. Similarly, the CHD mortality rate for
black women exceeds that for white women (Report of the Working Group on
Atherosclerosis, 1981). However, when these data are compared with the
mortality rates from the MRFIT screenee population, the American Cancer
Society (ACS), and the Evans County studies, the CHD mortality rates for
black men range from 78% to 90% that of white men. Only the excess CHD
mortality rate for black females (i.e., 107% in the ACS study) is
consistent with the national mortality data.
This picture is further complicated when the data on sudden death
are considered. The results of the Charleston Heart Study show that,
between 1960-1975, black males were three times and black females 1.5
307
times more likely to die suddenly (i.e., within 1 hour of onset of
symptoms) than were white males and females (Keil et al., 1984). On the
other hand, the Baltimore sudden death study revealed no black-white
differences in sudden death (Kuller, Perper & Cooper, 1975). Questions
were raised by Watkins (1984a) about whether these contradictory
findings are due to differences in death certification and/or to
differences in access to medical care.
Although many studies also report a lower prevalence of CHD in
blacks, other studies report that younger blacks and black women show
evidence of more CHD symptoms than do whites (Gillum, 1982; Langford et
al., 1984). Among MRFIT screenees followed for 5 years, blacks appeared
to be at greater risk for cerebrovascular accidents than whites, given
the higher overall prevalence of essential hypertension (Neaton et al.,
1984) and, in the Charleston Heart Study, blacks had a higher MI
case-fatality rate than their white counterparts (Table 2, Keil et al.,
1984). Furthermore, although CHD-related mortality has decreased
significantly in both blacks and whites since 1968, there is still a
large disparity in black-white CHD mortality rates because of the
persisting excess CHD mortality rates for black females (Figure 1,
Gillum & Liu, 1984). Important age, gender, socioeconomic status, and
geographic differences are also evident and must be considered in
interpreting these findings (Gillum & Liu, 1984; Savage et al., 1984;
Watkins, 1984a; Figures 1-4, Leaverton et al., 1984; Strong et al.,
1984; Keil et al., 1984).
These somewhat contradictory findings, along with the limited data
sources and the methodological limitations of many of the studies
reviewed, make it unwise to draw firm conclusions about the true
prevalence of CHD and its consequences in black populations. However,
it is clear that CHD is far from uncommon among blacks, and that blacks
are not immune to its effects. Rather, what we see is preliminary
evidence of gender differences in the pattern of CHD morbidity and
mortality when different races are compared. For example, if we look at
overall CHD mortality rates, then both black and white men have
significantly higher rates than both black and white women, but black
women have significantly higher mortality rates than white women (Figure
1, Gillum & Liu, 1984). On the other hand, if we consider sudden death
rates, than black men and women appear to be at greater risk than their
white counterparts (Gillum, 1982; Keil et al., 1984).
2. Risk Factor Differences
Several hypotheses have been proposed to explain the possible
reasons for these racial differences in CHD. The two most promisinq
hypotheses are (1) that there are racial differences in the operative
risk factors for CHD, and (2) that blacks may have some biologic and/or
psychosocial protective factors which may reduce their CHD risk. An
alternative hypothesis is that the standard CHD risk factors may be of
different degree of importance (i.e., different risk functions) (Currv
et al., 1984; Table 4, Figures 4 & 5, Tyroler, 1984; McDonald et al.,
1984). The available evidence also identifies several differences
between blacks and whites such as in the prevalence of hypertension, in
metabolic or biochemical factors, and in psychosocial characteristics
308
that suggest that different factors may potentiate coronary heart
disease in these group.
a. Biological Risk Factors
A strong family history of coronary heart disease is an
accepted risk factor for both blacks and whites. However, a family
history of essential hypertension may not be as strong a predictor of
coronary heart disease for blacks given the greater overall prevalence
of hypertension in black populations (Curry et al., 1984; Neaton et al.,
1984). For example, in the five-year follow-up of 361,620 men screened
for the MRFIT study, although elevated blood pressure was a strong
predictor of CHD mortality in whites, high blood pressure appeared to be
a better predictor of cerebrovascular disease and CVD mortality than of
CHD mortality in these black men (Neaton et al., 1984). This does not
mean, however, that hypertension in blacks is not a major CHD risk
factor. The evidence is incontrovertible that there is a high
population-attributable risk of hypertension for all-cause mortality and
for CHD mortality in blacks (See table 2 and Figure 1, Tyroler et al.,
1984; Figures 1 & 2, Neaton et al., 1984; Haywood, 1984). For these
reasons, aggressive prevention and treatment of hypertension must be
continued (Tyroler, 1984).
Similarly, the presence of such ECG abnormalities as minor S-T
segment depressions and T-wave abnormalities may not have the same
diagnostic significance for blacks as for whites (Bartel et al., 1971)
given the greater prevalence of these abnormalities in elderly U.S.
black populations (Riley et al., 1973) and even in black societies
in Africa and the Caribbean (Watkins, 1984b) where there is low CHD
prevalence. However, when abnormalities indicative of left ventricular
hypertrophy (LVH) are present in conjunction with other major risk
factors, then total mortality risk is likely to be even higher for
blacks than for whites (Table 1, Tyroler, 1984).
On the other hand, obesity and diabetes mellitus, which are not as
prevalent among whites, may be more significant risk factors for CHD
among blacks, especially for black women (Curry et al., 1984; Tables 6 &
7, Cooper et al., 1984; McDonald et al., 1984). For lipid profiles, the
situation is somewhat more complex. Typically, blacks tend to have
higher HDL-cholesterol (HDL = high-density lipoprotein) and
apolipoprotein Al levels, and lower levels of LDL-cholesterol (LDL =
low-density lipoprotein), VLDL-cholesterol (VLDL = yery low-density
lipoprotein), apolipoprotein CI I, and triglycerides than whites
(Gartside et al., 1984; Figures 1-4, Glueck et al., 1984; Figures 3-5,
Heiss et al., 1984; Rowland & Fulwood, 1984; Neaton et al., 1984). This
combination of higher HDL- and lower LDL-cholesterol levels for
equivalent total cholesterol level may confer some protection on blacks.
Unfortunately, there is some preliminary evidence from the MRFIT study
suggesting that an unexpected by-product of aggressive
pharmacotherapeutic intervention in hypertension is a significant
reduction in HDL-cholesterol level especially when propranolol is added
to diuretic regimens. Concurrent changes in diet and weight may have
also contributed to these changes in the lipoproteins (Lasser et al.,
1984; Currv et al., 1984). Tyroler (1984), however, argues against
309
overinterpreting these results as directly relevant to the larqe
population of black hypertensives, since these findings were obtained in
a select sample of upper middle-class white men. Whatever reduction, if
any, in degree of protection against CHD that may result from diuretic-
and propranolol-induced HDL-cholesterol level changes is not comparable
in magnitude to the significant benefits derived from aggressive blood
pressure control in black communities.
McDonald et al. (1984) also point to several apparent biochemical
risk factor differences between blacks and whites that include
differences in sodium/potassium ratios in urine, in plasma renin and
epinephrine levels, in hematocrit values, in differential rates of G6PD
enzyme deficiency, and in possible differences in transport of these
electrolytes via the sodium/potassium pump in the red blood cells. All
of these differences may be related to blood pressure differences
between the groups. However, as noted by Watkins (in press), the Evans
County, Georgia study found that black-white differences in blood
pressure were not due to higher sodium intake in blacks (Grim et al.,
1980). Blaustein (1984) and Trevisan et al. (1984) also discount
disturbances in the sodium transport mechanism as accounting for racial
differences in hypertensive populations.
b. Psychosocial Risk Factors
When we consider the host of psychosocial risk factors
implicated in coronary heart disease, the picture is even more complex.
Psychosocial risk factors for CHD that are generally accepted or
suggested include cigarette smoking and heavy alcohol consumption,
social isolation and inadequate social support, and sustained disturbinq
emotions (e.g., anxiety, hostility, etc.), especially as part of the
Type A behavior pattern (Coronary Prone Behavior Review Panel, 1981;
McDonald et al., 1984).
In the case of blacks, these factors do not appear to operate as
directly or to have the same demonstrated importance as they do for
whites. For example, socioeconomic disadvantage, including experiences
of racism and discrimination, appears to make a more significant risk
contribution for blacks than for whites (Tyroler et al., 1984; James,
1984a). On the other hand, risk behaviors such as smoking, alcohol
consumption, and limited physical activity appear to be pathogenic to
blacks and whites to the same degree. However, although more blacks
smoke, black smokers typically smoke fewer cigarettes than white smokers
(See Table 6, Garfinkel, 1984). Similarly, the relationship between
cigarette smoking and pattern of CHD and risk appears to be different
for blacks and whites. Neaton et al. (1984) note that, in the MRFIT
screenee follow-up studies, different 5-year, age-adjusted, CHD
mortality rates were obtained for black and white men as a function of
the number of cigarettes smoked (Figure 8). They also noted that black,
5-year, cerebrovascular mortality rates were significantly higher than
for whites, for a comparable number of cigarettes smoked (Figure 9).
In addition, there are complex interrelationships between cigarette
smoking, cholesterol levels, and blood pressure that impact on CHD
mortality; these appear to be discordant between blacks and whites
310
(Neaton et al., 1984; Garfinkel, 1984). The relative risk (RR) of CHD
death over 5 years, in smokers compared to nonsmokers, was relatively
constant in subgroups of black and white MRFIT screenees categorized
according to serum cholesterol level (250 mg/dl) and diastolic blood
pressure (DBP), both)90 mm Hg and<90 mm Hg. The RRs lay in the ranqe
1.62 - 1.83. In contrast, for men with a serum cholesterol level of 250
mg/dl, the corresponding RRs lay in the range 2.23 - 3.72, and were
highest for black males with a DBP of 90 mm Ha (RR = 3.72) and for white
males with a DBP of 90 mm Hg (RR - 2.87). However, the highest
mortality rates were observed among smokers with elevated serum
cholesterol levels, in black normotensive men, and in white hypertensive
men (Table 7, Neaton et al., 1984).
Also, blacks as a group tend to be more physically active than
whites (Rowland & Fulton, 1984), although this difference may well be
due to socioeconomic status-related differences in the proportion of
white- vs. blue-collar workers in these groups.
Research on the role of Type A behavior pattern and related effects
of strong emotions on CHD risk, although extensive for whites (Review
Panel, 1981) is extremely limited for blacks (James, 1984b). The
absence of relevant research on this question is a major lacuna in the
literature. The related work on suppressed anger (Diamond, 1983) and,
most recently, on the interaction of low education and the John
Henry-type coping pattern in hypertensive black men (James, 1984c)
suggests that these psychological processes need to be seriously
considered as possible risk factors in CHD in blacks as well. Similar
attention should be given to occupational stresses (House, 1974; James
et al., 1984d), and to social mobility (Gillum & Paffenbarger, 1978) as
additional, potential risk factors for CHD, especially qiven the unique
pressures faced by increasing numbers of black men and women who are
entering professional and managerial occupations.
At the broader socioecologic level, blacks face disproportionately
greater CHD risks due to higher life stresses (Harburg et al., 1973) and
to lower medical care access, utilization, and, possibly, lower quality
care (Yelin, Kramer & Epstein, 1983).
In addition to the consideration of risk factors, there is also the
need to explore the role of possible biologic and psychosocial
protectors against CHD. Given the higher prevalence of hypertension and
comparable prevalence of other CHD risk factors in blacks, it is
surprising that the prevalence of CHD and CHD mortality rates in blacks
is not even higher (Gillum, 1982). One possible explanation for the
current lower-than-expected rates in blacks is the presence of factors
that confer some degree of protection against CHD on blacks. We have
already reviewed the evidence of possible biologic protection in the
lipid profile that combines higher HDL-cholesterol and apolipoprotein Al
levels with total cholesterol level, which is more common in blacks than
in whites (Heiss et al., 1984; Glueck et al., 1984). It would also be
useful to explore the possible protective role that social supports
(Broadhead et al., 1983), psychological hardiness (Kobasa, Maddi & Kahn,
1982), a high sense of personal, social, and cultural coherence
(Antonovski, 1979), low "John Henryism" (James et al., 1984c), and other
311
adaptive stress-coping styles (Billings & Moos, 1981) may play in
reducing CHD risk in blacks.
In sum, these data point to the need to pursue actively this
question of possible racial differences in CHD risk factor levels and
risk functions, as well as in protective factors. In this process, a
multidimensional perspective that includes biological, psychological,
and social risks, as well as possible protectors, should be considered.
3. The Salience of Socioeconomic & Sociocultural Factors
A major recurrent theme in the debate over black/white differences
in the pathogenesis of coronary heart disease is the apparent
differential significance of socioeconomic status (SES) and
sociocultural factors. There seems to be some consensus of opinion
that, for blacks, social status and related sociocultural influences
probably contribute in some as-yet-undefined way to the observed pattern
of CHD risks and outcomes (Myers et al., 1984; James, 1984a, b; Kasl,
1984). This consensus appears to be based on a collection of
theoretical formulations, clinical observations, and on provocative
empirical evidence. The absence of more conclusive data seems to be due
to deficits in the conceptualization, specification, and measurement of
social status variables; to inconsistencies in the consideration of
these variables in studies of CHD; and to the frequent omission of these
variables, or to the confounding of these variables, with race in
studies of CHD in multiethnic populations. A related point is that
investigators typically look for main effects of SES and related
variables rather than testing the hypothesis that these factors may
operate interactively with other factors. The hypothesis that these
variables may be important to different degrees in different
populations, and may operate at different points in the CHD process is
also typically ignored.
An alternative conceptualization of social status and of this
selective effects' hypothesis was articulated in the Working Group III
report (Myers et al., 1984). The contributors suggested that
socioeconomic and sociocultural factors should be subsumed under the
generic heading of social status, and that this construct should be
defined multidimensionally. Sociostructural and sociopsychological
characteristics were distinguished and speculations about their
contributions to CHD were made. Sociostructural features of social
status include such factors as race, education, occupation, income,
marital status, and social mobility. These factors define social status
through the social meanings, institutions, and practices that govern
life opportunities and obstacles for blacks. The sociopsychological
features of social status, on the other hand, include the host of
individual differences in experiences and personal attributes,
resources, and liabilities, all of which determine individual
vulnerability or resistance to objective external social conditions.
These include personality characteristics, life stresses, coping styles,
the availability and use of social supports, patterns of help-seeking,
and characteristic levels of anxiety, happiness, anger, and other
similarly strong emotions.
312
In the assessment of these factors, careful attention must be given
to distinguishing objective, concrete events and experiences that blacks
face from the subjective interpretations and meanings conferred on these
experiences. The latter include consideration of both individual and
collective group meanings (McDonald et al., 1984; James, 1984a; Kasl,
1984; Myers, 1982).
In addition, consideration should be given to the analysis of main
effects and interactions of social status as predictors of CHD outcomes.
Most of the available evidence seems to provide more support for an
interactional contribution of these variables toward predicting illness
outcomes (Harburg et al., 1973; Kasl, 1984).
Finally, there is growing justification for considering separately
the influence of social status on the presence of factors that either
increase or decrease CHD risk status; on factors that influence the
management of risk (i.e., early symptom identification, intervention,
and disease prevention); on factors that influence the level of CHD
morbidity observed; and on factors that ultimately affect the level and
pattern of CHD mortality observed in the black population. Social
status factors may also exert their impact through such health care
system factors as the timing and availability of medical services, the
accuracy of clinical diagnosis, and the appropriateness and
effectiveness of the treatment received (Myers et al., 1984; Cooper et
al., 1981; James, 1984a; Kasl, 1984). Figure 1 in Myers et al. (1984)
describes these hypothesized influences in a simplified diagram.
4. Racial Differences in the Diagnosis, Treatment, & Course of
Coronary Heart Disease
The final substantive concern is whether the observed black/white
differences in CHD mortality might be due, in part, to differences in
the natural history and treatment of CHD. This concern over possible
differential health care system effects as a function of race and social
class is based on anecdotal, clinical, and preliminary research reports
that suggest that there are important differences between blacks and
whites in rates of access and utilization of preventive and emergency
medical services (Jackson, 1981; Yelin et al., 1983). Also, reports of
differences in risk status at the point at which treatment is initiated
(Haywood, 1984a, b; Francis et al., 1984; Curry et al., 1984), and
differential use of coronary arteriography and coronary artery bypass
grafting (CABG) procedures with black and white CHD patients (Oberman &
Cutter, 1984) have been noted. Physicians have also reported greater
resistance to, and lower compliance with, medical regimens among black
patients: This is believed to contribute toward diminishing the
effectiveness of treatment (Jackson, 1981). Data are inadequate with
respect to secondary prevention efforts (Oberman & Cutter, 1984), but
those studies that used standardized diagnostic and intervention
procedures (e.g., MRFIT & HDFP) show that blacks often derive similar or
greater benefit than whites from such intensive approaches to CHD risk
reduction and treatment (Tables 6 & 7, Rowland & Fulwood, 1984; Table 5,
Connett & Stamler, 1984; Table 5, Langford et al., 1984).
313
The data on surgical outcomes for black CHD patients are also
inadequate (Haywood, 1984). However, preliminary evidence suggests that
blacks show no greater operative mortality risk to myocardial
revascularization procedures when hypertension, diabetes, and prevalence
of hyperlipidemia are taken into account (Table I, Sterling et al.,
1984).
It is apparent from these reviews that no strong conclusions about
black/white differences in the natural course of CHD are justified at
this time, given the paucity of good data. However, there is enough
evidence to justify the suspicion that some racial and SES differences
in CHD course do exist, and that these differences are probably
attributable to differences in level of risk, pattern of health care
utilization, and in the pattern of health care system characteristics.
These factors probably interact to produce a more pathogenic process,
high CHD mortality, and higher CHD-related sudden death rates in black
Americans.
RECOMMENDATIONS FOR FUTURE RESEARCH
The present evidence supports the contention of Gillum and others
(Gillum, 1982a; Gillum & Grant, 1982) that CHD is a major health problem
for black Americans. Further, though there is growing and provocative
evidence suggesting that blacks and whites may not differ significantly
in overall prevalence and incidence rates for CHD, these groups do
appear to differ in overall CHD mortality and sudden death rates.
Furthermore, low-income blacks, and black women in particular, appear to
be at greater mortality risk than their male, white, and upper-SES
counterparts. In addition, the evidence suggests that many of these
racial differences may well be due to differences in biologic and
psychosocial risk factors, as well as to differences in the usual
diagnostic and treatment practices for suspected CHD.
Because of such significant deficits in the available data on CHD
in blacks, these statements should be treated as tentative and viewed
more as interesting hypotheses to be pursued vigorously rather than as
firm conclusions. The significance of these issues to the health of the
nation, however, clearly justifies an aggressive approach toward
answering major questions about CHD in black populations. The chief
areas of deficit and the appropriate recommendations for future research
are organized programrnatically as follows:
1. The most glaring lacuna results from the limited availability
of epidemiologic and clinical data on CHD in blacks. This
deficit can be corrected by a two-stage process consisting of:
a. first, existing NCHS data bases should be improved by
separating the data on blacks from the "non-white"
category, and by including large, nationally
representative samples of blacks in all existing or
proposed national health studies (e.g., NHANES, the
Coronary Artery Risk Development Study, and the Community
CHD Surveillance Studies); and
314
b. second, population-based prospective studies of black
cohorts similar to the Framingham Heart Study should be
funded.
In all of these studies great care should be exercised in the
selection of appropriately representative black samples, with
consideration given to such sources of group variability as urban vs.
rural residency, geographic location, socioeconomic status, and national
origin. The reliability and appropriateness of the assessment and
diagnostic tools and procedures used with this population must be
demonstrated.
2. The second major research priority should be a series of
studies addressing the issue of differential CHD risk pattern
and functions in blacks and whites. This priority could be
addressed by:
a. a more complete risk profile analysis of the black
participants of the HDFP and MRFIT studies should be
supported. This is a cost-effective strategy that avoids
the high start-up costs typically associated with new
research efforts with large samples; and
b. the development of multi-center, multi-disciplinary,
case-control studies focused specifically on such issues
as sudden death in the community, hospital admission and
discharge of patients with diagnoses compatible with CHD,
emergency room visits for chest pain and related
complaints, and surveillance of the offspring of indexed
cases should be supported. The latter is probably more
cost-effective than separate studies, and would take
better advantage of existing research teams in
geographically diverse areas with access to different
black populations.
Risk factor studies should be based on a multifactorial, biobehavioral
perspective that includes possible biological, psychological,
behavioral, and social sources of differences in risk factors and
protective factors. Consideration of possible differences in both risk
factor level and risk function should also be included.
3. Finally, there is considerable justification for supporting studies
that address the interface of patient and community characteristics on
the one hand, and health care system characteristics and practices on
the other, as predictors of CHD risk, natural course, and outcome.
Priority should be placed on studies that focus on physician beliefs and
attitudes, and the usual diagnostic and intervention practices used to
treat black patients with suspected or confirmed CHD. Attention should
also be given to how social status and associated sociopsychologic
factors influence the host of CHD-related health beliefs and behaviors
of blacks and how these, in turn, interact with the characteristics of
community health care providers to affect the observed pattern of
coronary heart disease morbidity, natural course, and mortality in black
315
populations. (See Appendix for a summary list of the specific research
recommendations made).
Underlying all of these recommendations is the need to give
priority to sound conceptualization and methodological rigor. Most
studies on CHD in blacks, as previously noted, suffer from a variety of
conceptual and methodological deficiencies which must be avoided in
future studies. Central among these are problems in the specification
and adequacy of measurement of the variables of interest, and inadequate
size and representativeness of the sample of blacks studied. Particular
attention to the issues of socioeconomic status and to gender must be
given in all of these studies.
In addition to aggressive support for research on the causes of CHD
in blacks, there is need also to increase support for prevention efforts
directed at reducing CHD risk factors in blacks. Ultimately, little
will be gained by knowing how prevalent CHD is in black populations or
what factors contribute to its occurrence if we do not also act
aggressively to prevent it. Results from the NHANES I & II studies
(Rowland & Fullwood, 1984), from the HDFP study (Langford et al., 1984),
and from the MRFIT study (Connett & Stamler, 1984) show significant
reductions in CHD risk-related factors in blacks through aggressive
programs of education and treatment. Such efforts must be continued and
should include greater black representation in future samples.
In sum, the present evidence points to the significance of CHD as a
major health problem for black Americans. Further, these data argue for
the need for more aggressive and focused support for studies targeted at
the major questions about CHD epidemiology, risk status, and
patient-health care system transactions that might account for the
observed CHD differences between black and white populations. Support
for targeted primary prevention programs in black populations is also
justified.
This paper was prepared under personal services contract No. 263SGX13736
from the Secretary's Task Force on Black and Minority Health, Department
of Health and Human Services. Dr. Myers is also a Scholar-In-Residence
at the Fanon Research & Development Center, Charles R. Drew Postgraduate
Medical School, Los Angeles. The author wishes to express his
appreciation to Dr. Laurence 0. Watkins and Elisabeth Pitt for their
careful review and suggested revisions.
316
APPENDIX
SUMMARY RECOMMENDATIONS FROM:
The National Heart, Lung, and Blood Institute's
Working Conference on Coronary Heart Disease in Black Populations
Bethesda, Maryland
September 29-30, 1983
PURPOSE: To review current knowledge about coronary heart disease in
blacks and identify areas for priority research effort. The
areas recommended included:
Prospective studies of the incidence of coronary heart disease in
blacks.
Research to determine why black women apparently have higher
coronary heart disease mortality rates than white women.
Research to determine the impact of antihypertensive treatment on
coronary heart disease in blacks.
Research on ways to modify, in school-age populations, the
development of eating patterns and physical activity behavior that
may result in obesity in later life.
Research on variables such as risk factor patterns associated with
coronary heart disease treatment, includina coronary artery bypass
surgery and angioplasty and its outcome in blacks compared with
whites.
• Studies of beliefs, awareness, and pre-hospital behavior that might
delay appropriate diagnosis and treatment for individuals in the
black community who have symptoms of coronary heart disease.
• Studies of risk factors for coronary heart disease in blacks that
include investigation of the impact of socioeconomic status and
ethnic diversity.
• Special efforts be made to aid minority researchers and those in
minority research settings to be competitive in seeking research
funding.
317
SUMMARY RECOMMENDATIONS FROM:
The National Heart, Lung, and Blood Institute's
Working Group to Discuss Strategies for Minimizing Coronary Heart
Disease in Black Populations
February 21-22, 1984
PURPOSE: To develop research strategies to answer priority issues
related to the gaps in our knowledge concerning coronary heart
disease in blacks.
Five task groups were convened to focus on priority issues
developed by the previous conference.
Task Group I focused on the problem of a paucity of epidemiologic
data available on the occurrence of coronary heart disease among
blacks and on the uncertain quality of mortality and morbidity data
available for blacks.
• They recommended further development of NHLBI research in
community and cohort surveillance of coronary heart disease
risk factors and events in black Americans.
They recommended a specific, prospective, community-based
cohort study with oversampling of blacks in one geographic
area which would ensure an adequate number and diversity of
blacks to assess prevalence of coronary heart disease, and
physiologic and psychosocial risk factors of coronary heart
disease.
• Longitudinal follow-up for at least five years would then
provide natural history data for an adequate number of blacks.
The Task Group suggested that cooperation with the NHANES III
study (to be carried out by the National Center for Health
Statistics) would be desirable. The phase one validation and
pilot studies, the definitive study, and the final data
analysis would require an estimated eight years.
• In addition, they recommended cohort studies among black
professionals and among industrial populations or medical
insurance groups.
• This Task Group also recommended a mortality data follow-back
survey to focus on the comparability of the accuracy of cause
of death, as reported on death certificates and in hospital
records, for blacks and whites, with particular concern for
the sensitivity and specificity of coronary heart disease
ascertainment. The goal would be to determine causes of
noncomparability and to try to develop programs to reduce the
problems.
318
Task Group II focused on the research strategies for ascertaining
the distribution of known and suspected risk factors for coronary
heart disease (biochemical and psychosocial) for
race-sex-socioeconomic status subgroups of the population and their
relative contribution over time to the development of coronary
heart disease in these subgroups."
• They recommended that a large, multicenter, prospective study
in diverse settings be initiated to determine differences in
the prevalence of coronary heart disease and associated risk
factors between blacks and whites. This study would include
prospective follow-up to determine the relative contribution
of these risk factors to coronary heart disease events over
time. Risk factors to be measured would include the standard
risk factors, health habits, and psychosocial environmental
factors. Cooperative efforts with the National Center for
Health Statistics were also recommended. Various instruments
for measurement of risk factors, especially psychosocial
variables, would need to be validated in blacks. (This
recommendation is compatible with the similar recommendation
from Task Group I.)
Task Group III focused their attention on possible research efforts
to determine the effects of various antihypertensive therapies on
coronary heart disease events in high-risk populations
(particularly blacks) and to determine whether the metabolic,
hemodynamic, and side-effects of these treatments are different in
blacks as compared with whites.
• The task aroup recommended a multicenter, randomized,
double-blind, clinical trial as the best type of study to
address these issues. Phase I pilot studies, as well as the
phase II definitive trial, were recommended. The latter would
be at least five years in duration.
Task Group IV focused on the issue of obesity as a risk factor for
coronary heart disease in black females.
• They recommended that research is needed to determine the
relative importance of obesity as a risk factor for coronary
heart disease in black females. Case-control studies to
obtain estimates of relative risk were recommended initially
and then prospective epidemiologic and intervention studies.
• Methodologic studies to develop tools for assessing coronary
heart disease risks in blacks compared with whites were also
recommended.
• Studies were recommended to assess the value of weight
reduction on modification of other coronary heart disease risk
factors in black and white women, stratified by different
levels of obesity. Methodologic studies may be needed to
identify effective means for achieving weight loss in
different subgroups.
319
Research was recommended to determine factors associated with
and potentially responsible for the observed divergence in
development of obesity after adolescence in black compared
with white females.
Task Group V focused on the problem of apparent greater incidence
of pre-hospital and sudden death and the lower hospital survival
rates of blacks following heart attack.
This task group recommended survey efforts to learn what level
of awareness is present among adult blacks regarding risk
factors and symptoms of coronary heart disease, and to
investigate and assess the appropriateness of pre-hospital
behavior by blacks, in response to such symptoms. The goal of
this research is to obtain information to assist in
implementing interventions that will reduce mortality and
morbidity resulting from CHD in black populations. Pilot
studies and pretests of measurement instruments may be
necessary.
This task group also recommended a study to assess the extent
of knowledge, attitudes, and practices of health providers in
diagnosing and treating coronary heart disease in black
populations. Such a study would also develop appropriate
educational interventions.
320
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treatment. American Heart J 108(3;2):688-694, 1984.
46. Rowland ML, and Fulwood R: Coronary heart disease risk factor
trends in blacks between the first and second National Health and
Nutrition Examination Surveys, United States, 1971-1980. American
Heart J 108(3;2):771-779, 1984.
47. Savage D, et al.: Summary of Workshop I: Working group on
epidemiology. American Heart J 108(3;2):699-703, 1984.
48. Shapiro S, Weinblatt, Frank CW, and Sager RV: Social factors in
the prognosis of men following first myocardial infarction.
Milbank'Memorial Fund Quarterly 48:37-50, 1970.
49. Sterling R, Graeber GM, Albus RA, Burton NA, Lough FC, and Fleming
AW: Results of myocardial revascularization in black males.
American Heart J 108(3;2):695-699, 1984.
50. Strong JP, Oalman MC, Newman WP, Tracy RE, Malcom GT, Johnson WD,
McMahan LH, Rock WA, and Guzman MA: Coronary heart disease in
young black and white males in New Orleans: Community Pathology
Study. American Heart J 108(3;2):747-759, 1984.
323
51. The Review Panel on Coronary-Prone Behavior and Coronary Heart
Disease. Coronary-prone behavior and coronary heart disease: A
critical review. 'Circulation 63(6):1199-1215, 1981.
52. Trevisan M, Ostrow D, Cooper RS, Sempos C, and Stamler J: Sex and
race differences in sodium-lithium counter-transport and red cell
sodium concentration. American J of Epidemiology 120(4):537-541,
1984.
53. Tyroler HA: Overview of risk factors for coronary heart disease in
black populations. American Heart J 108(3;2):658-660, 1984.
54. Tyroler HA, Knowles MG, Wing SB, Logue EE, Davis CE, Heiss G,
Heyden S, Hames CG: Ischemic heart disease risk factors and
twenty-year mortality in middle-age Evans County black males.
American Heart J 108(3;2):738-747, 1984.
55. Watkins LO: Epidemiology of coronary heart disease in black
populations: Methodologic proposals. American Heart J
108(3;2):635-640, 1984a.
56. Watkins LO: Coronary heart disease and coronary disease risk
factors in black populations in underdeveloped countries: The case
for primordial prevention. American Heart J 108(3;2):850-862,
1984b.
57. Watkins LO: The epidemiology of cardiovascular disease in black
populations. In R.A. Williams (Ed.), Textbook of Ethnic Medicine.
New York, McGraw-Hill, in press.
58. Yelin EH, Kramer IS, and Epstein WV: Is health care use equivalent
across social groups? A diagnosis-based study. American J of
Public Health 73(5):563-571, 1983.
324
Fig. 1: S.V. Kasl. p. 661
I. Asynptonatic status, risk factor(s) absent
II. Asymptcnatic status, risk faetor(s; present
III. Subclinical disease susceptible to detection
i
• su
I
IV. Initial tymptan experience
l~
V. Initial event (diagnostic criteria net)
l~
VI. Course of disease (repeat episodes, residual disability, etc.)
Via. Natural course
VTTb. Treatment experience
I*
VII. Mortality (oase fatality)
Fig. 1. Developmental schema for coronary heart dis-
ease: the possible role of race and psychosocial factors.
325
Table 2: Keil et al, 1984
T«bl« II. Incidence* of CHD manifestations by race and sex, 1960-1961 to 1974-1975
Black males Black males , high Black fema les White fema les
(N - 322) White males (TV '601) SES (N - 101) (N - 440) (N = 71b
Manifestation n Rate SE n Rate SE n Rate SE n Rate SE n Rate SE
11 CHD 43 131.7 18.3 114 188.4 15.5 4 61.2 34.5 72 161.0 17.1 84 113.8 11.3
CHD living 16 50.7 12.6 60 95.2 11.6 2 26.0 26.6 42 100.9 14.8 50 67.4 9.2
AMI 9 28.5 9.9 51 80.5 10.8 2 26.4 26.9 15 36.3 9.4 27 36.3 6.9
Angina pectoris 7 22.2 9.1 8 12.8 4.8 0 0 27 63.6 12.1 22 29.8 6.4
HD death 27 79.8 14.2 54 93.8 11.7 2 38.3 37.4 30 62.2 10.5 34 46.3 7.1
AMI 12 35.8 10.2 35 60.5 9.7 0 0 17 35.6 8.4 18 24.4 5.5
Sudden death 11 32.2 9.3 6 10.2 4.6 0 0 6 13.0 5.8 6 8.2 3.7
ASHD 4 11.7 7.3 13 23.2 6.4 2 44.0 43.0 7 13.8 5.7 10 13.8 4.4
ASHD - Atherosclerotic heart disease.
'Rates per thousand, age adjusted by indirect method. Rates for subheadings not additive.
326
FIG. 1: GILLUM £ LIU , p. 729
1000
_ 500-
F 400
1940
Fig. 1. Age-adjusted CHD mortality rates per 100,000
population for U.S. nonwhites aged 34 to 74 years, from
1940 to 1978. WM = White males; NM = nonwhite males;
WF - white females; NF = nonwhite females.
327
FIGS. 1 & 2: LEAVERTON, FEINLIEB & THQM, p.p. 733-73*<
3 LOWFST
Fig. 1. U.S. age-adjusted CHD mortality for white males
aged 35 to 74 years.
IKS-1972
1978
Fig. 2. U.S. age-adjusted CHD mortality for white
females aged 35 to 74 years.
328
FIGS. 3 & A: LEAVERTON, FEINLIEB & THQM, p.p. 735-736
W68-1972
1968-1972
1978
1978
LOWEST
NO OATA
HIGHEST
SECOND
Third
LOWEST
NO OATA
Fig. 3. U.S. age-adjusted CHD mortality for black males
aged 35 to 74 years (34 states with data).
Fig. 4. U.S. age-adjusted CHD mortality for black
females aged 35 to 74 years (34 states with data).
329
TABLE k: TYROLER et. al., p. 7^1
Table IV. Multivariate association of risk indicators with time to death (PH) and 20-year cumulative risk of death
(LRF) in males aged 40 to 64 years (all-cause mortality) in Evans County
Blacks Whites
LSS HSS
PH LRF PH LRF PH LRF
Intercept -5.653 4.054 -6.943
Age 0.075* 0.103' 0.059* 0.086* 0.059* 0.076+
SBP 0.016* 0.022* 0.015* 0.019' 0.012+ 0.017+
Cholesterol^ -0.020 -0.041 -0.033} -0.05SJ 0.0661 0.0921
Cholesterol2^ 0.005 0.010 0.009+ 0.015J -0.0131 -0.0181
Smoking current 0.547+ 0.492j| 0.701 + 1.071+ 0.862' 1.195+
Smoking past -0.037 -0.115 0.54 2} 0.909§ 0.347 0.489
Quetelet index*; -0.480 0.399 -2.903 J -3.513§ -3.676t -6.0131
Quetelet index:^ 0.053 -0.081 0.369 J 0.429§ 0.428+ 0.7361
Deaths/population 129/294 126/276 88/236
XJ 73 64 68 55 48 47
•p < 0.001.
tO.001
0 1 1 1
1 P6) 1 C7S-S0) HI 111-151 IV (•6-91) V <>ti)
Diastolic Blood Pressure Ouintile (mm Hg)
■ lack Men: wrui. u.n 6 3.602 7.418 3.724 65242 3.955 61.351 4.708 65.051 7.491 66.322
Fig. 1. Five-year age-adjusted total mortality rate (per
1000) by diastolic blood pressure level by race.
• Btack Men
O WNte Men
£| a t> • < Is I < ■ • > n 2 ^ 1 ' '
No. Bi.o Man. Mo. wrvi. Umn. 0'— 1 1.76) 3602 67.418 i «i rv (76-60) <»1-6S) C8f-»0 Diastolic Blood Pressure Ouintile (mmHg) 3.734 3955 «-7n0 65.242 61.251 65.051 V M1I 7,491 66.322
Fig. 2. Five-year age-adjusted CHD mortality rate (per
1000) by diastolic blood pressure level by race.
332
TABLE 1: H. A. TYROLER , p. 659
Table I. Five-year mortality rates in black and white males by education and presence of LVH at baseline for ail
HDFP stratum I participants and those not receiving medication at baseline: Referred-care males ages 40 to 69 years,
with entry diastolic blood pressure of 90 to 104 mm Hg*
% Mortality
(Deaths) N
Crude
Age -adjust edf
LVH-t
LVH+
LVH-
LVH+
LVH-
LVH+
All stratum I participants
WM > HS (18) 446
WM «= HS (26) 402
WM < HS (42) 335
BM < HS (56) 344
Participants not receiving medication at baseline
WM>HS '(13)347
WM «= HS (21) 315
WM < HS (22) 260
BM < HS (41) 268
( D 8 4.0 12.5 4.5 10.2
( 2)10 6.5 20.0 7.0 21.9
( 7)16 12.5 43.8 10.6 28.6
(11)32 16.3 34.4 15.4 32.3
ne ( D 8 3.8 12.5 4.4 10.2
( 0) 7 6.7 0.0 7.4 0.0
( 5)12 8.5 41.7 7.2 12.4
( 6) 18 15.3 33.3 14.9 33.2
WM = White males; BM * black males: HS «= high school education completed.
•From TyToler HA: Race, education, and 5-year morulity in HDFP stratum I referred-care males. In Gross F, Strasser T, editors: Mild hypertension:
Recent advances. New York. 19S3, Raven Press.
♦Age-adjusted rates by direct method. Standard population is age decade distribution of all white males aged 40 to 69 years with entry diastolic blood
pressure of 90 to 104 mm Hg.
JLVH determined by ECG. LVH+ denned as major LVH by Minnesota Code; LVH- denned as all others..
333
TA3LES 6 & 7 COOPER et. al., p.o . 830-331
Table Vi. Mean values of cardiovascular risk factors in black and white males and females, by diagnostic category:
CHA Detection Project'
Risk factor Diagnostic category White males Black males White females Black females
Systolic BP (mm Hg)t DM/H 144.6 147.9 137.0 146.9
Non-DM/H 138.5 141.8 131.8 134.3
Diastolic BP (mm Hg)t DM/H 84.9 89.9 81.1 88.8
Non-DM/H 81.6 84.6 77.4 80.3
Serum cholesterol (mg/dl) DM/H 210.0 211.9 215.3 209.7
Non-DM/H 205.7 201.9 208.5 205.6
No. of cigarettes smoked/day DM/H 11.6 10.6 8.0 9.2
Non-DM/H 9.5 8.9 7.1 5.7
Relative weight DM/H 1.25 1.30 1.20 1.32
Non-DM/H 1.22 1.22 1.18 1.26
BP « Blood pressure; DM ■ diabetes mellitus; H
•Age standardized, ages 2? to 64 years.
♦ Excludes those treated for hypertension.
hyperglycemia.
Table VII. All-cause death rates (per 1000) in black and
white males with diabetes or hyperglycemia vs those with
normoglycemia: CHA Detection Project*
Black/
White Black white
Diagnostic group males males ratio
Diabetes or hyperglycemia 96.0 (240)+ 95.7 ( 9) 1.00
Normoglycemia 52.3 (618) 62.7 (45) 1.20
Ratio of diabetes and 1.84 1.53
hyperglycemia to
normoglycemia
•Age standardized, ages 25 to 64 years.
♦ Number of deaths.
334
FIGS. 1 - 3: GLUECK et. al., p.p. 8l6t 818
•Or
While 9
Black o*
Black 0
6-17. n-358
6-17. n«326
6-17. n«1l9
6-17. n-124
32 <1 26 18 5 10 50 00 95
Birth Birth TH TH TH TH TH
Fig. 1. Mean levels of HDL cholesterol (HDLC) in
healthy, full-term, black and white neonates. (Data from
Glueck et al.11) Percentile distribution of HDL cholesterol
in black and white males and females ages 6 to 17 years:
The Princeton School District Prevalence Study. (Data
from Morrison et al.15)
•s
•5
35
»S
20-59. ft'
20-59 n-
134
?C3
Bock o
White o
Black O*. 20-59. n»76
While O*. 20-59. n«306
6 10 25 60 75 90 95
TM TH TH TH TH TM TH
Fig. 2. HDL cholesterol distribution in black and white
males and females, ages 20 to 59 years: The Cincinnati
LRC's Princeton School District Prevalence Study. (Data
from Morrison et al.17)
100
90
BO
70
60
so
40
30
20
10
0
N-BO M'44
N*B6 N-56
N-673 N-30
nnn
i
ES0
EHldlci. holci
COlDICI. HOLCJ
E23lDLC|. HOlCt.#Blacka more
likely to have
ILDLC1. HOLC) predominant
N-433 N-30 f*7^
accounting for
their hjpei
Cho'e»t«'oiemia
than whites
lor both
Children and
aduiti. p • .02
JESSE
r*xr
WHITE BLACK
MALES
6-19 YRS
WHITE BLACK
FEMALES
6-19 YRS
WHITE BLACK
MALES
20-79 YRS
WHITE BLACK
FEMALES
20-79 YRS
Fig 3. PercenUge of hypercholesterolemic subjects (total cholesterol on two consecutive visits ^ the
90th percentile) having LDL and/or HDL cholesterol primarily accounting for their hypercholesterolemia.
These subjects were arbitiarily categorized by having LDL > the age-sex-race-specific 95th percentile
and HDL > the age-sex-race-specific 95th percentile (at visit 2); LDL > the 95th percentile and HDL
<95th percentile; LDL < the 95th percentile and HDL 2: th? 95th percentile; and LDL < the 95th
percentile and HDL < the 95th percentile. (Data from Morrison et al.:')
335
FIG. A: GLUECK et. a).t p.819
Black Excess HDLC, mg/dl
0 2 4 6.8
n = 434
n=459
n = 174
n=188
"I---1---1---1---1---I---1---1
L • ry-'-TKfflrfrffltG.rls
n = 434
n = 45
n = 174
n = 188
E^BaBBBSSatBoys
Women
gaS^EESSBBi t Men
Covariance Adjusted Means
Quetelet Calories
White Black White Black
1.88 1.93 1939t 1642
1.90 1.95 2364 2156
2.39t 2.61 1746* 1464
2.65 2.72 2520 2450
Means covariance adjusted
for age and education of
the head of the household
t, p<.01
'J tAgM** ^lif 'ifi%'4ttipi *;
tGirls
tBoys
Women
g^gT^BSatMen
Means covariance adjusted
for age and occupation of
the head of the household
t, p<.01
1.88 1.94 1920t 1669
1.90 1.95 2345 2186
2.39* 2.61 1746* 1451
2.65 2.71 2515 2440
Fig. 4. Covariance-adjusted mean levels of HDL cholesterol, Quetelet index, and calories per day in
randomly recalled, blacks and whites. Means were covariance adjusted, separately for age and education of
head of household and for age and occupation of head of household. Mean excess of HDL cholesterol
(blacks above whites) is displayed. (Data from Khoury et al.1)
336
FIGS. 3-5: HEISS et. al., p.p. 809-810
-20 -15 -10
-5 0 5
mg/dl
C-TOTAL (p-19)
C-HDL 250 mg/dl
Smokers
Serum cholesterol <250 mg/dl
Serum cholesterol >250 mg/dl
Diastolic BF ^90 mm Hg
Nonsmoker
Serum cholesterol <250 mg/dl
Serum cholesterol >250 mg/dl
6mokcrs
Serum cholesterol <250 mg/dl
Serum cholesterol >250 mg/dl
Total
No. of men
Black
6.094
1.056
6.215
925
3.669
929
3.771
831
23.490
White
127.864
21.182
72.635
14,905
46.016
13,419
22.010
7,353
325,384
Age-adjusted rate (5 yr)
Black
1.67
6.86
6.21
11.OS
2.88
4.92
6.42
9.04
4.83
White
2.40
6.12
5.62
10.78
3.66
9.88
11.06
17.49_
5.22
Black/u-hiie ratio
0.70
1.12
1.10
1.03
0.75
0.50
0.58
0.52
0.93
339
FIG. 1: MYERS et. al. , p. 708
FIGURE 1. CONCEPTUAL MODEL OF THE ROLE OF SOCIAL STATUS IN CHD RISK, CHD MORBIDITY AND MORTALITY
SOCIOSTRUCTURAL
VARIABLES
©
SOCIAL
STATUS
©
PERSONAL,
SOCIOPSYCHOLOGICAL
VARIABLES
©
• ETHNICITY
• EDUCATION
• INCOME
• OCCUPATION
• GENOER
• AGE
• NATIONALITY
• SOCIAL MOBILITY
• SOCIAL POSITION
• SOCIO ENVIRONMENTAL FACTORS
• BEHAVIORAL CHARACTERISTICS
• PSYCHOLOGICAL TRAITS* STATES
MORTALITY
®
TABLES: 6 & 7: ftQV'UND & FULWOOD, p.p. 776-777
Table VI. Mean systolic and diastolic blood pressure and mean serum cholesterol level of adults 25 to 74 years old b>
race, sex, and survey period, showing standafd errors and age-adjusted means: United States, 1971-1975 and
1976-1980't
1971-1975 1976-1980
1971-197 1976-1 no
Age-adjusted meant Age-adjusted meanf
Risk factor and race-sex group Mean SE Mean SE SE SE
Systolic blood pressure (mm Hg)
White males 132.8 0.5 130.5 0.6 132.8 0.5 130.6 0.7
White females 130.1 0.5 125.6 0.7 129.4 0.4 125.1 0.7
Black males 140.0 1.6 133.2 1.1 140.4 1.7 133.7 1.1
Black females 137.8 1.4 130.6 1.2 138.6 1.4 131.7 1.1
Diastolic blood pressure (mm Hg)
White males 83.7 0.3 82.3 0.5 83.6 0.3 82.2 0.5
White females 80.4 0.4 78.1 0.5 80.1 0.3 78.0 0.5
Black males 89.9 1.0 85.3 0.8 89.8 1.0 85.5 0.8
Black females 87.0 0.9 82.3 0.6 87.1 0.8 82.6 0.6
Serum cholesterol level (mg/dl)
White males 218.0 1.1 216.6 1.2 217.5 1.0 216.7 1.1
White females 222.8 1.1 220.7 1.2 221.4 1.0 219.9 1.2
Black males 225.5 4.5 215.0 3.3 225.7 4.9 215.4 3.0
Black females 219.4 2.9 217.1 3.2 221.2 2.6 219.2 2.7
SE = Standard error of the mean.
•Data from the National Health and Nutrition Examination Survey. Division of Health Examination Statistics, National Center for Health Sutistics,
HyatLsville. Md.
tApe adjusted by direct method to the total U.S. population as estimated at the midpoint of the 1976-1980 NHANES.
fable VII. Age-adjusted percent distribution among risk factor groups with standard error of age-adjusted percent for
selected race-sex groups ages 25 to 74 years by survey period: United States, 1971-1975 and 1976-1980*______________
Risk factor groupst
None}
One§
Two or more \\
1971-1975 1976-1980 1971 ■ 1975 1976-1980 1971-1975 1976-1980
Racc-scx group % SE % SE % SE % SE % SE % SE
White males White females Black males Black females 390 45.4 23.4 28.0 1.3 1.1 3.2 2.4 42.5 47.0 29.3 41.4 1.1 0.9 2.0 2.3 46.2 41.9 44.3 49.2 1.3 1.0 3.9 2.5 44.5 42.9 50.9 43.7 1.1 0.8 2.3 2.0 14.8 12.7 32.3 22.8 0.8 07 4.1 1.8 13.0 0.6 10.1 0.5 19.8 2.1 14.9 1.2
cs,
•L^om^he^tional Health and Nutrition Examination Survey. Division of Health Examination Statistics. National Center for Health Statisti
rAyr.djuesied t direct method to the total U.S. population estimated at the midpoint of the 1976-1980 NHANES
tlSten "of the following: systolic blood pressure of at least 100 mm Hg and/or d.aslol.c blood pressure of at least 95 mm Hg. serum cholesterol level of at least
260 mg/dl. of smoker.
jOnly one of the above.
rjVo or more of the above.
341
TABLE 5: COHMETT & STAMLER, d. 8^3
Ta&le V. Mean values at sixth annual visit and percent changes in risk factors from baseline, by study group and
race
SI group UC group
White (N ^5338) Black (N - 416) White (N «= 5227) Black (N = 411)
Sixth ann. Sixth ann. Sixth ann. Sixth ann.
Risk factors visit % Change visit % Change visit % Change visit % Change
DBP (mm Hg) 80.4 -11.4 81.3 -13.6 83.5 -7.9 85.6 -8.1
SBP (mm Hg) 121.4 -10.3 122.3 -11.7 126.5 -6.4 129.4 -5.8
Percent smokers* 33.3 -46.2 38.0 -43.0 43.8 -29.0 42.9 -22.5
Serum cholesterol (mg/dl) 235.8 -7.3 231.0 -6.0 240.5 -5.6 237.3 -3.7
Plasma cholesterol (mg/dl) 228.5 -6.4 224.4 -6.5 233.3 -4.5 230.2 -4.3
Plasma HDL cholesterol (mg/dl) 41.3 -2.6 46.0 -6.5 41.4 -2.6 47.6 -4.8
Plasma LDL cholesterol (mg/dl) 148.7 -8.6 148.3 -8.5 152.8 -6.4 153.8 -5.4
Plasma triglycerides (mg/d#l) 200.9 +1.7 153.9 +7.2 203.0 +3.3 147.1 +4.0
Weight (lb) 187.7 -0.7 192.3 -0.2 190.1 +0.7 190.1 +0.7
HDL - High-density lipoprotein; LDL ■ low-density lipoprotein.
•Thioeyanau-adjusted rates, as defined by Neaton et al.'
342
Table 5: Langford et al, p. 800
Table V. Five-year incidence of angina, ECG MI, history of MI, and MI by RQ for SC participants in HDFP
Angina ECG Ml
Sa mple size Events Rate Sample size Events Rate
White males 1799 89 4.9 1868 12 O.fi
Black males 983 54 5.5 1056 15 1.4
White females 1078 103 9.6 1172 3 0.3
Black females 1211 79 6.5 1329 10 0.8
Total 5071 325 6.4 5425 40 0.8
343
Table 1: R. Sterling et al, p. 696
Table I. Operative mortality (1970-1982)
Black male patients Other WRAMC patients
Year No. /c No. %
1970-1977* 1978-1982 1970-1982 2/14 1/40 3/54 14 2.5 5.6 22/407 33/916 55/1323 5.4 3.6 4.2
WRAMC - Walter Reed Army Medical Center.
'Prior to use of cardioplegia.
344
Prevalence and Incidence of
Ischemic Heart Disease in
United States' Black and
White Populations
Melford J. Henderson, M.A., M.P.H.
Research Fellow
Association of Black Cardiologists
Daniel D. Savage, M.D., Ph.D.
Medical Advisor
National Center for Health Statistics
Hyattsville, Maryland
A major deficiency of epidemiologic research on ischemic heart disease
(IHD) in the United States has been the limited amount of reliable
information published on blacks (1). Published information on the
prevalence and incidence of IHD in blacks is incomplete and, at least on
the surface, inconsistent (1). Reliability of data on prevalence of IHD in
blacks has been compromised by the inclusion of relatively small numbers of
blacks in population-based studies and/or selection bias in the reported
study groups. Varying diagnostic criteria and study methods have
contributed to the apparent confusion. The purpose of this paper is first,
to review current information on the prevalence and incidence of IHD in
U.S. black and white populations; second, to document the inadequacy of
available information; and third, to suggest implications of these data for
the DHHS Task Force on Black and Minority Health.
Definition of Ischemic Heart Disease
Ischemic heart disease in this review includes all of the disorders of
the heart that result from inadequate supply of oxygen to the myocardium.
Manifestations are:
* myocardial infarction (MI), or death of myocardial tissue
resulting from significant reduction or interruption of
coronary blood flow;
* angina pectoris (AP), a varied symptom complex (most
commonly including substernal chest discomfort) caused
by transient ischemia that falls short of producing
infarction;
* arteriosclerotic heart disease, defined as obstruction
of coronary vessels by atherosclerotic plaques leading
to functional and structural changes in the myocardium
with or without symptoms;
* sudden death, defined as death within seconds to several
minutes (for some studies, several hours) after the onset of
symptoms.
Gillum (2) emphasized that IHD is a major cause of illness in both
U.S. black and white populations, and is the leading cause of death.
National data derived from death certificates indicate that it is the cause
of death in 30-40% of all adult blacks and whites (2). Death from IHD
occurred at a lower rate in black men than white men in 1940, increased
until it exceeded the white death rate in 1968, and then declined to a
level comparable to that in white men in 1976, but still exceeded the 1940
rate (2). Black women appear to have had IHD mortality rates similar to or
higher than those of white women (2), but comparisons of morbidity and
mortality are difficult because absolute numbers of cases of IHD in studies
involving black women are small (2).
The 1960-62 National Health Examination Survey (NHES) conducted by the
National Center for Health Statistics (NCHS) indicated little difference
between U.S. blacks and whites in prevalence of IHD (3). In a random
population sample, black and white persons were equally likely to have
arteriosclerotic heart disease, but the sampling error was too large for
meaningful, detailed comparison. Electrocardiographic (ECG) data from two
national probability samples (NHANES 1 and 2) are currently being analyzed
at NCHS. The data consist of ECGs from nearly 17,000 subjects (age range,
347
25-74 years) with a total of about 2000 blacks in the two studies, combined
(Tables 1 and 2). These data sets are deceptively large. The number of
black men and women in individual age groups is small, as is the percentage
with MI-associated ECG changes. For example, the percent with
Ml-associated Q-wave Minnesota codes (1-1-1 to 1-1-7)(4) in the white men
ranged from less than 2% in those age 44-55 years to about 3% in those age
65-74 years. For black men, the percentages with such codes were similar
to those of whites in younger men but substantially lower (about 1/2 the
white male rate) in those over age 65 years.
In contrast to those for black men, the prevalence estimates for white
men are relatively stable. For example, the addition of two "cases" in the
55-64 year age group would double the prevalence of Ml-associated ECG
findings in black men. The small numbers of blacks in the sample and low
number of such ECG findings in black and white men in the general
population do not allow comparisons of prevalence. Differences in ECG
criteria for Ml-associated changes has added to the confusion in various
studies. The use of a standardized code (e.g., the Minnesota code)
contributes to the comparability of various epidemiologic studies.
However, even this has not resolved all criteria-related issues. For
example, use of the Minnesota coding system for major Q wave findings
(e.g., codes 1-1-1 to 1-1-7) allows comparison of these studies with
others. However, it is possible that this would leave undetected a group
of individuals who have clinically accepted ECG evidence of MI but do not
quite^meet the criteria for these codes. The addition of other Minnesota
codes (e.g., 1-2-1 to 1-2-5, 1-2-7, 1-2-8 and various ST and T wave codes)
increases sensitivity but at the expense of specificity. If these various
ECG manifestations have the same meaning in blacks and whites, these
technical considerations would not necessarily invalidate comparisons.
However, there is some evidence that the meaning of at least some of the
ECG markers (e.g., some ST-T changes) may be different in blacks and whites
(4a).
Some preliminary comparisons can be made between blacks and whites in
the NHANES studies despite the indicated limitations of the data. The
prevalence of Ml-associated ECG changes is similar in 45 to 64 year old
black and white men but greater in older white men than in black men.
This might be related to the 5 to 7 year shorter life span of black men
(average life span of about 65 years) such that the group that lives to 65
includes a larger proportion of those who have not succumbed to IHD at an
earlier age. Differential case-fatality (discussed below) could also be
involved. The prevalence of IHD in black women was greater than or equal
to that of white women (0% in the young to about 1% over age 64) with no
cross-over.
The 1972 Health Interview Survey (5) indicated higher age-specific
self-reported prevalence of heart disease in nonwhites (predominantly
blacks) than in whites in both age groups 17-44 and 45-64 years. However,
nonwhites reported the diagnosis of coronary heart disease less often than
whites in ages 45-64 years (15.5 vs. 36.8 per 1000).
In some studies, prevalence of IHD was estimated from surveys or
baseline examinations of population-based cohorts. In 1960, the Evans
County, Georgia study (6) surveyed nearly all residents in this rural
county 40-74 years old and 50% of those aged 15-39 years; this resulted in
3102 participants. Nearly three times as many white men as black men
348
reported syndromes of IHD (Table 3A), with fewer black men reporting IHD at
all ages. When black and white women were compared, there was no
significant racial difference in prevalence (14 vs. 18 per 1000).
In the Charleston, SC study, 2275 blacks and whites were examined in
1960/61 (7). Age-adjusted IHD rates were computed indirectly using
standard age-specific rates for the total study sample. In the cohort
intake of 1960/61, white men of all ages had greater IHD prevalence than
black men (Table 3B). Prevalence in black women was identical to that in
white women (26.6 per 1000). Black women aged 75 years and over had a
greater IHD prevalence than black men (though not statistically
significant). Thus, the Charleston and Evans County studies reported
similar findings on the order of prevalence of IHD (Tables 3A and 3B).
White men were more likely to have IHD than black men. White and black
women had almost identical prevalence rates.
In the Hypertension Detection and Follow-Up Program (HDFP)(8),
hypertensive participants were evaluated by ECG for evidence of MI and were
administered the Rose Questionnaire to detect symptoms of AP. AP was found
to be more prevalent in black men than white men (7.7 vs. 5.1 per 100) and
more prevalent in black women than white women (9.9 vs. 8.6 per 100).
Compared to those without AP, those subjects with AP had twice the
likelihood of death during the ensuing five years. This applied to all
race-sex groups except black women.
The prevalence of MI at baseline as determined by the Rose
Questionnaire was higher in whites (5.9 per 100) than blacks (4.6 per 100),
and higher in white women (7.2 per 100) than black women (4.2 per 100).
Incidence of IHD in Black and White Populations
The study of incidence requires thorough assessment of the population
at risk, thorough tabulation of cases, and recognition of all indicated age
and sex differences. Completed population studies yield too few incidence
cases of acute myocardial infarction (AMI) and do not permit adequate
assessment of comparative incidence among men and women in black and white
populations.
Prior to 1970, studies that compared IHD incidence in blacks and whites
lacked population-based age-specific data. They usually involved only one
hospital or group of hospitals. For example, Mihaley and Whiteman (9)
studied AMI at Harlem Hospital in 1950-54, but during that time only 152
such cases were admitted. Whites, accounting for 5.8% of admissions,
constituted 13.1% of infarctions. The investigators maintained that AMI
was as common in blacks as in whites, but they did not have adequate data
to support their conclusion.
Data from NCHS Hospital Discharge Surveys in 1972, 1975, 1978, and
1981 (10) indicate that men and women over age 45 maintained nearly
constant hospital discharge rates for AMI. During 1981, rates for black
men were about 45% of total white rates, while rates for black women were
about 70% of white rates (ages 45-64). However, these data may be not
reflect true incidence because they do not take into account subjects who
died suddenly before hospital admission.
Few major studies involving the epidemiology of IHD yield data on
racial incidence. Ongoing prospective studies, such as those conducted in
Framingham, MA (11) and by the Hospital Insurance Plan of New York (HIP)
349
(12), involve predominantly white samples. The HIP study of insured
persons found the annual age-adjusted rate of incidence of first MI in
nonwhite (predominantly black) men to be half the rate in white men and the
case-fatality rate to be higher in nonwhites (47.5%) than in whites
(35.3%). However, the total number of nonwhite cases was too small to
yield statistically significant conclusions.
Additional studies of interest are those carried out in Nashville, TN
(14); Baltimore, MD (15); Newark, NJ (16); and Columbia (17,17a) and rural
Pee Dee (17a), SC. These studies reported incidence of hospitalization for
IHD in blacks and whites by age and sex (Table 7).
In the Nashville study (14), 1967-68, hospital surveillance was used
to detect all cases of AMI and sudden coronary death in persons ages 35-74
years. Although only 20% of the population group was black, the total
number of subjects was large (167,000). Annual incidence of MI was
substantially lower for black men than for white men at each age (Table 4).
White men had more than double the rate of black men. Annual incidence of
AMI was also greater in white women than in black women (Table 4). In this
study, black men had greater incidence than black women. In the 1970-72
Baltimore study (15), the number of nonfatal Q wave ("transmural AMIs") was
determined from a review of hospital records in the Baltimore area.
One-third of the 500,000 population sample was black. The incidence of
"transmural" AMI in white men ages 25-64 years was more than twice the
incidence in black men; but white women had only slightly greater incidence
than black women. Black and white women had similar nonfatal MI rates, and
in Nashville and Baltimore the occurrence of nonfatal MI was twice as
frequent as sudden death.
The Newark study (16) involved review of 89.5% of all 1973 hospital
admissions (15,124) in that city. Age-decade specific MI hospitalization
rates were reported for seven age groups (Table 5) . When analyzed by
decade, data revealed no statistically significant difference in incidence
between white men and black men, but the incidence was slightly higher for
white men at every decade except 40-49. AMI rates for black women were
slightly higher than for white women at every decade, but these differences
were not statistically significant.
The Columbia, S.C. study (17) in 1978 examined age-adjusted incidence
of AMI. The population included patients with prior heart disease and MI,
as well as those whose sudden death was associated with MI. Both proven
and suspected MI incidence were included, and in each age group over age 35
years, white men had higher incidence of MI than did black men. Black and
white women under age 65 years showed no consistent difference in
incidence, but black women ages 66-75 years had somewhat lower incidence.
Overall frequency was greatest in white men and decreased in the following
order: black men, white women, black women.
These studies differ in various ways making a firm conclusion
regarding the relative incidence of IHD in blacks and whites impossible.
Inadequacy of the available incidence data is related to several problems
including:
* the limited number of studies that have been carried out;
* the inadequate numbers of blacks in the populations studied;
* the use of varying standards for age-adjustment;
* the use of varying diagnostic criteria;
* varying lengths of follow-up.
350
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from the studies do suggest that the lower number of hospital admissions of
black men for AMI may at least partially, be explained by the greater
number of out-of-hospital deaths.
Incidence of Sudden Death
Sudden death comprises a large segment of total IHD death in U.S.
black and white populations; however, as with other IHD end points, few
reliable population-based data are available with regard to blacks. It is
generally acknowledged that sudden death results from some type of
arrhythmia--either asystole or ventricular fibrillation--and may have
different underlying pathophysiological mechanisms from those of
demonstrable AMI. The Charleston study (7) revealed sudden death in black
men (32.2 per 1000) to be three times the rate in white men (10.2 per
1000). The rate in black women (13 per 1000), was 1.5 times the rate in
white women (8.2 per 1000).
In the 1967-68 Nashville study (14), investigators identified likely
cases of sudden death from death certificates of people aged 35-74 years
and then interviewed relatives or friends to confirm the diagnoses. The
study showed black men to be at slightly greater risk of dying suddenly
from apparent IHD than white men. The death rate was greater in black men
(2.80 vs. 2.20 per 1000) than in white men. Black women had greater rates
than white women (1.48 vs. 0.70 per 1000).
The Baltimore study (15) measured total IHD rate and sudden death
rate. Sudden death rates were similar for black and white women. The rate
for black men was somewhat higher than for white men. No significant
racial differences were found in the incidence of sudden death, with or
without prior history of heart disease, but the number of sudden deaths was
very small for black women. The incidence of instantaneous death (defined
as death within 15 minutes of onset) was the same in black and white women,
but was slightly lower in black men than in white men.
In the Nashville study, more sudden deaths occurred within two hours
of symptom onset than in the Baltimore study, but fewer unwitnessed deaths
were recorded. Ratios of sudden death between white men and women were 5:1
for Baltimore and 3:1 for Nashville. Male-to-female ratios in blacks were
identical (2:1) in both studies.
The variation in statistics on incidence of sudden death may be
traceable at least partially to the following:
* varying definitions of terms,
" varying population samples, and
•'" inaccurate death certificates.
The Charleston study defined sudden death as death within one hour.
The Baltimore and Nashville studies defined it as death within 24 hours of
symptom onset. The HIP study (12) defined sudden death as death occurring
within 48 hours of symptom onset. Such conflicts in definition limit
possible inferences from the studies.
Population samples, too, varied from study to study. Baltimore studied
a slightly younger population than Nashville, and the HIP study included
only first MI, while the Nashville study included subsequent Mis. In
addition, the HIP cohort consisted mostly of employed (and therefore
relatively healthy) individuals, in contrast to the free-living population
353
in the Nashville study. These variations may account for the rate of
sudden death in Nashville being higher for all age groups than in the HIP
study.
Inaccuracy of death certificates may also be a significant problem in
available data. This is suggested by the comparison of the Baltimore study
results with the 1975 findings of Kuller et. al. who reviewed government
vital statistics published for Baltimore (18). Nonwhite death rates from
IHD were found to be higher here than those reported in the 1970-72
Baltimore study, with a higher sudden death rate for black women than white
women; little racial difference was found among men. In a representative
sample, death certificate diagnosis of IHD was confirmed by other data for
only 67% of black men and 52% of black women. The black male-female rate
ratios was higher in the Baltimore study than in the official vital
statistics, suggesting that vital statistics may not be a valid source of
information on IHD trends in urban black populations. Since death
certificates were also a primary source in the Nashville study, these
findings call into question its conclusions.
Incidence of IHD as Determined by Post-mortem Examination
Another method for assessing the incidence of death from IHD is
postmortem examination, particularly those in which autopsied cases are
representative of either all deaths or a definable sample of deaths.
Investigators in the Baltimore study performed detailed autopsies of 87% of
all sudden deaths occurring in a section of Baltimore and certified by the
medical examiner (15,18). In a total of 169 sudden deaths, 58% of black
men and women had severe three or four-vessel coronary artery stenoses
compared with 70% of white men and 34% of white women (18). In the 118
cases without prior history of coronary heart disease, black men had acute
coronary thrombi less frequently than white men (16% vs. 26%). However,
black and white men had approximately the same frequency of hemorrhage and
plaque. As noted by Gillum (2) these investigators found greater heart
weights in blacks, but they found fewer recent (6% vs. 13%) and old (26%
vs. 43%) myocardial infarctions in black men.
Assessment of Trends in Morbidity and Mortality in Blacks and Whites
Moriyama et. al. (19) and Cooper (20) have summarized cardiovascular
mortality in the U.S. in the last four decades. Gillum (2) points out that
prior to the 1940s, mortality trends were difficult to assess due to
inadequacies in reporting, diagnosis, and certification. Data from
national statistics have consistently shown rates for white men to exceed
those of nonwhite men, while rates for nonwhite women have exceeded those
of white women since 1950 (21). It should be noted that in these early
data, national statistics compared whites and nonwhites, with no direct
comparison between whites and blacks (who comprise 85% of U.S. nonwhites)
(19).
The data show that mortality due to IHD seems to be greater in urban
than suburban areas, but that mortality has declined nationwide (2,20).
The only exceptions are the Pacific and Mountain states, where the number
of deaths attributed to IHD increased in nonwhites aged 35-74 years in both
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Table 1
TOTAL NUMBER OF SUBJECTS WITH ECG READINGS
IN THE NATIONAL HEALTH AND NUTRITION
SURVEY 1971 - 1975 (Preliminary-1/28/85)
Age Group
ALL 25-44 45-54 55-64 65-74
Black men 379 120 97 75 87
White men 2688 1037 636 528 487
Black women 465 191 105 84 85
White women 3152 1329 739 556 528
Table 2
TOTAL NUMBER OF SUBJECTS WITH ECG READINGS
IN THE NATIONAL HEALTH AND NUTRITION
SURVEY 1976 - 1980 (Preliminary-1/28/85)
Age Group
ALL 25-44 45-54 55-64 65-74
Black men 528 209 62 129 128
White men 4302 1554 617 1086 1045
Black women 635 248 100 135 152
White women 4794 1726 647 1176 1245
356
Table 3A
PREVALENCE OF CORONARY HEART DISEASE IN BLACKS AND WHITES AGE 15-75+
YEARS PER ONE THOUSAND SUBJECTS, (1960) EVANS COUNTY, GA
N n Rates*
Black men 537 12 22.4
White men 947 54 59.0
Black women 646 9 13.6
White women 972 18 18.2
N= number of persons in each race/sex group
n=number of cases
* Age-adjusted rates by indirect method using total population
as standard
Source: JC Cornoni et al, Ref 6a
Table 3B
PREVALENCE OF CORONARY HEART DISEASE IN BLACKS AND WHITES AGE 35-75+
YEARS PER ONE THOUSAND SUBJECTS, (1960-61) CHARLESTON, SC
N n Rates*
Black men 333 11
White men 650 49
Black women 453 13
White women 738 20
32.7
75.8
26.6
26.6
* Age adjusted by indirect method
Source: Keil JE et al, Ref 7
357
Table 4
INCIDENCE OF ANTERIOR MYOCARDIAL INFARCTION IN BLACKS AND WHITES AGE
35-74 YEARS PER ONE THOUSAND SUBJECTS, (1967-68) NASHVILLE, TN
N n Rates*
Black men 14,628 31
White men 64,478 379
Black women 16,236 18
White women 71,469 137
2, .12
5. .88
1. .11
1. .92
N= number of persons in each race/sex group
n= number of cases of AMI
* Age group specific data showed similar trends
Source: Hagstrom RH et al, Ref 14
Table 5
INCIDENCE OF ACUTE MYOCARDIAL INFARCTION IN BLACKS AND WHITES
PER ONE THOUSAND SUBJECTS BY AGE DECADE, (1973) NEWARK, NJ
Age Decade Total Cases
20-29 30-39 40-49 50-59 60-69 70-79 80+
Black men „ _ 1.16 2.41 4.61 4.04 2.27
- - (ID (15) (17) (6) (D 50
White men 0.10 0.78 1.09 3.38 5.37 6.28 2.41
(D (7) (11) (34) (41) (27) (4) 125
Black women 0.10 0.19 0.85 1.64 2.18 4.04 5.58
(2) (3) (4) (12) (10) (8) (4) 43
White women 0 0.11 0.28 0.88 1.31 3.43 3.28
- (D (3) (10) (12) (21) (8) 55
Numbers in parentheses represent numbers of cases
Source: AB Weisse et al, Ref 16
358
Table 6
INCIDENCE OF IHD MANIFESTATIONS BY RACE AND SEX, 1960-1961
TO 1974-1975, CHARLESTON,SC
Black men
(N=322)
White men Black men, high SES
(N=601) (N=101)
Manifestation
Rate
Rate
n
Rate
All IHD 43 131.7
All nonfatal IHD 16 50.7
AMI 9 28.5
Angina pectoris 7 22.2
Black women
(N= =440)
Manifestation n Rate
All IHD 72 161.0
All nonfatal IHD 42 100.9
AMI 15 36.3
Angina pectoris 27 63.6
___
114 188.4
60 95.2
51 80.5
8 12.8
Whit e women
(N= 718)
n Rate
84 113.8
50 67.4
27 36.3
22 29.8
""
4 61.2
2 26.0
2 26.4
0 0
N= Total number of persons in each race/sex group
n= Total number of cases in each IHD category
SES=socioeconomic status
* Rates per one thousand, age adjusted by indirect method
Source: JE Keil et al, Ref 7
359
Table 7
INCIDENCE OF HOSPITALIZATION RATES FOR AMI IN U.S . BLACK AND WHITE
POPULATIONS PER ONE THOUSAND SUBJECTS
Age/Sex Evans County,GA
1960-1967
Nashville Baltimore Newark Columbia,SC
1967-1968 1970-1972 1973 1968
35-44
Black men 1.79 1.02 - 0.84
White men 8.28 1.84 0.783 1.25
Black women 3.72 0.19 0.193 0.38
White women 0.69 0.20 0.113 0.06
45-54
Black men 5.79 1.55 0.6 1.16 3.97
White men 10.48 5.50 1.9 1.09 5.76
Black women 5.10 1.41 0.2 0.85 0.68
White women 4.14 1.05 0.4 0.28 1.33
55-64
Black men 1.52 3.47 0.8 2.41 7.61
White men 17.79 9.82 2.9 3.38 10.75
Black women 8.97 1.64 1.0 1.64 2.91
White women 5.52 2.77 1.1 0.88 2.56
65-74
Black men 8.69 3.87 4.61 6.27
White men 32.14 12.75 5.37 18.82
Black women 6.21 1.77 2.18 5.75
White women 19.72 6.49 1.31 8.47
Source: RF Gillum, Ref 2
360
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Langford H, Mebane I, Neser W, Potts J, Saunders E, Savage D,
Schachter J, Stamler J, Tillotson L, Watkins L, Williams R:
Report of Epidemiology Working Group on Coronary Heart Disease
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2. Gillum RF: Coronary heart disease in black populations I.
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3. National Center for Health Statistics: Coronary heart
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Office. NCHS publication No. 1000, Series II, No. 101, 1965.
4. Prineas RJ, Crow RS, Blackburn H: The Minnesota Code Manual
of Electrocardiographic Findings. Boston, 1982. John Wright-
PSG Inc.
4a. Watkins LO: Epidemiology of coronary heart disease in black
populations: methodologic proposals. Am Heart J 1983;108:
635.
5. National Center for Health Statistics: Prevalence of chronic
circulatory conditions, U.S. 1972. Washington, D.C, U.S.
Dept. of Health, Education, and Welfare. Publication No. (HRA),
75-1521. 1974.
6. McDonough JR, Hames CG, Stulb SC, et al: Coronary heart
disease among Negroes and Whites in Evans County, Georgia.
J Chronic Dis 1965;18:433.
6a. Cornoni JC,Waller LE,Cassel JC,Tyroler HA,Hames CG:The Incidence
Study-Study Design and Methods. Arch Intern Med 1971;128:896.
7. Keil JE, Loadholt CB, Weinrich MC, Sandifer SH, Boyle E, Jr:
Incidence of coronary heart disease in blacks in
Charleston, South Carolina. Am Heart Journal 1984;108:779.
8. Langford HG, Oberman A, Borhani NO, Entwisle G, Tung BS:
Black-white comparisons of indices of coronary heart disease and
myocardial infarction in the stepped care cohort of the
Hypertension Detection and Follow-Up Program. Am Heart Journal
1984;108:797.
9. Mihaley JP, Whiteman NC: Myocardial infarction in the negro:
Historical survey as it relates to negroes. Am J Cardiol
1958;21:464.
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10. Feldman, J: National morbidity studies. In Havlik RJ,
Feinleib M, editors: Proceedings of the conference on the
decline in coronary heart disease mortality. NIH
publication No. 79-610, Washington, DC 1979, U.S. DHEW.
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The Framingham Study: Section 11. Washington, D.C, U.S.
Government Printing Office, September, 1968.
12. Shapiro S, Weinblatt E, Frank CW, et al: Incidence of coronary
heart disease in a population insured for medical care.
(HIP). Am J Public Health 1969; 59 (supp 2):1.
13. Cassel J, Heyden S, Bartel AG, Kaplan BH, Tyroler HA, Coroni
JC, Hames CG: Incidence of coronary heart disease by ethnic
group, social class and sex. Arch Intern Med 1971;128:901.
14. Hagstrom RH, Federspeil CF, Ho Y: Incidence of Myocardial
infarction and sudden death from coronary heart disease in
Nashville, Tennessee. Circulation 1971;44:884.
15. Kuller H, Cooper M, Perper J, et al: Myocardial Infarction
and sudden death in an urban community: Bull NY Acad Med 1973;
49:532.
16. Weisse AB, Abiuso PD, Thind IS: Acute myocardial infarction
in Newark, NJ: A study of racial incidence. Arch Intern Med
1977;137:1402.
17. Zmyslinski R, Lackland DT, Keil JE, and Higgins JE: Increased
fatality and difficult diagnosis of in-hospital acute myocardial
infarction: Comparison to lower mortality and more easily
recognized pre-hospital infarction. Am Heart Journal 1981;
101:586.
17a. Keil JE, Saunders DE, Jr, Lackland DT, Weinrich MC, et.al: Acute
myocardial infarction: Period prevalence, case fatality, and
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Carolina. Am Heart J 1985;109:776.
18. Kuller L, Perper J, Cooper M: Demographic characteristics
and trends in arteriosclerotic heart disease mortality: Sudden
death and myocardial infarction. Circulation, 1975; 51 and 52
(suppl III):III-1.
19. Moriyama I, Krueger DE, Stamler J: Cardiovascular Diseases
in the United States. Cambridge, 1971. Harvard University
Press, p. 49.
20. Cooper R, Stamler J, Dyer A, Garside D: The decline in
mortality from coronary heart disease, U.S.A., 1968-1975.
J Chronic Disease 1978;31:709.
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21. Rosenberg, HM and Klebb, AJ: Trends in cardiovascular mortality
with a focus on ischemic heart disease: US, 1950-76 in
Proceedings of the Conference on the Decline in Coronary Heart
Disease Mortality. U.S. DHEW, Public Health Services, NIH
Pub. No. 79-1610, May 1979.
22. Keil JE, Lackland DT, Hudson MB, Saunders DE Jr, et al:
Coronary heart disease and stroke mortality in South Carolina
geographical and temporal trends. J SC Med Assn 1983;
79:65.
23. Savage DD: Echocardiographic assessment of cardiac anatomy
and function in black and white hypertensive subjects. In
Williams R, ed. Textbook of Ethnic Medicine (in press).
24. Haywood LJ: Coronary heart disease mortality/morbidity
and risk in blacks. Clinical manifestations and diagnostic
criteria: The experience with the Beta BLocker Heart Attack
Trial. Am Heart Journal 1984;108:787.
Supplemental References
Ahmed SS, Razefort R, Franciato R: Incidence of acute
myocardial infarction among blacks in an urban community.
J Med Soc NJ 1977;74:1058.
Five-year findings of the hypertension detection and follow
up-program II. Mortality by race, sex and age. JAMA 1979;
242:2572.
Kleinbaum DG, Kupper LL, Cassel JC, Tyroler NA: Multivariable
analysis of risk of coronary heart disease in Evans County,
Georgia. Arch Intern Med 1971;28:943.
Kleinman JC, DeGruttola VG, Cohen BB, Madans JH: Regional
and urban-suburban differentials in coronary heart disease
mortality and risk factor prevalence. J Chronic Dis 1981;34:11.
Kuller L: Sudden and unexpected nontraumatic deaths in adults.
A review of epidemiological and clinical studies. Journal of
Chronic Diseases 1966;19:11652.
National Center for Health Statistics: Mortality, United States,
1977. By Number of Deaths. Washington, D.C, 1981, U.S.
Government Printing Office.
Stamler J, Berkson DM, Lindberg HA, Miller OW, Hall Y: Racial
patterns of coronary heart disease: blood pressure, body weight,
and serum cholesterol in whites and negroes. Geriatrics
1961;16:382.
363
Differences in
Socioeconomic Status and
Acculturation among
Mexican Americans and
Risk of Cardiovascular
Disease
Helen P. Hazuda, Ph.D.
Division of Clinical Epidemiology
Department of Medicine
University of Texas Health Science Center at San Antonio
San Antonio, Texas
Introduction
The purpose of this paper is to review the available literature
to assess the extent to which increasing differences in socioeco-
nomic status (SES) and acculturation among Mexican Americans are
associated with differences in cardiovascular risk factors and to
make public health recommendations based on the findings. It
should be noted initially that there is no commonly agreed upon
definition of Mexican American (MA) ethnicity and that the
several indicators most commonly used to classify persons as
Mexican American identify populations which differ significantly
in composition and size (1-5). The studies reviewed in this
paper relied on a variety of indicators for Mexican American eth-
nicity, ranging from simple self-definition to a complex
algorithm which considers surname and birthplace of subject's
parents, ethnic origin of subject's grandparents, and subject's
preferred ethnic identity. The study populations were referred
to variously as Hispanics, Spanish-Americans, persons of Spanish-
surname, Mexican Americans, or Mexican origin Hispanics. I have,
nonetheless, restricted this review to studies which explicitly
identified the target population as Mexican origin Hispanics or
were carried out in a geographic region where the overwhelming
majority of Hispanics are known to be Mexican origin, (e.g., over
80% of Hispanics in California and over 92% in Texas are Mexican
origin (6)). To place the review in context I will begin by pre-
senting a brief overview of changes in socioeconomic status and
acculturation which have occurred among Mexican Americans during
the last several decades, and, then, document the role of car-
diovascular disease as a cause of mortality in this ethnic group
before moving to a review of cardiovascular risk factors.
Socioeconomic Status and Acculturation of_ Mexican Americans1
The three major indicators of socioeconomic status are education,
occupation, and income. Of these, education is perhaps the most
important since it is closely linked to upward mobility and the
acculturation process. At the time of the 1970 census, Mexican
Americans still lagged about a generation behind the total U.S.
population in educational attainment and, together with the
Puerto Ricans, ranked as the least schooled Hispanic subgroup.
Nevertheless, Mexican Americans had made substantial gains in
schooling over the last several decades. Around the time of
World War I only about 10 percent of high-school-completion age
"^Statistics reported in this section, unless otherwise indicated,
were abstracted from Reference 7: Jaffe AJ, Cullen RM, Boswell
TD: The Changing Demography of Spanish Americans. New York:
Academic Press, 1980.
367
Mexican Americans had actually completed high school. By the end
of World War II about 20 percent were high school graduates and,
ty 1970, over 50 percent of the school-age cohort of U.S.-born
Mexican Americans and 32 percent of the Mexico-born cohort were
high school graduates. Gains were made in higher education as
well, but in 1970 only about 4 percent of Mexican Americans aged
25-29 who entered college had actually completed a 4-year degree.
Occupations held by Mexican American men in 1970 were the lowest
among the Hispanic subgroups and fell substantially below those
of non-Hispanic Whites. Nonetheless, considerable upward move-
ment occurred among Mexican Americans during the past several
decades. In fact, the movement of Mexican Americans up the occu-
pational ladder between 1930 and 1970 was relatively greater than
that for the total U.S. White male population. A major reason
for this was the movement of Mexican American men out of agri-
culture. In 1970 only 10 percent of Mexican American men were
employed in agriculture compared to 40 percent in 1930. In addi-
tion, in 1970 less than 25 percent of Mexican American men were
on the bottom rungs of the occupational ladder (nonfarm and farm
laborers) compared to 66 percent in 1930. While 61 percent of
Mexican American men in 1970 were employed in lower level blue
collar jobs compared to only 45 percent of non-Hispanic Whites,
this figure represented a substantial decline from 1930, when 87
percent of Mexican American men were employed in such jobs. In
addition, the number of Mexican American men employed in white
collar jobs at both upper levels (professionals, nonfarm mana-
gers) and lower levels (sales and clerical workers) tripled bet-
ween 1930 and 1970. Within equal levels of schooling the
occupational positions of Mexican American men closely approached
those of non-Hispanic Whites; among college graduates, there were
few differences between the two ethnic groups.
Overall, about 37 percent of Mexican American women aged 16 and
over were in the labor force in 1970, compared to 41 percent of
non-Hispanic White women. The occupational position held by
Mexican American women in 1970 were the lowest for all the
Hispanic subgroups and fell substantially below those of
non-Hispanic Whites. Between 1950 and 1970, however, Mexican
American women had experienced considerable upward occupational
mobility comparable to that for Mexican American men. The number
of Mexican American women in upper level white collar jobs
increased from 7 percent in 1950 to 8.5 percent in 1970. In
lower level white collar occupations, the number of Mexican
American women increased from 21 percent in 1950 to 31 percent in
1970. At comparable levels of schooling, Mexican American women
closely approximated the occupational levels achieved by
non-Hispanic Whites.
368
The income of Mexican Americans still lags substantially behind
that of non-Hispanic Whites. In 1969 the median family income of
Mexican Americans was $6,960, ranging from a median of $1,800 in
families with no earners to a median of $9,080 in familes with
two or more earners. These figures compared to a median family
income among non-Hispanic Whites of $10,100, ranging from a
median of $2,970 in familes with no earners to a median of
$12,350 in familes with two or more earners. In general, fami
lies headed by men had higher median incomes than families headed
by women, and families headed by U.S. born MAs had higher incomes
than families headed by Mexican born MAs. There is some indica-
tion, however, that MAs are gaining ground on non-Hispanic
Whites. In 1969, MA families headed by males averaged about 65%
of the income of non-Hispanic White male-headed families. By
1976-1978, this percentage had increased to about 70 percent (MA
median income, $12,600). Similarly, in 1969 MA families headed
by females averaged about 50 percent of the income of
non-Hispanic White female-headed families. By 1976-1978, this
percentage had also increased to about 70 percent (MA median
income, $6,200).
Acculturation can be understood as a complex process whereby
individuals whose primary learning has been in one culture take
over characteristic ways of living from another culture (8-10).
This process is complex in that it usually proceeds somewhat un-
evenly in two major areas of life: the social and the cultural.
The social area involves interaction with members of the host
society which results in the adoption of the public behaviors,
language, and material culture of the host society, while pre-
serving the primary attitudes, values, language and behaviors of
the culture of origin for participation in the private spheres of
life. The cultural area involves psychological integration with
the host society which results in the adoption of the central
attitudes and values of the host society for participation in
both public and private spheres of life. On a national level,
two statistical measures can be examined as indicators of
acculturation among Mexican Americans: the proportion who are
first, second and third generation Americans; and the proportion
who marry outside their own ethnic group (outmarriage), par-
ticularly those who marry non-Hispanic Whites.
In 1910 about 58 percent of all MAs in the U.S. were first
generation Americans (born in Mexico); by 1970 that number had
dropped to about 32 percent (7). In the five Southwestern states,
2 which contain about 90 percent of the total Mexican American
California, Texas, Colorado, New Mexico and Arizona.
369
population, only 12 percent of MAs were first generation
Americans in 1970 (11). Another 30 percent were second genera-
tion (U.S. born of Mexico-born parents), while 58 percent, the
vast majority, were third generation Americans (U.S.-born of
U.S.-born parents) (11).
The rate of outmarriage among U.S.-born MA women in 1970 was the
lowest among U.S.-born Hispanic women.3 Only 16 percent of
U.S.-born MA women had non-Mexican American husbands. However,
84 percent of these outmarriages were to non-Hispanic White
males; this was the highest rate for such marriages among the
Hispanic subgroups examined. Younger women were somewhat more
likely to marry outside their own ethnic group than older women.
The rate of outmarriage among U.S.-born MA women under 35 years
old was 19 percent compared to only 13 percent for those aged 35
and over. The percentage of outmarriages increased substantially
with increased schooling. For women younger than 35, the rate of
outmarriage among high school graduates was 30 percent compared
to only 11 percent among those who had not completed high school.
For women aged 35 and over, the corresponding rates of out-
marriage were 37 percent among high school graduates and 8 per-
cent among those who had not completed twelfth grade.
In summary, Mexican Americans are becoming an increasingly
heterogeneous population, both socioeconomically and culturally.
The majority of Mexican Americans, however, are still located in
the lower SES strata and have experienced low or intermediate
levels of acculturation into mainstream (non-Hispanic White)
American society.
Cardiovascular Disease As A Cause of Mortality Among Mexican
Americans
Two studies have examined the relative importance of car-
diovascular disease (CVD) as a cause of death among Mexican
Americans (12,13). One was conducted in California, the other in
Texas, the two states where over 86 percent of the nation's
Mexican American population resides (6). Both studies examined
mortality data for the period 1969 to 1971. Persons were
classified as Mexican American or non-Hispanic White using the
U.S. Census surname identifier. Methodologies differed in that
the California study compared cause-specific mortality using life
table deaths computed for 5-year intervals ages 0 to 85 and stan-
3
Rates of outmarriage were based on the Public Use Sample tabula-
tions for husbands and wives living together at the time of the
1970 Census enumeration. Rates could be determined for Mexican
Americans, Puerto Ricans, Cubans, and Hispanos, but not for
Central and South Americans(7).
370
dardized death rates directly standardized using the total popu-
lation of California in 1960; while the Texas study compared only
standardized death rates directly standardized on the Texas
non-Spanish surname White female age distribution (13).
The two studies yielded strikingly similar results. Both found
cardiovascular disease to be the leading cause of death among
Mexican Americans, just as it is among non-Hispanic Whites. CVD
mortality rates were lower for Mexican American males, however,
than for non-Hispanic White males (in California, 82% of the
non-Hispanic White rate; in Texas, 85% of the non-Hispanic White
rate). CVD mortality rates for Mexican American females, on the
other hand, were virtually identical to those for non-Hispanic
White females (in California, 99.8% of the non-Hispanic White
rate; in Texas, 7% higher than the non-Hispanic White rate). The
sex differential in CVD mortality was less favorable for Mexican
American females than for non-Hispanic Whites (in California: a
male-female sex ratio of 1.43 for MAs vs. 1.72 for non-Hispanic
Whites; in Texas, a male-female sex ratio of 1.46 for MAs vs.
1.78 for non-Hispanic Whites).
Two other studies have examined secular trends in cardiovascular
mortality during the first half of the 1970s to determine whether
Mexican Americans shared in the nation-wide decline in CVD mor-
tality which occurred during that period (14,15). The first
study, using data only from Bexar County (San Antonio) Texas,
found that standardized CVD mortality rates4 for the period 1970
to 1976 declined significantly in both MA men and women and in
non-Hispanic White males (14). Furthermore, the CVD mortality
decline in Mexican Americans was equal to that in non-Hispanic
whites. The second study, using state-wide data from Texas,
found that standardized proportional CVD mortality rates for the
period 1970 to 1976 declined in Mexican Americans, but that, par-
ticularly for MA males, the decline was much less steep than in
non-Hispanic Whites (15). Each of these studies suffered from
the limitation that 1975-76 population denominators were derived
from population estimates rather than actual census data. A new
study, not yet published, which uses denominators from the 1980
census for the state of Texas, indicates an interesting sex-
differential in the rate of CVD mortality decline in Mexican
Americans during the period 1970 to 1980 (16). The rate of
decline in Mexican American men was about only half as steep as
in non-Hispanic Whites, while the rate of decline in Mexican
4Directly standardized to the 1970 U.S. population.
371
American women was one-third to two-thirds steeper than in
non-Hispanic Whites.
Socioeconomic Status, Acculturation, and Cardiovascular Risk
Factors in Mexican Americans
Evidence concerning the level of cardiovascular risk factors in
Mexican Americans is growing, but research in this area has been
quite limited over the past 15 to 20 years. This is particularly
true for research on the association between differences in
socioeconomic status and acculturation among Mexican Americans
and the risk of cardiovascular disease. Table 1 provides a list
of 21 research reports found in a search of the literature for
the period 1966 to October 1984. These 21 reports are based on
eight separate studies: 4 carried out on populations in
California, 3 in Texas, and 1 in the four states along the
U.S.-Mexico Border. Over half of the reports are from the San
Antonio Heart Study (SAHS), a large population-based investiga-
tion which compared diabetes and cardiovascular risk factors in
Mexican Americans and non-Hispanic Whites residing in three
socioculturally distinct neighborhoods of San Antonio, Texas.
Almost one-fourth of the 21 reports, including all of those from
the Starr County study, deal exclusively with diabetes or with
the relationship between diabetes and obesity. Only about half
of the reports, primarily those from the San Antonio Heart Study,
examine the relationship between either SES or acculturation and
cardiovascular risk factors in Mexican Americans. The evidence
contained in these reports deals with six risk factors: lipids
and lipoproteins, blood pressure and hypertension, cigarette
smoking, exercise, obesity, and diabetes.
1. Lipids and lipoproteins. Cholesterol levels in Mexican
Americans have been examined in five separate studies (17-21).
All of these compared cholesterol levels in Mexican Americans
with those in non-Hispanic Whites. One study looked only at
very low SES Mexican Americans and found that the age-adjusted
serum cholesterol levels in Mexican Americans of both sexes were
higher than those recorded for non-Hispanic Whites in a national
comparison sample (HANES I), which was undoubtedly of higher SES
(17). Two studies used mixed samples which included both lower
and middle SES Mexican Americans and non-Hispanic Whites, but did
not carry out stratified analyses or adjust for differences in
SES between the two ethnic groups (18,19). In one study Mexican
Americans were predominantly of lower SES, while non-Hispanic
Whites were predominantly of middle SES; cholesterol levels were
no higher in Mexican Americans than in non-Hispanic Whites (18).
In the other study lower and middle SES subjects were nearly
equally distributed in the two ethnic groups; cholesterol levels
372
in Mexican American men, however, were higher than those in
non-Hispanic Whites, while cholesterol levels in Mexican American
women were similar to those in non-Hispanic Whites (19). These
three studies revealed no consistent pattern of ethnic differen-
ces in cholesterol levels nor do they permit inferences about the
relationship between socioeconomic status and cholesterol levels
in Mexican Americans. Two of the five studies do provide this
this information; one of these was done in central California
(20), the other in South Texas (21).
The California study compared the proportion of hypercholestero-
lemic males (cholesterol > 260 mg/dl) in six different levels of
socioeconomic status. The overall prevalence of hypercholestero-
lemia in Mexican Americans was higher than in non-Hispanic Whites
(16.7 vs. 13.9%). There was some evidence of an inverse rela-
tionship between SES and cholesterol levels in non-Hispanic
Whites, but no evidence of a similar SES gradient in Mexican
Americans (20). The South Texas study (SAHS) examined cho-
lesterol as a continuous variable. SES diffrences were examined
by comparing cholesterol levels for a random sample of Mexican
Americans and Non-Hispanic Whites who resided in three
socioculturally distinct neighborhoods of San Antonio, Texas.
These neighborhoods had been purposively selected by the
researchers to represent low, middle and high levels of SES and
acculturation of Mexican Americans. Non-Hispanic Whites were
sampled only in the two higher socioeconomic neighborhoods.5
Overall, cholesterol levels tended to be somewhat higher in
Mexican American than in non-Hispanic White men, but similar in
the two ethnic groups for women. Among Mexican Americans, cho-
lesterol levels were nearly identical in the two lower SES groups,
but increased markedly and significantly in the high SES group.
For women, on the other hand, cholesterol levels remained similar
in all three SES groups. For non-Hispanic Whites, similar sex
difference was observed in the relationship between socioeconomic
status and cholesterol.
5Strictly speaking, these neighborhood analyses do not permit a
clear distinction between any purely socioeconomic or cultural
factors which might be operating. Neighborhood differences pro-
bably reflect the combined effect of socioeconomic status and
acculturation. Nonetheless, since the three neighborhoods repre-
sent significantly different levels of socioeconomic status (21),
the investigators feel justified in referring to the three neigh-
borhoods as "SES groups."
373
In men, cholesterol levels were significantly higher in the upper
SES group than in the middle group; in women, cholesterol levels
were similar for both SES groups.
Four studies also examined triglyceride levels (17-19,21). All of
them found triglyceride levels in Mexican Americans to be higher
than those in non-Hispanic Whites, although the differences
tended not to be statistically significant. Ethnic differences in
triglyceride levels persisted in both sexes even when comparisons
were made within the same SES strata6 (21). Among Mexican
Americans triglyceride levels in men were similar in the two
lower SES groups, and increased markedly, though not statisti-
cally significantly, in the highest SES group. In Mexican
American women, there was a clear tendency for triglyceride to
decrease in the higher SES group.
Two lipoproteins were also examined in the San Antonio Heart
Study: low density lipoprotein cholesterol, associated with
increased risk of coronary heart disease (CHD); and high density
lipoprotein cholesterol, a protective factor against CHD (21).
For low density lipoprotein cholesterol (LDL-C)7, the rela-
tionship with socioeconomic status closely paralleled that for
total cholesterol. In Mexican American men, LDL-C levels were
similar in the two lower SES groups, but increased markedly and
statistically significantly in the highest SES group. In
non-Hispanic men LDL-C also increased significantly from the
middle to upper SES group. For women in both ethnic groups, on
the other hand, LDL-C levels were similar in all SES groups. For
high density lipoprotein cholesterol (HDL-C), there was also a
sex difference in the relationship with socioeconomic status. In
men of both ethnic groups HDL-C remained constant across levels
of SES. On the other hand, in women of both ethnic groups, HDL-C
Strictly speaking, these neighborhood analyses do not permit a
clear distinction between any purely socioeconomic or cultural
factors which might be operating. Neighborhood differences pro-
bably reflect the combined effect of socioeconomic status and
acculturation. Nonetheless, since the three neighborhoods repre-
sent significantly different levels of socioeconomic status (21),
the investigators feel justified in referring to the three neigh-
borhoods as "SES groups."
7A1though SES was not considered, a related report suggests that
ethnic differences in triglyceride levels persist even when
adjustments are made for a number of relevant behavioral
variables (i.e., age, obesity, cigarette smoking, coffee and
alcohol consumption and, in women, estrogen and oral contracep-
tive usage) (22).
374
rose significantly with increasing socioeconomic status.
In terms of lipids and lipoproteins, then, it appears that
increased socioeconomic status may be associated with greater
protection against CHD in women (i.e., lower triglyceride levels
and higher levels of HDL-C), but with increased risk of CHD in
men (higher cholesterol levels and higher levels of LDL-C).
Two other reports from the San Antonio Heart Study have examined
SES differences in dietary practices which may influence serum
cholesterol (23,24). One report used data from a diet frequency
questionnaire to devise a scale measuring avoidance of saturated
fat and cholesterol (23). In Mexican Americans of both sexes, fat
and cholesterol avoidance increased significantly with increasing
socioeconomic status. Although non-Hispanic Whites in the middle
SES group still scored significantly higher on the fat avoidance
scale than Mexican Americans, no ethnic differences were present
in the highest SES group. No difference in fat avoidance was
observed between Mexican Americans born in the U.S. and those
born in Mexico.
The other SAHS report looked at how well-informed individuals
were about the role of dietary cholesterol and saturated fat as
risk factors for cardiovascular disease and at the extent to
which individuals modified their diet to reduce heart disease
risk (24). Overall, Mexican Americans were less well-informed
than non-Hispanic Whites and were less likely to have attempted
any dietary modifications to reduce risk of heart disease.
Although increased socioeconomic status was associated with
increased knowledge and preventive behavior in both ethnic
groups, the gap in knowledge and behavior between Mexican
Americans and non-Hispanic Whites began to close at the higher
SES levels.
2. Blood pressure and hypertension. Three studies have
compared blood pressure levels in Mexican Americans and
non-Hispanic Whites (17-19). All three found diastolic blood
pressure, in men, and systolic blood pressure, in both men and
women, to be similar in the two ethnic groups. Two of the stu-
dies (17,18) found diastolic blood pressure in Mexican American
women to be lower than in non-Hispanic Whites, while the third
found no ethnic differences (19). The Laredo Project (17) also
examined prevalence of hypertension in Mexican Americans, using
two separate definitions utilized in the Hypertension Detection
and Follow-up Study (HDFP). One definition of hypertension
("elevated diastolic blood pressure") included only individuals
with diastolic blood pressures (DBP) greater than or equal to
95mm Hg. The second definition ("actual" hypertension) included
individuals with currently elevated diastolic blood pressures
375
plus those whose diastolic blood pressures were below 95 mm Hg,
provided they gave a history of hypertension and were also
currently taking anti-hypertensive medications. The second defi-
nition provides for differences in treatment levels which may
occur across ethnic groups or geographic regions.
The prevalence of elevated diastolic blood pressure in Laredo
Mexican Americans (very low socioeconomic status) was compared to
that of HDFP Whites and Blacks. In Mexican American males the
prevalence of hypertension was intermediate between those of HDFP
Whites and Blacks. In Mexican American females, on the other
hand, hypertension prevalence was lower than in either HDFP
Whites or Blacks. Mexican American males had substantially
higher rates of elevated diastolic blood pressure in each of
three age groups (40-49 year olds: 19.4 vs. 7.9%; 50-59 year
olds: 23.3 vs. 7.1%; 60-69 year olds: 23.8 vs. 5.7%) (17).
The rate of "actual" hypertension in Laredo Mexican Americans was
also intermediate between the rates for HDFP Whites and Blacks
until age 59, after which it became essentially similar to the
HDFP Black rate. For Mexican American women, however, the rate
of actual hypertension was slightly higher than that in HDFP
Whites except in the 60-69 year-old age category where the rate
was as high as that in HDFP Blacks. The large sex differences
observed for rates of elevated diastolic blood pressure in Laredo
Mexican Americans were greatly reduced for actual hypertension
and were, in fact, reversed in the oldest age category (40-49
year olds: 29.0 vs. 21.1%; 50-59 year olds: 37.2 vs. 26.2%; and
60-69 year olds: 38.1 vs. 44.3%). The latter finding suggests
that among Laredo hypertensives, women were more likely than men
to have their hypertension controlled (17).
SES differences in hypertension prevalence were examined in a
California study (20) and in the San Antonio Heart Study (21),
but with two different definitions of hypertension. The
California study looked at elevated diastolic blood pressure,
while the SAHS examined actual hypertension. The California
study found a clear inverse relationship between SES and preva-
lence of elevated diastolic blood pressure in Mexican American
males, ranging from a rate of 8.2 percent in the highest SES
category to 19.6 percent in the lowest SES category (20). A
similar SES gradient was present in non-Hispanic Whites. The
overall prevalence of elevated diastolic blood pressure in
Mexican American males was 15.6 percent; intermediate between the
rates found for non-Hispanic Whites and Blacks.
The San Antonio Heart Study found no SES gradient in prevalence
of actual hypertension in either Mexican American or non-Hispanic
White males (26). In Mexican American males, rates of actual
376
hypertension were 10.7 percent in the lowest SES group, 7.3 per-
cent in the middle SES group, and 11.5 percent in the highest SES
group. The corresponding rates for non-Hispanic White males were
10.0 percent in the middle SES group and 9.5 percent in the high
SES group. In contrast to the finding for men, there was a
strong inverse relationship between socioeconomic status and pre-
valence of actual hypertension in women of both ethnic groups.
For Mexican Americans, the rates declined from 9.2 percent in the
low SES group to 8.4 percent in the middle SES group, and 4.7
percent in the high SES group; for non-Hispanic Whites, the rate
declined from 10.7 percent in the middle SES group to 8.7 percent
in the high SES group. Rates of hypertension appeared to be
similar in males of both ethnic groups, but lower in Mexican
American women than in non-Hispanic Whites, although this ethnic
difference was not statistically significant. When adjustments
were made for obesity (higher in MAs), Mexican Americans tended
to have a lower rate of hypertension than non-Hispanic Whites at
the same SES level.
Data on the proportion of hypertensives previously diagnosed and
under treatment with antihypertensive drugs were also reported
from the San Antonio Heart Study. The proportion of hyperten-
sives previously diagnosed and under treatment was lower in
Mexican Americans of both sexes than in non-Hispanic Whites.
Interestingly, the proportion of previously diagnosed hyperten-
sives under treatment was as great among low SES Mexican American
men as high SES men, and actually decreased from the low to high
SES group in MA women. Among non-Hispanic Whites, on the other
hand, there was either no SES difference in the proportion of
previously diagnosed hypertensives under treatment (for women) or
the proportion increased with increased socioeconomic status (for
men). These data suggest that health care deliverers may be par-
ticularly sensitive to the potential presence of hypertension
among low SES minorities. Nonetheless, the proportion of Mexican
American hypertensives both under treatment and under control
(DBP < 95 mm Hg) was lower in both sexes at the lower SES levels.
In addition, lower SES Mexican Americans of both sexes were also
somewhat less likely than those at higher SES levels to report
that they had attempted to control hypertension as a means of
preventing heart attacks (24).
The overall proportion of SAHS Mexican Americans under adequate
control was greater in women than in men (87 vs. 64 percent).
Comparable data from the Laredo Study showed 77 percent of MA
hypertensive women and only 37 percent of hypertensive men under
adequate control (17). While the figures for Mexican American
women are similar to national figures for hypertension control in
women, Mexican American men lag far behind national figures for
hypertension control in men.
377
3. Cigarette smoking. Six studies have compared smoking
behavior in Mexican Americans and non-Hispanic Whites
(18-20,26-28). Overall rates of current smoking appear to be the
same or higher in Mexican Americans than in non-Hispanic Whites.
Overall rates, however, obscure an important sex-ethnic interac-
tion: for males, the proportion of Mexican Americans who are
current smokers is the same or higher than for non-Hispanic whi-
tes; for women, on the other hand, the proportion of current smo-
kers is much lower among Mexican Americans than among
non-Hispanic Whites (19,27,28). Regardless of sex, however,
Mexican Americans smoke significantly fewer cigarettes per day
than non-Hispanic Whites (18,27,28).
SES differences in smoking behavior were examined in three stu-
dies (20,27,28). One study which included only women found that
in both Mexican Americans and non-Hispanic Whites, the proportion
of current smokers decreased with increasing socioeconomic status
(27). At comparable levels of SES, though, the proportion of
non-Hispanic White smokers was double that of Mexican Americans.
Among Mexican Americans, similar proportions of U.S.-born and
Mexico-born women were current smokers. The central California
study (20) examined the proportion of heavy cigarette smokers (>
20 cigarettes per day) among males only. In both Mexican
Americans and non-Hispanic Whites, the proportion of heavy smo-
kers decreased with increasing socioeconomic status. For Mexican
Americans, the proportion ranged from 6.1 percent in the highest
SES category to 23.5 percent in the lowest category. For
non-Hispanic Whites, rates were somewhat higher, ranging from
16.3 percent in the highest SES category to 48.3 percent in the
lowest.
Two reports from the San Antonio Heart Study compared SES dif-
ferences in smoking behavior in both men and women. In the first
report cited, subjects were grouped into two SES categories: low
and high. Since no low SES non-Hispanic Whites were available in
the SAHS sample, SES comparisons within ethnic groups could be
made only for Mexican Americans. For men, the proportion of
current smokers was greater among Mexican Americans of both SES
levels than among high SES non-Hispanic Whites. For women, on
the other hand, the proportion of current smokers was lower among
Mexican Americans at both SES levels than among high SES
non-Hispanic Whites. In Mexican Americans of both sexes the pro-
portion of current smokers decreased markedly in the higher SES
group. Within SES levels, the proportion of current smokers was
twice as high among Mexican American men than among women. Among
high SES non-Hispanic Whites, on the other hand, a slightly
higher proportion of women were current smokers than men. High
SES non-Hispanic Whites of both sexes smoked almost twice as many
378
cigarettes per day as Mexican Americans in either SES group.
Among Mexican Americans, high SES men smoked slightly more
cigarettes per day than low SES men (16.8 vs. 13.3), while
Mexican American women in the two SES groups smoked about the
same number (9.2 cigarettes per day).
A second SAHS report focussed on how well-informed individuals
are about the role of smoking as a risk factor for heart disease
and whether they had modified their smoking behavior (i.e., quit
or never started) to reduce heart disease risk (24). Mexican
Americans of both sexes tended to be less well-informed about the
risks of cigarette smoking than non-Hispanic Whites. High SES
Mexican Americans, however, were much better informed on this
issue than low SES Mexican Americans; ethnic differences in
knowledge decreased at the higher SES levels. Within the same
SES level, Mexican American men tended to be better informed
about the risk of cigarette smoking than women (in the low SES
group: 10% of men vs. 6% of women; in the middle SES group, 16
vs. 18%; and in the high SES group, 31 vs. 26% of women).
For men, about equal proportions of Mexican Americans and
non-Hispanic whites in the middle SES group reported modifying
their smoking behavior to reduce CHD risk (11% of MAs vs. 12% of
non-Hispanic Whites); but more non-Hispanic Whites than Mexican
Americans were likely to report prevention-oriented behavior in
the high SES group (18% of MAs vs. 24% of non-Hispanic Whites).
A similar pattern was found for women; in the middle SES group,
10% of MAs vs. 11% of non-Hispanic Whites reported modifying
their smoking behavior compared to 16% of MAs and 20% of
non-Hispanic Whites in the high SES group. Low SES Mexican
Americans of both sexes lagged far behind in prevention-oriented
behavior only 6% in both sex groups reported modifying their
behavior to reduce CHD risk.
4. Exercise. Three studies have compared the level of phy-
sical exercise in Mexican Americans and non-Hispanic Whites
(19,24,27). All three reported a lower level of physical exer-
cise outside of work in Mexican Americans than in non-Hispanic
Whites. Only one study (24) examined differences in physical
exercise by level of SES. Although non-Hispanic Whites were
generally better informed about the role of exercise in reducing
risk of CHD and reported more prevention-oriented behaviors than
Mexican Americans, both knowledge and preventive-behavior
increased among Mexican Americans with increasing SES. For
women, while only 21 percent of low SES Mexican Americans were
informed about the role of exercise in reducing CHD risk, 37 per-
cent of middle SES women and 52 percent of high SES women were
informed on this issue. Similarly, the proportion of Mexican
379
American women reporting that they engaged in physical exercise
to reduce risk of heart disease increased from 13 percent in the
low SES group to 21 percent in the middle group, and 33 percent
in the high SES group. Even in the highest SES group, though, MA
women lagged substantially behind non-Hispanic Whites in both
knowledge and preventive behaviors. For men, the proportion of
Mexican Americans informed about exercise and CHD rose from 22
percent in the low SES group to 40 percent in the middle group,
and 66 percent in the high SES group. This proportion in high
SES Mexican American men equalled that observed in high SES
non-Hispanic Whites. The proportion of Mexican American men
reporting that they exercised to reduce CHD risk increased from
18 percent in the low SES group to 28 percent in the middle SES
group, and 50 percent in the high SES group. Again the propor-
tion of high SES Mexican American men reporting this prevention-
oriented behavior equalled the proportion among high SES
non-Hispanic Whites. On the four risk factors examined in this
SAHS report (dietary fat, blood pressure, cigarette smoking, and
exercise), Mexican American men ranked highest on exercise in
their level of knowledge and prevention-oriented behavior.
5. Obesity. The available evidence clearly indicates that
obesity is a major health problem in Mexican Americans, par-
ticularly among women and those of low socioeconomic status
(17,18,21,27,30-32). In the Laredo study of very low SES Mexican
Americans, the age-adjusted prevalence of obesity (defined as
being 20 percent or more over desirable weight) was 25.8 percent
in men and 44.8 percent in women (17). Corresponding figures
derived from the Health and Nutrition Examination Survey (HANES
I) for the general U.S. population were only 15.6 percent for men
and 29.0 percent for women (33). Another study of very low SES
Mexican Americans in Starr County, Texas, found that the preva-
lence of obesity (defined as body mass index > 30) was typically
30 percent or higher in adults of both sexes (30).
Data from the San Antonio Heart Study found that body mass index
decreased only slightly in Mexican American men with increasing
SES, but decreased markedly and significantly in women at each
higher SES level. Ethnic comparisons within SES-matched strata,
however, still indicated greater adiposity among Mexican
Americans of both sexes than among non-Hispanic Whites (21).
Comparisons of attitudes and behavior related to obesity in
middle and high SES subjects revealed that a greater percentage
of Mexican Americans than non-Hispanic Whites at each SES level
were likely to express the belief that Americans are too con-
cerned about losing weight (34). Mexican Americans in both SES
groups also scored lower than non-Hispanic Whites on scales
measuring sugar avoidance and dieting behavior, but the ethnic
380
differences were statistically significant only for women in the
middle SES group. Mexican Americans in the high SES group scored
significantly higher on these scales than those in the middle SES
group. In non-Hispanic Whites SES differences were statistically
significant only for men and only for the dieting behavior scale.
Only one report, also from the San Antonio Heart Study, examined
the relationship between acculturation and obesity in Mexican
Americans (35). Acculturation was measured using a multi-
dimensional scale which reflected adoption during adulthood of
non-Hispanic White behaviors, attitudes, and values. Even after
adjusting for socioeconomic status, increased levels of
acculturation were found to be associated with significant
decreases in body mass index in Mexican Americans of both sexes.
This finding suggests that SES and acculturation may play inde-
pendent and distinct roles in reducing obesity in Mexican
Americans. Mechanisms (e.g., diet, exercise, stress, attitudes
toward obesity) which may mediate the SES-obesity and
acculturation-obesity relationships are in need of further
investigation.
In addition to the role played by overall adiposity, there is
evidence that the distribution, or patterning, of body fat may be
an important determinant of some metabolic disorders (such as
diabetes) which may be related to heart disease. Limited evi-
dence, based on subscapular and triceps skinfolds, suggests that
Mexican Americans have a relatively more central distribution of
body fat compared to non-Hispanic Whites (32,36). There is also
some data to suggest that the centrality of the fat distribution
in Mexican American men increases with increasing SES, while for
Mexican American women centrality decreases (32). Interest has
been expressed recently as well in the hypothesis that persons
with upper body obesity have a greater propensity toward metabo-
lic disorders (e.g. diabetes) than persons with lower body obe-
sity. While no data are currently available on ethnic
differences in upper and lower body obesity between Mexican
Americans and non-Hispanic Whites, the Starr County study has
reported that Mexican American diabetics have relatively more
upper body fat and less lower body fat than non-diabetics
(30,31). Data needed to examine ethnic difference in upper vs.
lower body fat distribution across SES levels are currently being
collected in the San Antonio Heart Study II.
6. Diabetes. A recent review of current research on diabe-
tes mellitus in Hispanics indicated that the prevalence of
insulin-dependent diabetes mellitus (IDDM) is less than 5 percent
and found no evidence for increased prevalence of IDDM in Mexican
Americans relative to non-Hispanic Whites (37). Non-insulin
381
dependent diabetes mellitus (NIDDM), on the other hand, appears
to be a major health problem in Mexican Americans, particularly
those of low socioeconomic status (17,21,37-41). In Laredo,
Texas, the age-adjusted prevalence of NIDDM in low SES Mexican
Americans was 15.7 percent in males and 16.1 percent in females
(17,37); corresponding rates for low SES Mexican Americans in
Starr County, Texas were 8.3 percent in both sexes (38).
Comparisons to the general U.S. population made in both studies
suggest that low socioeconomic status Mexican Americans are at
substantially greater risk of NIDDM.
The San Antonio Heart Study compared the prevalence of NIDDM
(defined according to the National Diabetes Data Group (NDDG)
criteria (42)) in Mexican Americans and non-Hispanic Whites
across three SES levels (21). In the lowest SES group the age-
adjusted prevalences for Mexican Americans were comparable to
those reported in the Laredo study: 13.7 percent in males and
14.8 percent in females. NIDDM prevalence declined in both sexes
and in both ethnic groups with increasing levels of socioeconomic
status. In the middle SES group the age-adjusted prevalence for
males was 14.6 percent in Mexican Americans and 7.0 percent in
non-Hispanic Whites; the corresponding rates for females were 8.2
percent in Mexican Americans and 7.3 percent in non-Hispanic
Whites. In the highest SES group the rates for males dropped to
6.1 percent in Mexican Americans and 3.6 percent in non-Hispanic
Whites; for females the corresponding rates fell to 3.7 percent
in Mexican Americans and 2.2 percent in non-Hispanic Whites.
Further analyses of the data for Mexican Americans indicates that
the inverse relationship between socioeconomic status and NIDDM
may be largely mediated through obesity in MA women, but not in
men (41). In addition, when SES and acculturation were examined
separately in relation to NIDDM prevalence, acculturation was
consistently associated with a reduction in NIDDM prevalence for
both MA men and women, even after linear adjustments for
socioeconomic status. The effect of acculturation on NIDDM
appeared to be largely mediated through obesity in women, but was
largely independent of obesity in men (42).
Since Mexican Americans tend to be much more obese than
non-Hispanic Whites, efforts were made to determine whether obe-
sity could explain the excess prevalence of diabetes. Even when
Mexican Americans were closely matched to non-Hispanic Whites on
degree of obesity, the prevalence of NIDDM was significantly
greater in Mexicans than in non-Hispanic Whites (40). The sum-
mary prevalence ratio, after matching for obesity, was 2.54 for
men and 1.70 for women. While obesity contributes to NIDDM in
Mexican Americans, particularly Mexican American women, it does
382
not entirely explain the excess prevalence rate that has been
observed relative to non-Hispanic Whites.
There is limited evidence to suggest that the excess NIDDM preva-
lence in Mexicans which cannot be attributed to obesity may have
a genetic component related to degree of native American admix-
ture. In the San Antonio Heart Study NIDDM prevalence in Mexican
Americans was intermediate between the rates observed for the
predominantly non-Hispanic White HANES II population (3.1%),
which presumably has few if any native American genes, and for
Pima Indians (49.9%), who are believed to have close to 100 per-
cent native American genes (39). NIDDM prevalence for
non-Hispanic Whites in the SAHS sample was nearly identical to
that observed for the HANES II population (3.0%). In addition,
the stepwise decline in NIDDM prevalence from the low to high
Mexican American SES groups observed in the San Antonio Heart
Study was paralleled by a similar stepwise decline in percent
native American admixture (39,43). Low SES Mexican Americans had
about 46 percent native American admixture, MAs middle SES
Mexican Americans about 26 percent native American admixture, and
high SES Mexican Americans about 18 percent native American
admixture. It should be kept in mind, however, that this evi-
dence is currently ecological in nature, although more definitive
studies are now in progress.
Summary and Recommendations
This review confirms that the profile of cardiovascular risk fac-
tors is less favorable in Mexican Americans than in non-Hispanic
Whites. Within the Mexican American population, those in the
lowest socioeconomic group and those who are the least
acculturated have a significantly worse profile of cardiovascular
risks than those in higher socioeconomic groups and those who are
more acculturated. Obesity and non-insulin dependent diabetes
mellitus rank as major health problems in Mexican Americans of
both sexes. For Mexican American males, hypertension and
cigarette smoking rank as significant health problems, as well.
Finally, the less favorable profile of lipids and lipoproteins in
Mexican Americans (greater hypertriglyceridemia and lower levels
of high density lipoprotein cholesterol in both sexes; and
greater hypercholesterolemia and higher levels of low density
lipoprotein cholesterol in males) relative to non-Hispanic Whites
should also be recognized as a public health concern. In light
of these findings, the following recommendations seem warranted:
1 Major priority should be given to public health ini-
tiatives directed toward reducing the high rates of obesity and
non-insulin dependent diabetes mellitus in the Mexican American
383
population. Toward this end, research monies should be
appropriated to determine whether genetic as well as lifestyle
factors are related to excess NIDDM prevalence in Mexican
Americans.
2. Educational programs and improvements in health care
delivery should be directed toward increasing compliance with
antihypertensive regimens and reducing the rate of current
smoking in Mexican American males.
3. Health care deliverers should be alerted to the need for
careful monitoring of lipids and lipoproteins in Mexican
Americans associated with increased risk of coronary heart
disease. This seems particularly important in low SES Mexican
Americans of both sexes and in upwardly mobile Mexican American
males.
4. Public health initiatives to lower the profile of coro-
nary risk in Mexican Americans should be directed primarily
toward those at lower levels of socioeconomic status. However,
since Mexican Americans at all SES levels tend to lag behind
non-Hispanic Whites in levels of knowledge and behavior related
to the prevention of coronary heart disease, educational programs
designed to reduce CHD risk should be directed toward Mexican
Americans at all socioeconomic levels.
384
Table 1. Research Reports on Cardiovascular Risk Factors in Mexican Americans
Researchers
Locale
ex
1. Stern et al
(18)
2. Roberts and
Lee (27)
3. Kraus et al
(20)
4. Friia et al
(19)
5. Stern et al
(17, 25)
Three semi-rural
communities in
northern California
Alameda County, CA
Sacramento, CA
Orange County, CA
Year Rink Factors
1972 Lipids and Lipoproteins
Dietary Fat
Blood Pressure
Cigarette Smoking
1974 Cigarette Smoking
and Exercise
1975 Obesity
_5*5Pi.? Characteri^stics_
Examined Differences
in Acculturation or
SES: Yes or No?
Laredo, TX
1975- Lipids and Lipoproteins
1976 Blood Pressure
Cigarette Smoking
1978 Lipids and Lipoproteins
Blood Pressure
Cigarette Smoking
Exercise
Obesity
Glucose Levels
1979 Lipids and lipoproteins
Hypertension
Overweight
299 Mexican American and 1367 non-Hispanic
White men and women, aged 35-59, residing in
households randomly sampled in each community
MAs: predominantly lower SES; non-Hispanic
Whites: predominantly middle SES
417 MA, 382 Black, and 2638 non-Hispanic White
men and women, aged 20-65+, residing in house-
holds randomly sampled from the county;
Mixed lower to upper SES; SES structure for MAs
significatnly lower than that for non-Hispanic
Whites
19,141 employed male volunteera, aged 35-57
738 MAs, 923 Blacks, 818 Asians, and 16,412
non-Hispanic Whites;
Five levels of SES, ranging from lower to upper;
SES structure for MAs substantially lower than
for non-Hispanic Whites
450 MA and non-Hispanic men and women who were
incoming government employees of Orange County
County in 1978; age ranges not reported;
Mixed lower and middle SES
127 MA men and 262 MA women, aged 40-47,
residing in household* randomly sampled
from two low SES cenaua tracts
No
No; SES used as a
control variable in
ethnic comparisons
Yes—SES only
No
6. Stern et al
(21)
7. Hasuda et al
(24)
8. Haffner et al
(23)
9. Haffner et al
(22)
10. Franco at al
(26)
San Antonio, TX*
San Antonio, TX*
San Antonio, TX*
San Antonio, TX*
San Antonio, TX*
1979-
1982
1979-
1981
1979-
1981
1979-
1982
1979-
1982
Lipids and Lipoproteins
Obesity
Diabetes
Dietary Fat and
Cholesterol
Blood Pressure
Cigarette Smoking
Exercise
Dietary Fat and
Cholesterol
Dietary Factors Related
to Lipida and Lipoproteins
1288 MA and 929 non-Hispanic Whit* men and women,
aged 25-64, residing in households randomly
sampled from three neighborhooda;
Neighborhoods were purposively selected to
represent three distinct levels of SES
and acculturation of MAs; low, middle, and high
932 MA and 382 non-Hispanic White men and women,
aged 25-64, residing in households randomly
sampled from three neighborhoods;
Neighborhoods were purposively selected to
represent three distinct levels of SES and
acculturation of MAs: low, middle, and high
Same as Research Report 7; sample sise varies
slightly (MAs: 915; non-Hispanic Whites: 388)
Same as Research Study 6; sample site variea
slightly (MAs: 1241; non-Hispanic Whites: 923)
Hypertension
Same as Research Report 6
"••—SIS and
Acculturation
Combined
Yea—SES and
Acculturation
Combined
Yes—SES and
Acculturat ion
Combined
Yes—SES and
Acculturat ion
Combined and
Separately
Yea—SES and
Acculturation
Combined
Table I. Continued
Researchers
Locale
11. Haffner et al San Antonio, TX*
(29)
12. Hoick et al
(28)
51 U.S. counties
in four states
along the U.S.-
Mexico border
13. Malina et al San Antonio, TX*
(32)
1979-
1982
1979
1979-
1981
Risk Factors
Cigarette Smoking
Cigarette Smoking
Obesity and Fat
Patterning
SamplejCharscteristic«__
1605 MA and non-Hispanic White men and women,
aged 25-64, residing in households randomly
selected from three neighborhoods;
Neighborhoods were purposively selected to
represent three distinct levels of SES end
scculturation of MAs: low, middle, and high
1255 MA, 798 non-Hispanic White, and 82 other
ethnic group women, aged 15-44, residing in
a sample of households;
Three SES levels and two levels of acculturation
represented among MAs
Same aa Research Report 7; Sample sice variea
slightly (MAs: 934; non-Hispanic Whites: 394)
Examined Differen
in Acculturation
SES: Yes or No?
Yes--SES snd
Acculturstion
Combined
Yes —SES and
Acculturation
Separately
Yes—SES and
Acculturation
Combined
14. Mueller et al Starr County, TX*
(30)
15. Stern et al San Antonio, TX*
(34)
16. Hasuda et al San Antonio, TX*
(35)
1981- Obesity and Fat
1983 Patterning
1979- Obesity-related Attitudes
1980 Knowledge, and Behavior
1979- Obesity
1982 Glucose Intolerance
1155 MA men and women, ages 15-70*. residing
in households randomly selected from three
densely populated towns in the County;
SES is extremely low, 52X of familiea were
classified below the poverty level in the 1970
Census
454 MA and 395 non-Hiapanic White men and women,
ages 25-64, residing in a random aample of
households in two neighborhoods;
Neighborhoods were purposively selected to
represent two distinct levels of SES and
acculturation of MAs
Same as Research Report 6, MAs only
No
Yes—SES and
Acculturation
Combined
Ye*—SES and
Acculturatioa
Separately
17. Stern et al San Antonio, TX*
(40)
1979-
1981
Obesity and Diabetes
Same aa Research Report 7
Yea—SES and
Acculturation
Combined
18. Jooa et al Starr County, TX*
(31)
19. Gardner et al San Antonio, TX*
(39)
1981-
1983
Obeaity and Diabetea
20. Hasuda and
Haffner (41)
21. Hani* et al
(38)
San Antonio, TX*
Starr County, TX*
1979- Diabetes
1981
1979- Diabetes
1981
1981- Diabetea
1983
59 male and 109 female diabetica, agea 30-69,
and the same number of randomly aelected
matched non-diabetic controla; a subset of
the sample in Research Report 14
Same as Research Report 7
Same aa Reaearch Report 6; MA ethnic group
only
2498 MA Men and women ages 15-70+, residing
in households randomly sampled from three
towns in the county;
SES is extremely low
Yes—SES and
Acculturation
Combined
Yea—SES and
Acculturation
Combined
Yea—SES and
Acculturation
Separately
No
*Data preaented in theae studies were all collected as part of the San Antonio Heart Study, a population-based
study of diabetea and cardiovascular risk factors in Mexican Americana and non-Hispanic Whites.
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390
Ischemic Heart Disease
Risk Factors in Hispanic
Americans
Shiriki K. Kumanyika, Ph.D. M.P.H.
Department of Epidemiology
Johns Hopkins School of Hygiene and Public Health
Baltimore, Maryland
Daniel D. Savage, M.D., Ph.D.
Medical Advisor
National Center for Health Statistics
Hyattsville, Maryland
TABLE OF CONTENTS
1.0 INTRODUCTION.................394
2.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG MEXICAN AMERICANS
AND HISPANIC-HERITAGE POPULATIONS IN THE SOUTHWEST .... 395
2.1 Elevated Blood Pressure and Hypertension
2.2 Cholesterol
2.3 Cigarette Smoking
3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG PUERTO RICANS . . .405
3.1 Data Issue
3.2 Ischemic Heart Disease Risk Patterns
4.0 SUMMARY...................407
5.0 REFERENCES..................408
6.0 SUPPLEMENTARY REFERENCES ............. 410
393
1.0 INTRODUCTION
This paper presents selected data on three of the standard ischemic
heart disease (IHD) risk factors (hypertension, elevated cholesterol, and
cigarette smoking) among Hispanic Americans. In addition to the material
presented here, the Cardiovascular Diseases Subcommittee report analysis of
IHD risk among Hispanics draws upon information compiled by Hector F.
Meyers, Ph.D., one of the subcommittee's consultant writers, and upon the
commissioned paper by Hazuda on socioeconomic factors and CVD (1).
However, in their entirety, the data available at the time of the Task
Force deliberations do not provide an adequate picture of IHD risk patterns
among Hispanics--either in the aggregate, according to ethnic-regional
subgroups, or according to sociocultural and socioeconomic distinctions
which may have a direct bearing on IHD risk.
Some mortality, morbidity and risk factor data which relate to
Hispanics are inaccesible in that they are grouped within data for
"non-whites". "Spanish-surname" tabulations are ambiguous as to the
homogeneity of the population so classified, and the ethnicity of
"Spanish-surname" populations must be inferred on a geographical basis.
For example, according to Aday et al. (2), 83% of a southwest Spanish
surname sample drawn for a 1975-76 national survey were Mexican American
persons (Colorado, Texas, New Mexico, Arizona, and California were the
sample states). In the New York City area, most Spanish-surname persons
are Puerto Rican. In Florida, most are Cuban Americans. Other
Spanish-surname persons have origins in Central or Latin America or other
Spanish-speaking areas of the world.
The numbers of Hispanic respondents in health surveys of the overall
United States population (e.g., the National Health and Nutrition
Examination Survey (NHANES) and the National Health Interview Survey
(NHIS)) have been small, proportional to the relatively small numbers of
Hispanics in the population. However, the Hispanic Health and Nutrition
Examination Survey (HHANES), to be completed in 1985, has been specially
designed to provide data on a range of health status variables for
sizeable, representative samples of Mexican Americans, Puerto Ricans, and
Cuban Americans (3). HHANES will become the appropriate reference point for
many IHD risk factor considerations related to Hispanic populations after
late 1985 or early 1986.
Most of the information in this paper relates to Mexican Americans and
Hispanics in the Southwest who are presumed to be primarily Mexican
Americans. This information is presented, by risk factor, in section 2.
394
Section 3 includes relatively brief comments related to the assessment of
IHD risk among Puerto Ricans. Essentially no relevant data on Cuban
Americans were identified.
2.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG MEXICAN AMERICANS
AND HISPANIC-HERITAGE POPULATIONS IN THE SOUTHWEST
2.1 Elevated Blood Pressure and Hypertension
Kraus et al. (4) reported the prevalence of elevated blood pressure
(DBP >=95 mm Hg) for Hispanic men screened at the University of California
Multiple Risk Factor Intervention Trial (MRFIT) center during 1975-76. The
approximately 19,000 screenees included 738 Spanish American men: 340 and
398 in the 35-44 and 45-57 year age-groups, respectively. In the white
comparison group, a higher proportion of white men were in the 45-57 year
age-group compared to the Spanish American men. The prevalences of
elevated blood pressure among Spanish American men and white men are
compared in Table 1, overall and according to categories of a 77 point
education-occupation scale of socioeconomic status.
Table 1: Prevalence of elevated blood pressure among Spanish American
and white men in the U.C. Davis MRFIT screenee population,
overall and according to socioeconomic status (SES). Elevated
blood pressure is defined as diastolic blood pressure > or = 95
mm Hg) (from 4; Table 3)
SES Spanish White
American
% %
all SES 15.6 11.7
11-21 high SES 8.2 9.0
22-32 12.3 10.8
33-43 11.5 12.0
44-54 17.4 13.1
55-65 19.1 14.7
66+ low SES 19.6 16.1
The data in Table 1 indicate an overall higher prevalence of elevated
blood pressure among the Spanish American men. High blood pressure
prevalence increases with decreasing socioeconomic status among the men in
both ethnic groups. The excess prevalence among the Spanish American men
is most evident in the lower SES strata. The black men in this population
had the highest prevalence of elevated blood pressure of all the ethnic
groups reported (18.8% prevalence), but did not show the SES gradient.
395
Data for Hispanic men and women in California relating to several
hypertension variables are included in the report of the California
Hypertension Survey. This survey, conducted in 1979, used a multistage,
random, probability sample of households. The Hispanic sample included
1,647 persons. The survey results on hypertension prevalence, awareness,
treatment and control for Hispanic men and women in two age-groups are
shown in Table 2.
Table 2. Hypertension variables for Hispanic men and women-
California Hypertension Survey (from reference 5; Tables
4.3 and 4.4.) Comparison data for white respondents in
the same survey are shown in brackets.
H: Lspanic Hispanic Hispan ic Hispanic
Men 18- ■49 Men 50+ Women 18-49 Women 50+
% hyperten 14.1 39.4 7.6 44.7
(140/90+ or [ 16.3 45.6 6.4 46.7 ]
on meds)
%140/90+ 13.9 35.7 6.9 29.4
[ 15.0 38.5 4.8 36.4 ]
% hyperten 28 64 45 68
aware [ 42 60 61 70 ]
% hyperten 6 38 20 55
on drug Rx [ 15 40 41 52 ]
% hyperten 1 7 8 27
controlled [ 7 15 26 21 ]
Among men, the prevalence of hypertension by either of the criteria
shown is somewhat lower among Hispanic vs. whites in both age-groups.
Awareness, treatment, and control are lower among Hispanic men compared to
white men in the younger age-group. Among the older men (aged 50 or over),
hypertension awareness is slightly higher among Hispanics but treatment and
control are somewhat lower among Hispanics, compared to whites. Among
women, the prevalence of hypertension is higher in Hispanic women than in
white women in the younger age-group but somehwat lower in the older
age-group. Younger Hispanic women are less aware and less likely to be
treated and controlled than their white counterparts. For older women,
the treatment and control appear to be somewhat better among Hispanic than
among white women.
396
In comparisons of overall hypertension rates among the ethnic groups
surveyed, adjusting for differences in the age, sex, and body weight
distributions of the populations being compared, the prevalence of
hypertension (systolic blood pressure >140 mm Hg or diastolic blood
pressure >90 mm Hg or on medication) was 21.5% among Hispanics, compared to
23.4% among whites and 35.2% among blacks (5; Table 4.2). The adjusted
mean levels of systolic and diastolic blood pressure among Hispanics and
whites were not markedly different (e.g., Hispanics mean DBP was 74.9
compared to 76.4 for whites).
Additional probability sample data which permit comparisons of blood
pressure levels among Mexican Americans and whites have been reported from
cycle 1 of the NHANES. These comparison data are shown in Table 3, for
men, and Table 4 for women.
Table 3. Systolic and diastolic blood pressure levels of Spanish"/
Mexican American men, with comparison values for white
men, U.S., 1971-1974, NHANES I. (from reference 6;
Tables 25 and 27).
SYSTOLIC(mm Hg) DIASTOLIC (mm Hg)
AGE- Spanish/ Spanish/
GROUP Mex American White Mex American White
Men Men Men Men
18-24 119.1 123.7 73.4 76.4
25-34 121.6 125.2 78.4 80.8
35-44 124.7 127.0 81.8 84.2
45-54 140.1 134.7 86.5 87.5
55-64 139.9 139.6 86.8 86.4
65-74 146.0 146.0 82.4 84.9
* examinees who identified themselves as Spanish Americans or
Mexican Americans
397
Table 4. Systolic and diastolic blood pressure levels of Spanish"/
Mexican American women, with comparison values for
white women, U.S., 1971-1974, NHANES I. (from
reference 6; Tables 25 and 27).
SYSTOLIC(mm Hg) DIASTOLIC (mm Hg)
AGE Spanish/ Spanish/
GROUP Mex American White Mex American White
Women Women Women Women
18-24 109.6 115.1 67.1 71.3
25-34 117.2 116.2 74.4 74.6
35-44 122.4 122.6 78.3 79.3
45-54 130.0 131.1 83.7 82.6
55-64 144.8 143.0 85.8 86.2
65-74 150.1 151.6 81.6 85.4
" examinees who identified themselves as Spanish American or
Mexican American.
Among men in the NHANES I sample (Table 3), systolic blood pressures of
the Spanish/Mexican American men were lower than those of white men between
the ages of 18 and 44 but comparable to or higher than those of white men
in the 45-74 year age-groups. Diastolic blood pressures of the Hispanic
men were comparable to or somewhat lower than those of their white
counterparts. Among women (Table 4), systolic and diastolic blood presures
of the Spanish/Mexican American women were generally similar to those of
white women, slightly lower in several of the age groups.
Christensen et al. (7) reported blood pressure levels of Mexican
American and Anglo students (mean age 16 years) and parents (mean ages 46
and 43 years for fathers and mothers) from the Houston-Baylor Prevalence
Study. Data are for the 1972-75 period. The number of Mexican American
parents who participated was small. Data for Mexican Americans were
reported for 165 male and 169 female students but only 44 fathers and 80
mothers. Among Anglos there were 500 to 600 in each of the four categories
(i.e., male and female students and parents).
Mean systolic and diastolic blood pressure levels for Mexican American
and Anglo fathers were almost identical (e.g.,mean systolic blood pressures
were 126.6 mm Hg and 126.9 mm Hg for Mexican American and Anglo fathers,
respectively. Mean systolic and diastolic blood pressures of Mexican
American and Anglo male students were similar also--120.2 mm Hg systolic
for Mexican American boys vs. 118.7 mm Hg for white boys. Blood pressure
levels of the Mexican American mothers were higher than those of the Anglo
mothers--125.1 mm Hg systolic for Mexican American mothers compared to 118.2
mm Hg systolic for Anglo mothers; 80.5 mm Hg diastolic vs. 76.7 mm Hg
diastolic for Mexican American mothers vs. Anglo mothers. Blood pressure
398
levels of the Mexican American girls were approximately 2 mm Hg lower than
those of Anglo girls (109.6 vs. 111.3 mm Hg systolic and 68.6 vs. 70.4 mm Hg
diastolic). The large standard deviations and the lack of adjustment for
age or body weight limit the ability to interpret these small differences.
Stern et al. (8) reported blood pressure levels from a 1979
cardiovascular survey of Mexican Americans in Laredo, Texas. Eighty-eight
percent of 462 age-eligible Mexican Americans participated (the age range
was 40 to 74 years of age). Mean systolic and diastolic blood pressure
levels of the "Laredo Project" men and women were consistently lower than
the NHANES I levels for black men and women in all sex-age-groups (men and
women between 40 to 74 years). Compared to NHANES I data for whites and
Spanish/Mexican Americans (shown in Tables 3 and 4 above), mean systolic
blood pressure levels for Laredo Project men and women were lower in some
age-sex groups and higher in other groups (8; Tables 1 and 2).
The prevalence of hypertension (i.e., medication for hypertension
and/or uncontrolled high blood pressure taken together) among Mexican
Americans was estimated to be higher than among whites but lower than among
blacks, using estimates for the Hypertension Detection and Follow-up
Program (HDFP) as the comparison data—but only in the 40 to 59 year olds.
Hypertension prevalence rates among Mexican Americans in the 60-69 year
age-group were equal to the high levels reported for blacks. Hypertension
prevalences for Laredo Mexican American men ages 40-49 and 60-69 years were
29 and 38% respectively, compared to estimates of 20.6% and 18.5%
respectively for HDFP white men and 39% and 36.3%, respectively for HDFP
black men. The same data for women--Laredo: hypertension prevalences of
21.1% and 44.3% for 40-49 and 60-69 year old Mexican American women,
compared to 18.0% and 23.6% estimated for HDFP white women and 40.8% and
42.1% for HDFP black women (8, Table 4). Stern et al. (8) note that this
intermediate blood pressure prevalence status of Mexican Americans in
Laredo (between levels for blacks and whites) is similar to the findings of
Kraus et al. (4) among the MRFIT screenees. Hypertension awareness,
treatment and control levels were greater among Laredo women than men in
every age category. In addition, Laredo project women appeared to have
better awareness, treatment, and control than white or black women in a
comparison group (Impact of Hypertension Information (IHI) Program;
reference 9). Laredo Project men were somewhat less likely than white or
black men in the IHI population to be aware, treated or controlled.
Overall, these data on blood pressure levels and hypertension
prevalences among Hispanics are very difficult to interpret. Variances
around mean levels reported are often large and relevant tests of
statistical significance are not reported. Comparison data for some reports
are taken from external sources; thus situational or methodologic
differences across studies may affect results. The SES and weight effects
on blood pressure may contribute to the discrepancies in the results. With
these considerations in mind, it seems safe to infer that the problem of
hypertension among Mexican Americans and Hispanics in the southwestern
United States is generally not of the same magnitude reported for U.S. black
populations overall, although it may be substantial, and greater than for
whites, among certain subgroups.
399
2.2 Cholesterol
Kraus et al. (4) reported a 16.7% prevalence of elevated serum
cholesterol (defined as > or = 260 mg/dl) for the Spanish American men in
the MRFIT screenee population described above, compared to 13.9% prevalence
among the white men. Prevalences of elevated cholesterol by socioeconomic
status subgroup are shown in Table 5. The prevalence of elevated
cholesterol among Spanish American men is higher than for white men in all
SES classes. The direction or nature of the SES-cholesterol relationship,
if any, within these two ethnic groups is not clear, although a U-shaped
relationship is suggested.
Table 5: Prevalence of elevated serum cholesterol among Spanish American
and white men in the U.C. Davis MRFIT screenee population,
overall and according to socioeconomic status (SES) (from 4;
Table 3)
SES Spanish American White
% %
all SES 16.7 13.9
11-21 high SES 20.4 12.5
22-32 18.5 14.1
33-43 17.2 14.4
44-54 14.0 13.9
55-65 17.8 15.4
66+ low SES 19.6 16.1
The Houston-Baylor Prevalence Study data reported by Christensen et
al. (7) also compared plasma cholesterol levels of Mexican American and
Anglo parents and children. There were no differences between Mexican
American vs. white students of either sex. Among the adults, the
Mexican American men had cholesterol levels higher than either white or
black fathers (Mexican American fathers: 218 mg/dl; white fathers: 210
mg/dl; black fathers: 209 mg/dl). Mexican American mothers had the lowest
cholesterol levels of the three groups (Mexican American mothers: 192
mg/dl; white mothers: 198 mg/dl; black mothers: 200 mg/dl). As noted
earlier when reporting the blood pressure findings from this study, the
differences reported cannot be interpreted in light of the large standard
deviations and lack of age or relative weight adjustments. It should also
be noted that the overall cholesterol values in Houston were notably lower
than values reported in national surveys. Even with consideration of
methodological differences in cholesterol determinations, Houston values
were probably 15mg% lower than in NHANES I.
400
Fortmann et al. (10) report plasma cholesterol levels at baseline in
the Stanford Three Community Study and report changes in cholesterol levels
after the 1972-1975 intervention period. The three communities were
semi-rural agricultural communities. The Hispanic persons surveyed were
classified as either bilingual or Spanish-speaking. Five classes of the
Hollingshead SES index are reported for stratification of results; however,
the Hispanic persons are almost all confined to the two lowest categories
(70 out of 80 bilingual persons and 51 out of 52 Spanish-speaking, with 45
of the Spanish-speaking in the lowest category). The only useful
comparison seems to be of baseline plasma cholesterol levels across ethnic
groups within the lowest category (class 5). Within SES class 5, plasma
cholesterol levels were lowest in the Spanish-speaking group (199 mg/dl),
intermediate in the bilingual group (210 mg/dl), and highest among Anglo
persons (220 mg/dl) (10; Table 1).
Stern et al. (11) compared levels of serum cholesterol in the Laredo,
Texas population (described earlier) to cholesterol levels of the Lipid
Research Clinics' population (comparison data were from reference 12). The
values reported are shown in Table 6.
Table 6: Serum cholesterol levels of Laredo Project Mexican American men
and women with comparison data for white men and women in the
Lipid Research Clinics (LRC) population (from 11; Table 5).
Mexican Mexican
American American
Age Men White Men Women White Women
Mean cholesterol levels (mg/100 ml)
40-44 241.8 206.5 215.5 194.5
45-54 220.4 212.4 218.5 210.9
55-64 224.9 213.6 234.6 227.2
65-74 207.1 210.9 238.6 228.5
The prevalence of obesity in this Mexican American population was
intermediate between levels reported for U.S. whites and Pima Indians.
Prevalence of hyperglycemia was also intermediate between whites and Pima
Indians and this was apparently not due to differences in the % of
diabetics controlled. With the exception of 65-74 year old men, the serum
cholesterol levels of Mexican Americans were somewhat higher than those of
the LRC whites.
Stern et al. (13) reported total and HDL cholesterol and related
variables in Mexican and Anglo men and women in San Antonio Texas (San
Antonio Heart Study). The major purpose of this report was to look at
effects of cultural and socioeconomic status on these variables. However,
ethnic comparisons were briefly discussed. The prevalence of diabetes
401
among Mexican American men was twice that of Anglo men. It was also
somewhat higher in Mexican American women vs. Anglo women. The prevalence
of obesity was consistently higher in Mexican Americans vs. Anglos--in
both sexes. HDL cholesterol levels were consistently lower in Mexican
Americans in both sexes. No consistent patterns of ethnic differences in
total cholesterol were observed.
Overall, no consistent pattern of Hispanic-white cholesterol
differences can be inferred from these data. As noted earlier regarding
findings on blood pressure, some of the inconsistencies may be due to
weight and SES differences across comparison groups.
2.3 Cigarette Smoking
Samet et al. (14) reported smoking data from a survey in Bernillo
County, New Mexico. The survey was conducted around 1980. Data were
collected through mailed questionnaires supplemented by telephone and
home interviews to increase response rates. Response rates were
75-78% for Anglo men and women; 60 to 69% for Hispanic men and women.
The Hispanic sample was of lower SES than the Anglo sample. Thus, it
is not possible to separate ethnic and socioeonomic effects in the
smoking data.
Comparable smoking patterns (current, former, never smoked) were
observed in Hispanic and Anglo samples except that among 40-59 year
old Anglo men the proportion of ex-smokers was higher than the
proportion of ex-smokers among Hispanic men. The cumulative cigarette
exposure was lower among Hispanics due to fewer average cigarettes smoked,
not shorter smoking duration.
Smoking data for Hispanics (unspecified) and whites are given in
an Advance Data report from the National Center for Health Statistics
(15). Preventive health practices were surveyed in a 1977 National
Health Interview Survey. Age-, sex-, and ethnic-specific tables are not
given. Data are shown in Table 7. A larger proportion of Hispanics than
whites had never smoked, although the percentages of current smokers were
similar. A substantially larger percentage of Hispanic than white smokers
reported smoking less than 15 cigarettes per day.
402
Table 7. Reported smoking status of Hispanics and whites in a 1977
National Health Interview Survey (from reference 15)
Never
Smoked
% White 43.1
% Hispanic 54.1
Former Current
Smoker Smoker
21.7 35.2
12.3 33.5
Average # cigs/day
for smokers
<15 >25
25.2 29.8
59.1 13.6
Roberts and Lee (16) reported smoking data from the Human Population
Laboratory Studies (1974 and 1975). Households in Alameda County,
California census tracts were sampled (Table 8). In the 1975 sample, which
was much smaller than the 1974 sample, there is an impression that Chicanos
smoke less than whites. Smoking patterns of the two groups appear
comparable in the 1974 data. Multivariate analyses controlling for age and
education or income clarified the ethnic differences such that the authors
concluded that Chicano rates of "never smoking" were higher than for Anglos,
Table 8: Smoking behavior of Chicanos and Anglos in Alameda County
in two survey samples (from 16; Table 2)
n current former never
1974
White 2292 34.3 22.5 43.2
Chicanos 162 36.0 16.8 47.2
1975
White 346 45.1 17.7 37.2
Chicanos 225 36.2 16.5 47.3
Smoking patterns among Spanish American and white MRFIT screenees in
California are shown in Table 9. Spanish American men smoke less than white
men in all SES strata. The prevalence of smoking 20 or more cigarettes
per day decreases with increasing SES (4).
Table 9: Percentages of Spanish American and white U.C. Davis MRFIT
screenees smoking 20 or more cigarettes per day, overall and by
socioeconomic status (from 4; Table 3).
SES
Spanish
American
White
all SES 20. .7
11-21 high SES 6. ,1
22-32 10, ,8
35-43 21, ,7
44-54 22, .0
55-65 25, .7
66+ low SES 23 .5
30.2
16.3
25.6
32.6
36.7
42.2
48.3
404
Smoking status data for Hispanic men and women in the California
Hypertension Survey population are shown in Table 10. Rates of current and
former smoking are similar among Hispanic and white men, although Hispanic
men smoke fewer cigarettes per day. Among women, all smoking variables are
lower among the Hispanic women. Hispanic men who smoke may be less likely
to want to quit than white men, in both age-groups. Younger Hispanic women
smokers appear to be more likely to want to quit than white women in this
age-group.
Table 10: Cigarette Smoking Variables among Hispanic American men and women
in the California Hypertension Survey, 1979 (from reference 5;
Table 7.5). Comparison data for whites are shown in brackets
Men Men Women Women
18-49 50+ 18-49 50+
% current regular 38.8 34.0 21.3 20.2
smokers [ 34.6 30.5 36.5 25.9
% current or 58.1 73.6 37.1 37.2
former smokers [ 58.0 72.6 52.2 48.7
average cigarettes 17.7 16.7 9.7 16.4
per day among [ 26.5 28.3 23.4 23.2
current smokers
% of current smokers 66.3 50.8 72.3 57.9
who would like to quit [ 71.0 59.0 63.8 60.8
Overall, the smoking data are relatively consistent in showing lesser
smoking prevalences and less heavy smoking among Hispanics when compared to
whites, particularly when SES factors are controlled.
3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG PUERTO RICANS
3.1 Data Issue
A recently published paper by Rosenwaike and Preston (17) questioning
the validity of age-reporting in some data for Puerto Ricans may be of
interest regarding the interpretation of mortality patterns for this group.
The authors note that recent official statistics show a longer
life expectancy among both males and females in Puerto Rico compared to
that for males and females in the United States (and all but a few other
countries). They suggest, however, that there appears to be strong
evidence of widespread overstatement of age among Puerto Ricans at the
older ages, resulting in an underestimation of mortality rates.
405
Table 1 in the Rosenwaike and Preston paper (17) notes life
expectancies after age 45 (1969-71) of 30.3 for Puerto Rican men vs. 27.5
and 24.6 for mainland white and non-white men. For Puerto Rican women the
life expectancy after age 45 years is 34.2 years vs. 33.5 and 29.8 for
mainland whites and non-whites. The authors present several graphs and
tables which demonstrate an excess of "age-heaping" (tendency to report
ages with terminal digits of zero and five) in the distribution of ages
among Puerto Ricans over age 40. Also, there is some inconsistency in the
data from successive censuses regarding the numbers of persons at different
ages. In discussing this analysis, the authors note that an overstatement of
one year would introduce a 10% error and two years a 20% error.
3.2 Ischemic Heart Disease Risk
Nearly all of the papers on IHD in Puerto Ricans are for the San
Juan area. Gordon et al. have published two reports (18,19)
comparing men in Framingham, Honolulu, and Puerto Rico. Some baseline data
from this comparison are shown in Table 11. The Puerto Rican men have lower
levels in all IHD risk factor and morbidity categories except diabetes.
Table 11: Baseline data for Puerto Rican and Framingham men on IHD risk
variables (from reference 18; Table 2)
FRAMINGHAM PUERTO RI
Relative weight (%) 120.04 112.50
SBP (mm Hg) 136.41 130.35
DBP (mm Hg) 85.07 82.19
Serum cholesterol (mg%) 233.96 202.45
# cigarettes/day 12.26 percent of group 7.63
diabetes by Hx 3.7 5.3
LVH-ECG 2.3 1.5
Smokers 57.7 44.4
Angina Pectoris 3.8 1.3
Coronary Insuffici ency 0.5 0.5
Myocardial Infarct ion 1.2 0.1
- difference is 25mg% for Puerto Ricans after adjustment for laboratory
differences)
At two-year follow up (18), Framingham men were reported to have a
two-fold greater risk of coronary heart disease (CHD) than men in
Puerto Rico, even after adjustments for blood pressure and cholesterol. The
differences in rates between Puerto Rican men and Framingham rates were
small or nonexistent in younger men and larger in the older men. The
apparent absence of a smoking effect on CHD among Puerto Rican men was
noted as an important exception to the overall pattern of similar risk
factor/outcome associations across ethnic groups (19). Host risk
406
factor/outcome associations were generally similar in all three cohorts in
spite of lower overall risk in the Honolulu Japanese and Puerto Rican
cohorts compared to Framingham. However, a later analysis of the Puerto
Rican Heart Program data using 8 year incidence (which gave a larger number
of incident cases) established an association of smoking with increased
incidence of myocardial infarction in both urban and rural Puerto Rican men
(20). This association was not found with other CHD endpoints.
4.0 SUMMARY
Available data on patterns of IHD risk among Mexican Americans and
Puerto Ricans are limited. Data relating to Cuban Americans appear to be
lacking. Data from the HHANES, which will describe all three groups, are
not yet available. Concurrent data for whites will not be available for
comparison with HHANES; however, older data from NHANES II are available for
comparison. A comparison of age-adjusted heart disease mortality in
predominantly Hispanic census tracts in Los Angeles with rates of Los
Angeles whites, gives the impression that Hispanics are at lower risk of
dying of heart disease than whites (21). Levels of smoking appear to be
lower in Hispanic populations. Available data on other IHD risk factors do
not clearly establish whether levels for Hispanics are lower, higher, or
variable in relation to those of whites. Analyses are needed which examine
risk factor patterns within cultural and SES subgroups of Hispanics and
also adjust for levels of overweight and diabetes.
ACKNOWLEDGEMENTS
We gratefully acknowledge the editorial assistance of Sandra
J. Anderson and Elisabeth Pitt.
407
5.0 REFERENCES
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among Mexican Americans and Risk of Cardiovascular
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on Black and Minority Health. 1984.
2. Aday LA, Chiu GY, Andersen R. Methodological issues in
health care surveys of the Spanish heritage population.
Am J Pub Health 1980;70:367-374.
3. Transcript of remarks by Fernando M. Trevino, Ph.D., M.P.H.
to the Secretary's Task Force on Black and Minority Health.
National Institutes of Health. Bethesda, MD. August 8, 1984.
4. Kraus JF, Borhani NO, Franti CE. Socioeconomic status,
ethnicity, and risk of coronary heart disease. Am J Epidemiol
1980;111:407-414.
5. Igra A, Stavig GR, Leonard AR, with special contributions by
Gamber W, Hawthorne A, Jang VL, Ransom B. Hypertension and
Related Health Problems in California. Results from the 1979
California Hypertension Survey. Hyertension Clearinghouse.
Department of Health Services. Hypertension Control Program.
714 P. Street. Sacramento, California 95814.
6. U.S. DHEW. California Conference on High Blood Pressure
Control in the Spanish-Speaking Community. Summary Report.
Conference date April 1-2, 1978. NIH Publication No.
79-1959. August 1979.
7. Christensen BL, Stallones RA, Insull W, Gotto AM, Taunton
D. Cardiovascular risk factors in a tri-ethnic population.
Houston, Texas 1972-1975. J Chron Dis 1981;34:105-118.
8. Stern MP, Gaskill SP, Allen CR, Garza V, Gonzales JL, Waldrop
RH. Cardiovascular risk factors in Mexican Americans in
Laredo, Texas. II. Prevalence and Control of Hypertension.
Am J Epidemiol 1981;113:556-562.
9. Apostolides AY, Cutter G, Kraus JF, Oberman A, Blaszkowski T,
Borhani NO, Entwisle G. Impact of hypertension information
on high blood pressure control between 1973 and 1978.
Hypertension 1980;2:708-713.
10. Fortmann SP, Williams PT, Hulley SB, Maccoby N, Farquhar
JW. Does dietary health education reach only the privileged.
The Stanford Three Community Study. Circ 1982;66:77-82.
11. Stern MP, Gaskill SP, Allen CR, Garza V, Gonzales JL, Waldrop RH.
Cardiovascular risk factors in Mexican Americans in Laredo,
Texas. I. Prevalence of overweight and diabetes and distribution
of serum lipids. Am J Epidemiol 1981;113:546-555.
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12. The Lipid Research Clinics Program Epidemiology Committee.
Plasma lipid distribution in selected North American
Populations: Lipid Research Clinics program prevalence study.
Circulation 1979;60:427-439.
13. Stern MP, Rosenthal M, Haffner SM, Hazuda HP, Franco LJ.
Sex differences in the effects of sociocultural status on
diabetes and cardiovascular risk factors in Mexican Americans.
Am J Epidemiol 1984;120:834-851.
14. Samet JM, Schrag SD, Howard CA, Key CR, Pathak DR. Respiratory
disease in a New Mexico population sample of Hispanic and
Non-Hispanic whites. Am Rev Respir Dis 1982;125:152-157.
15. National Center for Health Statistics. Health Practices
Among Adults. United States, 1977, by Schoenborn CA, Danchik
KM. Advancedata. No 64, November 4, 1980.
16. Roberts RE, Lee ES. Health Practices among Mexican Americans.
Further evidence from the human population laboratory studies.
Prev Med 1980;9:675-688.
17. Rosenwaike I, Preston SH. Age overstatement and Puerto Rican
longevity. Human Biology 1984;56:503-525.
18. Gordon T, Garcia-Palmieri MR, Kagan A, Kannel WB, Schiffman
J. Differences in coronary heart disease in Framingham,
Honolulu, and Puerto Rico. J Chron Dis 1974;17:329-344.
19. Gordon T, Kagan A, Garcia-Palmieri M, Kannel WB, Zukel WJ,
Tillotson J, Sorlie P, Hjortland M. Diet and its relation
to coronary heart disease and death in three populations.
Circ 1981;63:500-515.
20. Sorlie PD, Garcia-Palmieri MR, Costas R, Cruz-Vidal M, Havlik
R. Cigarette Smoking and Coronary Heart Diseaes in Puerto Rico.
Prev Med 1982;11:304-316.
21. Frerichs RR, Chapman JM, Maes EF. Mortality due to all causes
and to cardiovascular disease among seven race-ethnic populations
in Los Angeles, County 1980. Int J Epidemiol 1984;13:291-298.
409
6.0 SUPPLEMENTARY REFERENCES
Ramirez EA, Garcia-Pont PH. Relationship of serum cholesterol
to socioeconomic and dietary factors in Puerto Rican veterans.
Dis Chest 1969;55:197-201.
Garcia-Palmieri MR, Tillotson J, Cordero E, Costas R, Sorlie
P, Gordon T, Kannel WB, Colon AA. Nutrient intake and serum
lipids in urban and rural Puerto Rican men. Am J Clin Nutr
1977;30:2092-2100.
Garcia-Palmieri MR, Sorlie P, Tillotson J, Costas R, Cordero
E, Rodriguez M. Relationship of dietary intake to subsequent
coronary heart disease incidence. The Puerto Rico Heart
Health Program. Am J Clin Nutr 1980;33:1818-1827.
Costas R, Garcia-Palmieri MR, Sorlie P, Hertzmark E. Coronary
heart disease risk factors in men with light and dark skin
in Puerto Rico. Am J Pub Health 1981;71:614-619.
Health of Minorities and Women. Chartbook. American Public
Health Association. 1015 Fifteenth Street, N.W. Washington,
D.C. August 1982. Stock No. 072.
Health of the Disadvantaged. Chartbook II. DHHS Publication
No. (HRA)80-633. September 1980.
Frerichs RR, Chapman JM, Nourjah P, Maes M. Cardiovascular
Diseases in Los Angeles. 1979-1981. Hansen VE, Ed. American
Heart Association. Greater Los Angeles Affiliate, Inc.
1984 edition.
Chapman JM, Frerichs RR, Maes EF. Cardiovascular Diseases
in Los Angeles. 1980. Hansen VE, Ed. American Heart
Association. Greater Los Angeles Affiliate, Inc. 1983 edition.
U.S. DHHS. Hispanic Health Services Research. NCHSR Research
Proceedings Series. Conference held September 5-7, 1979.
DHHS Publication No. (PHS) 80-3288.
Hayes-Bautista DE. Identifying "Hispanic" populations.
The influence of research methdology upon public policy.
Am J Pub Health 1980;70:353-356.
Roberts RE, Lee ES. The health of Mexican Americans. Evidence
from human population laboratory studies. Am J Pub Health
1980;70:375-384.
Benson H, Costas R, Garcia-Palmieri MR, Feliberti M, Aixala
R, Blanton JH, Colon AA. Coronary heart disease risk factors.
A comparison of two Puerto Rican populations. Am J Pub
Health 1966;56:1057-1060.
410
Costas R, Garcia-Palmieri MR, Nazario E, Sorlie PD. Relation
of lipids, weight, and physical activity to incidence of
coronary heart disease. The Puerto Rico Heart Study. Am
J Cardiol 1978;42:653-658.
Garcia-Palmieri MR, Costas R, Schiffman J, Colon AA, Torres
R, Nazario E. Interrelationships of serum lipids with relative
weight, blood glucose, and physical activity. Circ
1972;45:829-836.
Garcia-Palmieri MR. Precursors of coronary artery disease
in Puerto Rico. Am J Clin Nutr 1973;26:1133-1137.
Garcia-Palmieri MR, Sorlie P, Tillotson J, Costas R, Cordero
E, Rodriguez M. Relationship of dietary intake to subsequent
coronary heart disease incidence. The Puerto Rico Heart
Health Program. Am J Clin Nutr 1980;33:1818-1827.
Caetano R. Drinking patterns and alcohol problems among
Hispanics in the U.S. A Review. Drug and Alcohol Dependence
1983;12:37-59.
National Center for Health Statistics. Blood Pressure
Levels of Persons 6-74 years, United States 1971-1974,
By Roberts J and K Maurer. Vital and Health Statistics,
Series 11, No. 203. DHEW Publication No. (HRA) 78-1648.
Caetano R. Self-reported intoxication among Hispanics
in Northern California. J Stud Alcohol 1984;45:349-354.
Gordon AJ. The cultural context of drinking and indigenous
therapy for alcohol problems in three migrant Hispanic
cultures. J Stud Alcohol 1981;(Supp)9:217-240.
Ross CE, Mirowsky J. Social epidemiology of overweight. A
substantive and methodological investigation. J Health Soc
Behavior 1983;24:288-298.
Stern MP, Gaskill SP, Hazuda H, Gardner LI, Haffner SM.
Does obesity explain excess prevalence of diabetes among
Mexian Americans? Results of the San Antonio Heart Study.
Diabetologia 1983;24:272-277.
Ailinger RL. Hypertension knowledge in a Hispanic community.
Nurs Res 1982;31:207-210.
Hazuda HP, Stern MP, Gaskill SP, Haffner SM, Gardner LI.
Ethnic differences in health knowledge and behaviors related
to the prevention and treatment of coronary heart disease.
Am J Epidemiol 1983;117:717-728.
411
Nader PR, Baranowski T, Vanderpool NA, Dunn K, Dworkin
E, Ray L. The Family Health Project. Cardiovascular risk
reduction education for children and parents. Develop
and Behavioral Pediatrics 1983;4:3-10.
Stern MP, Pugh JA, Gaskill SP, Hazuda HP.
Knowledge, attitudes, and behavior related to obesity and
dieting in Mexican Americans and Anglos. The San Antonio
Heart Study. Am J Epidemiol 1982;115:917-928.
Ramirez AG, Herrick AG, Herrick KL, Weaver FJ. El asesino
silencioso. A methodology for alerting the Spanish-Speaking
community. Urban Health 1981;10:44-48.
Weaver FR, Herrick KL, Ramirez AG, Deatrick DA. Establishing
a community data base for cardiovascular health education
programs. Health Values 1978;2:249-256.
U.S. DHHS. Proceedings of the Conference on Communicating
with Mexican Americans. Por Su Buena Salud. (Comunicando
Con Mexico Americanos. For Their Good Health. Conference
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PL, eds. NIH Publication No. 81-1961. June 1981.
412
Ischemic Heart Disease
Risk Factors in Asian/
Pacific Islander Americans
Shiriki K. Kumanyika, Ph.D., M.P.H.
Department of Epidemiology
Johns Hopkins School of Hygiene and Public Health
Baltimore, Maryland
Daniel D. Savage, M.D., Ph.D.
Medical Advisor
National Center for Health Statistics
Hyattsville, Maryland
TABLE OF CONTENTS
1.0 INTRODUCTION..................416
1.1 Data Sources
1.2 Approach
2.0 ISCHEMIC HEART DISEASE MORTALITY AMONG ASIAN/PACIFIC ISLANDERS:
Trends and Geographic Comparisons ......... 417
3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG ASIAN/PACIFIC ISLANDERS . 419
3.1 Japanese Americans
3.1.1 Blood Pressure
3.1.2 Blood Cholesterol
3.1.3 Smoking
3.1.4 Overall Impact of Risk Factors on Ischemic Heart Disease in
Japanese Americans
3.1.5 Summary
3.2 Chinese Americans
3.3 Filipino Americans
3.3.1 Blood Pressure
3.3.2 Smoking
3.4 Other Asian/Pacific Islanders
4.0 CONCLUSION...................436
5.0 REFERENCES ...............437
415
1.0 INTRODUCTION
1.1 Data Sources
The census definition of Asian/Pacific Islanders refers to a set of
ethnically and culturally diverse U.S. population subgroups whose origins
were in the "Far East, Southeast Asia, or the Pacific Islands' (1).
Relatively recent (1980 or later publication date) ischemic heart disease
(IHD) or IHD risk studies on Asian/Pacific Islanders identified through the
Medline search related almost exclusively to Japanese Americans--drawing
primarily on the Ni-Hon-San Study comparisons of Japanese in Hawaii,
California, and Japan (2-7) and on the prospective study of the Honolulu
cohort of Japanese (Honolulu Heart Study) (8-20).
Papers on heart disease mortality in Hawaii and Los Angeles compare
mortality rates of several groups (the Hawaii paper includes data for
Hawaiian, Filipino, Japanese, and Caucasian men and women (8); the Los
Angeles County paper includes data for Japanese, whites, Filipinos,
Chinese, and Koreans (21)). A review of disease trends in Pacific Basin
countries (22) includes an overview of CHD mortality trends in Japan,
China, Hawaii, and the Philippines. A California statewide hypertension
survey presents cardiovascular risk factor data (except lipids) for white,
Japanese, Filipino, Chinese, and other Asian/Pacific Islander men and women
(23,24).
Even recognizing the relatively small amount of data available on
Asian/Pacific Islander subgroups other than Japanese Americans, the low
yield of studies of other Asian/Pacific Islander subgroups from the
computerized literature search suggests that the NLM searching protocol for
minorities (i.e. MEDLINE heading: "minorities") may need expanding to
ensure that Filipinos, Hawaiians, Koreans, and other Asian sub-groups (e.g.,
Vietnamese) are included. Several informative papers on Chinese,
Filipino-, and Hawaiian-Americans (25-36) were identified
through ad hoc methods, using the bibliograpy of a recent paper on diabetes
mortality among New York City Chinese (Current Contents citation) as the
index paper.
1.2 Approach
An attempt is made to summarize available data on levels and trends of
IHD risk factors among Asian/Pacific Islander subgroups in the United
States. Patterns of IHD or heart disease mortality and incidence are
presented to provide a perspective in considering the related risk factors
(and to some extent as a substitute for risk factor data to give at least a
general impression of patterns in various sub-groups). Available
information on risk factor levels, trends, and impact in the Asian/Pacific
Islander population is then presented by risk factor separately for
Japanese, Chinese, and Filipinos. Where possible, comparisons with levels
in the U.S. total population or the white population are made. Comparisons
between or among Asian/Pacific Islander subgroups are noted where they
appear to give insight into differential effects of migration and
adaptation among Asian/Pacific Islanders of different origins.
416
2.0 ISCHEMIC HEART DISEASE MORTALITY AMONG ASIAN/PACIFIC ISLANDERS:
Trends and Geographic Comparisons
A comparison of age-adjusted coronary heart disease (CHD) mortality
rates among males in the state of Hawaii between 1940 and 1978 (8)
indicates that rates for Caucasians followed very closely the pattern
observed for the total population of white men in the U.S. Hawaiian men had
the highest rates, Caucasian men second highest, Filipino men third, and
Japanese men lowest. Over the 38 year period between 1940 and 1978, rates
for Hawaiian and Caucasian men showed almost no net increase--a slight
upwards slope changed to a downward trend around 1970. Rates for Hawaiian
men were in the range of 3 per 1000 and for Caucasian men in the range of 2
per 1000.
The pattern for Filipino men in Hawaii was quite different from that
seen in Hawaiian and Caucasian men. CHD mortality among Filipino men
increased from less than 0.6 per 1000 in 1948 to slightly more than 2 per
1000 in 1978 with no evidence of the downturn seen in the other three
ethnic categories. In a detailed analysis of CHD mortality data for
Filipinos in Hawaii, Gerber noted that CHD mortality rates more than
doubled during the 20 year period between 1950 to 1970 (1970 rates 2.6
times 1950 rates), and were significantly related to degree of urbanization
and to marital status (lowest rates among married males)(27).
CHD mortality for Chinese in Hawaii was not reported in the paper by
Reed et al. (8). King reported that 1949-1956 CHD mortality rates for
Chinese in Hawaii were lower than for Hawaiians or Caucasians but higher
than for Japanese (28). More specific data for this period were reported
by Bennett et al. (29). Age-adjusted death rates for arteriosclerotic
heart disease including coronary disease (ICD 420) for Polynesian
(Hawaiian), Chinese, Caucasian, Filipino and Japanese men (ages 35-74 years
of age, 1949-1956) were 550, 357, 488, 140 and 161/100,000 respectively
(29). Chinese men had rates lower than Caucasians but considerably higher
rates than Filipinos and Japanese. Among women, equivalent rates for
Polynesians, Chinese, Caucasians, Filipinos, and Japanese were 303, 251,
190, 130, and 94 per 100,000. Thus, Chinese women were at higher risk of
mortality than women of all ethnicities other than Hawaiian. Data on the
slope of CHD mortality among Chinese men and women in Hawaii since 1956
have not been identified at this writing. Gerber and Madhavan reported
277 CHD deaths among Hawaii Chinese males age 25 or over in 1968-72, but no
denominator is given for conversion to a rate (30, Table 1). The remaining
data are presented as proportional mortality.
CHD mortality rates also increased substantially among Japanese men
in Hawaii between 1940 and 1978 (less than 0.3 in 1940 to about 1.5 in
1970) but declined somewhat between 1970 and 1978. Patterns for women in
Hawaii were similar to those of the men in the respective ethnic groups,
except that rates were lower and downward trends in rates were observed
among women in all four groups and began in 1960 (rather than 1970) for
Hawaiian and Filipino women.
417
Although the above findings, which were based on Hawaii state death
certificate data, indicate a decline in CHD mortality for Japanese men from
the late 1960's on, no such decline was indicated in data for the Honolulu
Heart Study cohort (8). In noting this discrepancy, Reed and coworkers
suggest that the apparent declines indicated in the state mortality records
may be artifacts of coding changes or misclassification of other
cardiovascular diseases.
Los Angeles 1980 age-sex adjusted mortality due to heart disease is
shown in Table 1, below; cerebrovascular disease rates are also shown, for
comparison. Heart disease mortality is substantially less among
Asian/Pacific Islanders vs. the white or overall U.S. populations. Among
Asian/Pacific Islanders, heart disease death rates were highest for
Japanese, intermediate for Chinese and Korean and lowest for Filipinos.
The relative mortality ranks for Japanese, Chinese and Filipinos were the
same for both heart and cerebrovascular disease, although Japanese American
cerebrovascular disease rates were higher than those for whites or for the
general U.S. population.
Table 1. Deaths due to heart and cerebrovascular diseases in
Los Angeles County, 1980 (from ref 21, Tables 3 and 4)
MORTALITY: LOS ANGELES COUNTY, 1980
US White Japanese Filipino Chinese Korean
Heart Diseases 309 331 162 58 99 82
Cerebrovascular Dis 69 76 80 20 49 48
" rate per 100,000 age adjusted for age and sex by direct method, Los
Angeles County population 1980 as standard.
# adjusted for age by direct method, LA county 1980 population as standard.
Comparison of the adjusted Hawaii and Los Angeles County death rates
is not appropriate. However, the difference in the relative positions of
Filipinos and Japanese in Hawaii in 1978 vs. Los Angeles in 1980 is noted.
In discussing the Los Angeles data, Frerichs et al. (21) suggest that the
recency of migration of the Chinese, Filipino and Korean populations to the
Los Angeles area may be responsible for a "healthy migrant" effect on
mortality rates in these groups. In the same vein, rates for the more
established Japanese population are closer to those of the Los Angeles
general population.
Gerber and Madhavan have compared proportional mortality due to CHD
among Chinese in Hawaii, native and foreign-born Chinese in New York City,
and whites in New York City between 1968 and 1972 (30). CHD deaths are
proportionately higher in Hawaii Chinese vs. New York City Chinese in every
age-group (for population ages 35 and over) with the size of the difference
418
narrowing with increasing age and disappearing in the 75+ age-group. Among
the Chinese in New York City, CHD deaths were proportionately greater in
U.S. born vs. foreign-born Chinese at all ages (ages 25 and over). CHD
mortality represented a lower proportion of deaths among Chinese in both
Hawaii and New York City vs. whites in New York City, except in the 25-44
year age-group where proportionate mortality was higher in Hawaiian
Chinese. Age at CHD death was later in Chinese populations than in New
York City whites and later in foreign-born New York City Chinese than in
the other two Chinese subgroups. These findings are consistent with an
increasing and earlier CHD risk with increasing U.S. exposure.
These limited data on IHD mortality data for Asian/Pacific Islanders
indicate generally lower IHD mortality among Asian/Pacific Islander
subgroups than among United States whites.
Asian/Pacific Islander women appear to have lower risk than men. The
subgroup variations in IHD mortality rates and trends among Asian/Pacific
Islanders are noteworthy and suggest the need to go beyond generalities to
analyses for each specific subgroup. Subgroup differences are related to
biocultural factors which are inherently different among groups classified
as Asian/Pacific Islanders and also to factors such as place of birth
(native-born or immigrant), age of migration, length of U.S. residence,
region of residence (e.g., Hawaii, California, New York City),
socioeconomic status, and level of acculturation in diet and lifestyle.
IHD risk appears to increase with increasing length of U.S. residence and
increasing acculturation.
3.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG ASIAN/PACIFIC ISLANDERS
3.1 Japanese Americans
3.1.1 Blood Pressure
[The high rate of stroke and potential effect of stroke mortality among
Japanese men with elevated blood pressure should be kept in mind when
considering the data on blood pressure distributions]
A report by Yano et al. gives mean baseline blood pressure levels in
45-54 year old men in the Honolulu Heart Study Cohort (1965) as 130.7/82.0
(systolic/diastolic, mmHg) and the prevalence of elevated blood
pressure (>160/95) as 16.7% (37). Gordon reported that mean blood pressure
levels of Honolulu Japanese men 45 to 64 years old (note that age span is
10 years longer than that cited from Yano et al.; i.e., more older men in
the Gordon data) were similar to those of men in Framingham (mean SBP 136
in both groups). Mean diastolic blood pressure levels were somewhat lower
in the Honolulu men compared to Framingham men (82.68 vs. 85.07) (38). A
substantially higher prevalence of ECG-LVH in Framingham vs. Honolulu men
was noted (2.3 vs. 0.7%) in spite of the similarity of blood pressure
levels. The authors note that the readings were not standardized.
419
Comparisons of (1967-1970) systolic blood pressure levels of
Japanese men living in Japan, Honolulu and California, reported by
Winkelstein et al. (6), resulted in an overall impression that blood
pressure levels of home-island Japanese men were intermediate between those
of Northern California Japanese men, who had the highest levels, and those
of Hawaii Japanese men. The concluding point of their abstract is that
. . . the blood pressure distributions of the Japanese populations residing
in Japan, Hawaii, and Northern California cannot of themselves account for
the observed differences in coronary heart disease and stroke occurrence
among these populations in which there is a gradient from high stroke rates
in Japan to low rates in California and a reverse trend for coronary heart
disease" (6).
The specific analyses indicated that Issei Japanese men (men born in
Japan who migrated to Hawaii or California) under age 55 in all three areas
have similar blood pressures, but that over the age of 55 California Issei
men had higher readings than their counterparts in the other two areas.
Blood pressures of Issei men over age 55 in California were somewhat higher
than those of the Issei Hawaiian men.
Diastolic blood pressure levels among Nisei men in California were
higher than those of the other cohorts at all ages studied. Systolic blood
pressure levels of both Hawaiian and California Nisei men under age 55 were
substantially higher than those of the Japanese men in Japan or the Issei
men in Hawaii and California. Diastolic blood pressures of the men in
Japan and those of first and second generation Japanese men in Hawaii were
similar. Systolic blood pressure levels increased with age for all
cohorts; diastolic blood pressure levels were unrelated to age in the Japan
and Hawaii cohorts and in the Nisei men in California. Appendix A in the
Winkelstein et al. paper gives mean blood pressure levels as shown in Table
2, below (however, most of the analyses presented by Winkelstein et al. are
based on comparisons of selected percentiles--means are presented here as a
convention; standard deviations are in the source Table: SDs range from 16
to 27 for SBP and from 11 to 15 for DBP).
420
Table 2. Baseline systolic and diastolic blood pressure levels
of cohorts of 45-64 year old Japanese men in three geographic regions
ref.6; Appendix A
age 45-49 50-54 55-59 60-64 65-69
JAPAN
SBP 126 130 136 140 143
DBP 81 82 85 83 83
HAWAII
Issei SBP 131 134 135 137 141
DBP 80 86 82 80 81
Nisei SBP 128 132 134 139 141
DBP 82 82 83 83 81
CALIFORNIA
Issei SBP 123 132 139 146 148
DBP 79 84 88 89 89
Nisei SBP 133 137 142 142 146
DBP 88 89 90 89 90
The differences in blood pressure levels among these cohorts were
primarily explained by weight. Weight-blood pressure relationships were
unstable in the men in Japan; weight and blood pressure were postively
associated in the other cohorts and adjustment for relative weight
decreased the blood pressure differences between cohorts. Blood pressure
levels of the California cohort remained somewhat higher than those of the
other two cohorts in most of the comparisons.
Mean blood pressure levels among Japanese men in California in 1979
were estimated from the California Hypertension Survey data, based on a
multistage probability sample of the state population, with oversampling in
primarily Asian American communities (24). The authors of this paper noted
that in the 1980 census, the Asian/Pacific Islander population of
California comprised 35.8% of the Asians and Pacific Islanders in the United
States.
The California Hypertension Survey (24) estimate of elevated blood
pressure prevalence (>140/90) among California Japanese men ages 18-49 was
slightly higher than for white men (19.2 vs. 15.0 %). For men over age 50,
the prevalence of elevated blood pressure among Japanese men by this
criterion was lower than for white men (29.1 vs. 38.5 %). Hypertension
prevalence (140/90) for Japanese women was much lower than for white women
421
at all ages: 0.4% vs. 4.8% among Japanese vs. white women ages 18-49 and
13.9 vs. 36.4% for Japanese vs. white women over age 50. (See Table 9 in
section 3.4 for 160/95+ prevalence comparisons with sexes pooled.)
The sex differences in hypertension prevalence among Asian/Pacific
Islander men and women were reduced 5% by adjustment for age and relative
weight and further by adjustment for alcohol intake and other environmental
variables. Rates for the men were only 2.3% higher than those of women
after adjustment for all significant predictors available (these included
psychological, social support, nutrition, smoking, and acculturation
factors).
In a more detailed report of the survey results, the prevalence of
hypertension (i.e., rather than elevated bp) (>140/90 or taking medication)
among Japanese men and women was as follows (from Table 4.3 in Reference
23):
Japanese American men 18-49: 19.8% (vs. 19.2% with bp > or =140/90)
50+: 32.3% (vs. 29.1% with bp > or =140/90)
Japanese American women 18-49: 0.9% (vs. 0.4 % with bp > or =140/90)
50+: 17.5% (vs. 13.9% with bp > or =140/90)
The parenthetical data are repeated here to indicate the relative
percents of the populations who are hypertensive under control vs. those
whose blood pressures were elevated at time surveyed, using the 140/90+
definition.
In the California Hypertension Survey (23), levels of hypertension
awareness, treatment and control differed depending on the definition of
hypertension used. In almost all instances higher percentages of
awareness, treatment and control were reported for the groups defined by
the more severe criteria (i.e., 160/95+ or 95+). (This also applies to the
whites, blacks, and the other Asian/Pacific Islander subgroups surveyed.)
Awareness among hypertensive Japanese adults ages 50 and older was 72%
(using 140/90 mm Hg) and 94% (using a diastolic blood pressure of 95 or
greater mm Hg) in men (60 to 87% in white men) and 60 to 87% in women
(white women, 70 and 93%). Awareness levels among Japanese males 18-49
were 35 to 30% (i.e., 35% aware using 140/90 and 30% aware using 95+ mm Hg,
a reversed trend); (white males 42 to 62%).
Percentage of hypertensives under drug treatment were as follows: 12
to 29% for Japanese men 18-49 (white men 15-38%); (no stable estimates for
Japanese women ages 18-49);37 to 61% for males ages 50 and over (white
males 40-75%) and 32 to 79% for women ages 50 and over (white women
52-87%). Percentages of hypertensives controlled were 3 to 29% for
Japanese men 18-49 (7-32% for white men) and 10-56% for men 50 and over
(15-58% for white men). Eight to 38% of Japanese women ages 50 and over
were controlled (21-78% of white women).
422
3.1.2 Blood Cholesterol
Yano et al. report a mean level of baseline serum cholesterol in the
younger segment of the Honolulu cohort (ages 45-54) as 219.4 mg% and a
13.4% prevalence of hypercholesterolemia (>=260 mg%) (37). Comparisons of
total cholesterol levels in 45-64 year old Japanese men in the Honolulu
cohort with levels of Framingham men were reported by Gordon et al. in 1974
(38). Methodologies for cholesterol determinations were sufficiently
similar for Honolulu and Framingham to support direct comparisons. Serum
cholesterol levels were approximately 15% lower in Honolulu vs. Framingham
(218.55 vs. 233.96 mg%).
Baseline comparisons of serum cholesterol levels in Honolulu, Japan,
and California were reported by Nichaman et al. (4). The essence of the
overall findings was that "in every age-group, mean, median and percentiles
for each of the biochemical variables are considerably lower for men in
Japan than in California or Hawaii. . . at all ages the cholesterol
values in Hawaii are somewhat lower than in California" (4, p. 494) (the
other biochemical variables examined were glucose, uric acid, and
triglycerides). Mean levels for the three cohorts are shown in Table 3,
below.
Table 3. Mean serum cholesterol levels at baseline (1967-1970)
for Japanese men in Japan, Hawaii, and California (from ref
4, Table 3; mg%)*
AGE JAPAN
45-49 179.8
50-54 182.5
55-59 181.5
60-64 182.2
65-69 180.9
AWAII CALIFORNIA
219.4 223.4
219.4 228.2
218.7 226.8
216.7 223.6
211.1 224.0
a footnote to the source table notes that the values from Japan
were taken from the 1967 cycle and that diabetics were excluded
from this analysis--therefore other published values may differ
slightly.
Serum cholesterol levels of a sample of men from the Honolulu and San
Francisco cohorts were among those analyzed in the Cooperative Lipoprotein
Phenotyping Study (9). White comparison groups were from Albany NY, Evans
County GA and Framingham. Mean HDL levels reported in Table 1 of that
paper are shown in Table 4, below.
423
Table 4. Mean HDL-cholesterol level in samples of white, Japanese,
and black men over age 50 by age-group (ref 9, Table 1)
GROUP AGE
50-59 60-69 70+
Albany (white) 48.7 49.6 51.4
Framingham ((white) 44.8 45.5 45.5
Evans County (white) 48.3 48.1 50.9
Evans County (black) 59.0 56.3 51.0
San Francisco (Japanese) 45.9 48.8 49.7
Honolulu (Japanese) 44.0 46.0 46.6
The focus of the Cooperative Lipoprotein Phenotyping analysis was the
relationship of lipoproteins to CHD. Total cholesterol levels and HDL-C to
total-C ratios were not reported as such. This limits the ability to
directly evaluate the data in Table 4. However, considering the
earlier-cited data indicating similar total cholesterol levels among
Framingham and Honolulu men and higher total cholesterol levels in San
Francisco vs. Honolulu men, the data in Table 4, above, do not suggest any
large difference in proportionate HDL-levels of Japanese American men
compared to white men in the same age range.
3.1.3 Smoking
The prevalence of cigarette smoking in the Honolulu cohort men ages
45-54 was reported by Yano et al. (37) as 46.4%. The percent of men
smoking a pack of cigarettes per day or less was 27.2; 19.2 smoked more
than one pack per day (37). In the comparison of 45-64 year old Framingham
and Honolulu men reported by Gordon et al. (38), 44.1% of Honolulu men vs.
57.7% of Framingham men were smokers; Honolulu men smoked 10.52 cigarettes
on average, vs. a 12.26 average among Framingham men. Robertson et al. (5)
reported the following frequency distributions of baseline smoking status
for home-island and Honolulu Japanese men ages 45-68 years (ref. 5; Fig. 1):
none'" <11 11-20 21+
Japan 24.4 7.9 56.1 11.6
Honolulu 55.8 2.5 25.1 16.6
( * includes former smokers )
Taken together, these data indicate that Japanese men in Honolulu were less
often smokers than Japanese men in Japan and white men in Framingham.
Marmot and Syme discuss smoking habits in relation to acculturation
of Japanese men in San Francisco (3). The data are based on a survey
conducted in 1969-70 (response rate 66% of the men enumerated in San
424
Francisco and Oakland plus additional men in Santa Clara County). The
study included 14.6% Issei men. The rest were Nisei (including some Sansei
(third generation)) men ages 30 and over. Issei men were the older men in
the cohort.
Defining traditional vs. nontraditional upbringing according to years
spent in Japan, age left parents' home, ever lived on a farm, where
schooling took place (Japan or U.S.), years spent in Japanese language
school, religion while growing up, friends while growing up, wife s
cultural background (if married) (3; pp.230-231)--the following data were
reported (3; p.232):
% of smokers who smoke:
1-14 15-24 25+
cigarettes per day
traditional 20.7 50.5 28.8
nontraditional 20.0 50.6 29.4
Thus, although there may be differences in the percentages of traditional
and nontraditional men who smoke, there are no differences in level of
smoking among those who do smoke. Also, the authors note a possible
interaction between Japanese vs. Western diet preference and smoking among
the men surveyed--there was a somewhat higher percent of smokers among men
who preferred a Japanese diet.
More recent estimates of cigarette use among Japanese Americans in
California are available from the 1979 survey results. Overall, 50.6% of
the Japanese American men were classified as "ever smoked" (24). A more
detailed breakdown of smoking habits in this population is shown in Table
5, below.
Table 5. Cigarette Smoking Variables among Japanese American men and women
in the California Hypertension Survey, 1979 (from reference 23, Table 7.5)
[percentages for comparable white sex-age-group]
^current regular smokers
^current or former smokers
average cigarettes smoked per
day among current smokers
%of current smokers who
would like to quit
Men Men
18-49 50+
34.8 17.7
[34.6 30.5
55.0 81.1
[ 58.0 72.6
19.3 19.9
[ 26.5 28.3
80.4 40.2
[ 71.0 59.0
Women Women
18-49 50+
19.0 18.1
36.5 25.9 ]
47.4 29.5
52.2 48.7 ]
17.6 11.7
23.4 23.2 ]
56.1 5.9*
63.8 60.8 ]
*=based on fewer than 20 cases
425
3.1.4 Overall Impact of Risk Factors on CHD in Japanese Americans
Earlier, the discrepancy between Hawaii state mortality data and
Honolulu Heart Study findings regarding CHD mortality was noted. The
Honolulu data did not show declines in CHD mortality in analysis of data
for 60 to 69 year old men between 1968 and 1978 using causes coded from
medical records review, whereas the data coded according to state mortality
codes did show a decline (see Reed et al. (8, Figures 3 and 6)).
Reed et al. present total and fatal myocardial infarction (MI)
incidence data for 50-59, 60-63, and 64-67 year old men in this cohort in
Figure 4 of their report. Incidence rates for total MI increased overall
between 1967-70 and 1975-78 for men ages 60-67 and appear to have remained
constant in the 56-59 year old men. Fatal MI rates showed a slight
increase in the 60-67 year old men with evidence of tapering off after
1971-74; fatal MI rates were constant in the 56-59 year old men.
Case-fatality rates for the three age groups are presented in Table 1 of
the report: 37, 39, and 36% in men 56-59 during the three time periods;
36, 42, and 33% in 60-63 year old men; and 46, 45, 45 percent in men ages
64-67. Analyses by birth cohort indicate upward slopes of total and fatal
MI incidence during this time period in all cohorts of men born between
1900 and 1919.
Gordon et al. (38) reported that although the standard risk factor
associations were observed among men in the Honolulu cohort, the 2 year CHD
incidence (by ECG) or mortality in Honolulu was less than in Framingham by
one-half to one fourth. Incidence was 2 times more in Framingham and
mortality was 4 times more i.e., the case-fatality in Honolulu was much
lower than in Framingham. CHD mortality in Framingham was greater by a
factor of 2.1 even after adjustment for differences in levels of blood
pressure, smoking, and cholesterol (this finding was not substantially
changed by exclusion of men with prior CHD from the analysis). Castelli et
al. point out that Honolulu men have CHD incidence half that of Framingham
men in spite of the fact that HDL cholesterol levels of the two groups of
men are similar (9). Framingham CHD rates were higher than Honolulu rates
even in the group with low risk factor levels. Differences in Framingham
and Honolulu rates increased in magnitude with increasing age.
In a later analysis of six year follow-up data (10) Gordon et al.
attempted to identify factors other than blood pressure, smoking and
cholesterol which could explain the differences between Framingham and
Honolulu CHD rates. Alcohol intake was found to be a strong inverse
predictor of MI and CHD death although the authors noted that total
mortality was increased with increased alcohol consumption (possibly
positive effect of alcohol on blood pressure and/or stroke). Higher starch
intake in the Honolulu cohort was also noted as a significant protective
factor for CHD. Elsewhere, the possible differential factor of later age
of acquisition of risk factors among Japanese migrants vs. U.S.-born men
has been noted as a possible explanation for CHD rates less than those
predicted with Framingham logistic functions (5).
426
Robertson compared risk factor-CHD associations in Japanese men in
Honolulu and Japan (5). Gradients for blood pressure and cholesterol on
CHD incidence were similar in both cohorts of men. Smoking was the most
significant risk factor in Honolulu but was not related to CHD incidence in
Japan (suggesting to the authors that cigarette smoking may be a less
important CHD risk factor in men with low serum cholesterol levels). An
influence of relative weight on CHD was observed in Honolulu Japanese men
but not among the men in Japan (this finding may have been due to the
relatively small number of obese men in the Japan cohort (authors' note)).
In spite of higher blood pressure levels in the California cohort, as
reported by Winkelstein et al. (6), the authors note that a separate study
of CHD prevalence in the three cohorts did not find a higher CHD prevalence
among the California men (there are several possible explanations for this
other than the lack of a true relationship). However, the Honolulu Heart
Study prospective data found a substantial impact of blood pressure on CHD
at ten-year follow-up (and throughout)(37).
In the ten-year Honolulu Study data, the significance of blood
pressure levels for total, fatal, and nonfatal CHD, nonfatal MI and acute
coronary insufficiency compared with nonCHD was great. In fact, systolic
(or diastolic) blood pressure was one of the strongest and most
consistently related risk factors of those measured, for all CHD measures
except angina pectoris (see Table 6, below).
Table 6. Impact of standard risk factors, body mass index and
alcohol intake on CHD among Japanese American men in Honolulu
at ten-year follow-up (from 37, Table 2 (age-adjusted means
for baseline characteristics)
SBP DBP CHOL* CIGS# BMI** ALCH!
nonCHD 133.2 81.9 217.0 10.2 23.8 14.3
Total CHD 144.7 86.6 229.9 13.0 24.7 9.7
Fatal CHD 151.6 89.0 231.3 14.2 24.8 9.1
nonfatal MI 143.2 86.0 223.0 14.6 24.8 8.3
Acute CI 147.1 87.4 222.7 14.2 24.8 15.6
uncomp AP 137.2 84.0 225.4 7.3 24.5 10.5
* serum chol mg%;#no. per day;** kg/m squared;!ml/day
Levels of these variables were significantly different from the nonCHD
group for the total CHD cases, for fatal CHD cases (except alcohol
consumption), and for nonfatal MI. Acute coronary insufficiency cases
differed from the nonCHD only for blood pressure (the authors note that
less than valid ascertainment of angina pectoris may be involved in the
apparent lack of associations with this CHD manifestation).
427
Multivariate analyses (see 31, Table 4) indicated that, in addition to
blood pressure, cigarette smoking was next in line as a strong predictor of
CHD in all categories except angina. Alcohol consumption was a strong,
independently associated protective factor for both fatal CHD and for
nonfatal MI. Serum cholesterol was strongly associated with total CHD and
nonfatal MI and significantly, but less strongly related to fatal CHD.
Relative weight was not independently associated with any of the CHD
manifestations in the multivariate analysis.
3.1.5 Summary
These data, although far from adequate in describing the overall IHD
risk patterns among Japanese American men and women, can be summarized as
follows.
Systolic blood pressure levels of Japanese men in the Honolulu Heart
Study cohort were similar to those of Framingham men; diastolic blood
pressures were somewhat lower. The EKG-LVH prevalence among the Japanese
men was lower than expected based on the Framingham model, possibly related
to methodology. A consistent gradient in blood pressure and blood pressure
related risk is not evident when comparing Japanese men in Japan, Hawaii,
and California. U.S. born Japanese men in California have higher blood
pressure levels than men in Japan or Japanese-born men in California; these
differences appear to be weight-related.
When compared to white men in California, Japanese men under age 50
had a hypertension prevalence slightly higher than that of white men
whereas Japanese men above 50 had a lower hypertension prevalence than
white men. Hypertension awareness was somewhat higher among Japanese men
over age 50 compared to white men in that age-group but was lower among
Japanese men under age 50 compared to white men. Percentages of Japanese
men under drug treatment were somewhat lower than for white men.
Percentages of those treated who were controlled were similar among
Japanese men and white men.
Japanese women in California had substantially lower hypertension
prevalence than white women in both the under 50 and 50 and over age
groups. Weight and other environmental factors would appear to explain
most of the gender differences in hypertension prevalence. Small numbers
precluded estimates of hypertension awareness, treatment, and control among
Japanese women under age 50. Data for hypertensive women over age 50
indicated lower levels of awareness, treatment, and control compared to
white women in this age-group.
The limited available data on serum cholesterol levels of Japanese men
indicate a consistent gradient in serum cholesterol levels from low levels
among Japanese men in Japan to intermediate levels among Japanese men in
Hawaii and the highest levels among Japanese men in California. Serum
cholesterol levels of Japanese men in all three areas were lower than for
men in Framingham. No data on cholesterol levels of Japanese American
women were identified.
428
Regarding smoking, the prospective study baseline data suggest that
Japanese men in Hawaii were less likely to be smokers than men in Japan or
Framingham. The more recent California survey data suggest similar smoking
rates among Japanese and white men under age 50, but lower smoking rates
among the older Japanese men compared to older white men. Smoking rates
among Japanese women respondents in the California survey were lower than
for white women, in both the younger and older age-groups. The average
number of cigarettes smoked by Japanese men and women was consistently less
than for the comparable white age-sex group. Somewhat more of the younger
Japanese men wanted to quit smoking compared to the white men in the same
age-group; otherwise, the Japanese surveyed were less likely than their
white counterparts to state that they wanted to stop smoking.
The impact of the standard risk factors on IHD morbidity and
mortality, although less than predicted at short-term prospective
follow-up, has been in line with expectations upon longer (10-year)
follow-up. Thus, at least tentatively, these data indicate that Japanese
Americans have IHD risks comparable to those of white Americans to the
extent that they acquire comparable risk factor profiles. The lower IHD
mortality rates among Japanese Americans may reflect somewhat lower levels
of certain IHD risk factors, particularly among the older Japanese men who
are primarily Japan-born.
3.2 Chinese Americans
Primary findings from the available data sources on risk factors among
Chinese Americans are summarized in this section. Refer to the earlier
description of CHD mortality data for Chinese Americans (section 2.0). A
report by Gerber of higher proportional diabetes mortality among Chinese in
New York City compared to whites and other nonwhites in New York City
should be noted as well (31). Among 45-64 year old foreign-born Chinese, the
proportion of diabetes deaths increased with increased length of residence
in New York City. Proportional mortality from diabetes was slightly higher
in foreign born vs. U.S. born Chinese above age 65, but slightly lower
among foreign-born Chinese ages 45-64.
A component of the Hawaii Cardiovascular Study compared cardiovascular
risk factors in 30 Chinese and 68 Japanese males who had Mis with those of
CHD-free controls in 1966 and 1967 (25). The comparison was prompted by
the higher risk of CHD in Chinese men--2.2 times that of the Japanese men.
Cases were identified through hospital discharge records. Examinations
were at least 3 months post-discharge. Controls were age- and race-matched
men identified through hospital records as well as an additional group of
population controls randomly selected from a health department survey
sample. Absence of CHD in controls was electrocardiographically confirmed.
Racially-mixed Chinese and Japanese men were not included in the study.
Chinese cases were older than Japanese cases by about 5 years (58.4 vs.
53.2 years of age). Racial comparisons were therefore age-adjusted.
Recognizing the inherent possibilities for sample biases among the
cases, the emphasis of the analyses was in racial rather than case-control
comparisons. Significant differences between the Chinese and Japanese
429
cases which were also seen in the population controls were considered to
have greater probable validity than differences which were apparent between
Japanese and Chinese controls only.
The Chinese men were more obese than the Japanese (skinfolds) and
appeared to have gained more weight since age 25, but were not more
overweight by a weight/height index (Quetelet). In a follow-up report on
the Chinese MI survivors and controls, these authors confirmed that the
moderate, "nonoverweight" adiposity among the Chinese men was of
pathological significance, i.e., it was related to higher levels of
CHD and CHD risk factors (32).
Serum cholesterol levels of the Chinese population controls were
approximately 20 mg% higher than those of the Japanese controls (242.7 vs.
220.7); higher cholesterol among the Chinese vs. Japanese men was generally
consistent in age-specific comparisons although not always statistically
significant. Blood pressure levels and LVH patterns were not consistently
or significantly different between the two racial groups. A slightly
higher proportion of Japanese vs. Chinese cases were smokers (75 vs. 70%)
in the immediate pre-MI period; higher proportions of Chinese patients and
both groups of controls had never smoked and fewer were current smokers
than the respective groups of Japanese men. Physical activity was lower in
the Chinese than Japanese men.
According to Stavig et al., the Chinese population of California
increased by a factor of 2.5 between the 1970 and 1980 censuses (24).
Estimates of elevated blood pressure prevalence (> or =140/90) among California
Chinese men ages 18-49 was slightly lower than for comparable white men
(11.8 vs. 15.0%). For Chinese men over age 50 the prevalence of elevated
blood pressure by this criterion was higher, 45.0 vs. 38.5% for white men.
Elevated blood pressure prevalence (140/90+) for Chinese women vs. white
women was similar: slightly higher in the 18-49 year age-group (6.4 vs.
4.8%) and essentially the same (34.3 vs. 36.4%) for women ages 50 and over
(also see Table 9, section 3.4).
The overall influence of age, relative weight and other predictive
variables on the prevalence of elevated blood pressure among Asian/Pacific
Islanders in the 1979 California survey was described earlier (section
3.1.1). Chinese in California were intermediate (between Japanese and
Filipinos) in reported alcohol intake, the least likely of the three
sub-groups to be foreign-born, and varied in comparability to the other two
groups on other blood pressure predictors.
In the more detailed report of the survey results, the prevalence of
hypertension (rather than elevated blood pressure) (> or =140/90 or taking
medication) among Chinese men and women was as follows (from Table 4.3 in
reference 23):
Chinese American men 18-49: 13.3 % (vs. 11.87% with bp > or =140/90)
50+: 50.3% (vs. 45.0% with bp > or =140/90)
Chinese American women 18-49: 7.1% (vs. 6.4 % with bp > or =140/90)
50+: 42.6% (vs. 34.3% with bp > or =140/90)
430
The parenthetical data are repeated here to indicate the relative
percents of the populations who are hypertensive under control vs. those
whose blood pressures were elevated at time surveyed, using the 140/90+
definition.
Levels of hypertension awareness among hypertensive Chinese ages 50
and older in California in 1979 were 58 to 83% in men (white men, 60-87%)
and 55 to 98% in women (white women 70-93%), depending on the definition of
hypertension used. Awareness levels among Chinese males 18-49 were 32 to
79% (white men 42-62%)(23, Table 4.4).
Percentages (of hypertensives) under drug treatment were 21 to 63% for
Chinese men 18-49 (white men 15-38%); no stable estimates for
Chinese women aged 18-49; 40 to 68% for males ages 50 and over (white
males 40-75%); and 52 to 97% for women ages 50 and over (white women,
52-87%). Percentages of hypertensives under control were 11 to 48% (white
men 7-32%) for Chinese men 18-49 and 11-59% for men 50 and over (white men
15-58%). Nineteen to 94% of Chinese women ages 50 and over (white women
21-78%) were controlled.
Smoking data for Chinese men and women from the detailed California
Hypertension report are summarized in Table 7.
Table 7. Cigarette Smoking Variables among Chinese American
men and women in the California Hypertension Survey, 1979 (from
reference 23, Table 7.5) [comparison data for whites]
Men Men
18-49 50+
% current regular 26.6 35.2
smokers [34.6 30.5
% current or 42.0 69.8
former smokers [58.0 72.6
average cigarettes
12.5 16.4
per day among [26.5 28.3
current smokers
% of current smokers 54.3 59.0
who would like to quit [71.0 59.0
Women Women
18-49 50+
3.6 9.7
36.5 25.9 ]
7.7 19.2
52.2 48.7 ]
12.0 17.1
23.4 23.2 ]
48.0* 66.5*
63.8 60.8 ]
based on fewer than 20 cases
431
In summary, pertinent data which permit interpretation of IHD risk
factor levels among Chinese American men and women in the context of levels
of risk typical for the U.S. white population are essentially limited to
the data from the California survey. The California data indicate higher
hypertension prevalence among Chinese men over age 50 compared to white
men, but somewhat lower rates among Chinese men compared to whites in the
under 50 age-group. Among Chinese and white women in both age-groups the
rates of hypertension are similar and are lower than for men.
No serum cholesterol data are available from the California survey.
The smoking data indicate that more of the older Chinese men, but fewer of
the younger men, smoke compared to their white age peers. Substantially
fewer Chinese women smoke than white women in both age-groups. At all
ages, the Chinese who smoke smoke fewer cigarettes per day. Younger
Chinese men and women are less likely than their white counterparts to
report wanting to quit smoking. Older Chinese men and women were equally
or more likely to report wanting to quit compared to whites.
Only proportionate mortality data were identified for the Chinese
population in New York City. These data indicate lower IHD risk among
Chinese relative to whites, although the proportion of diabetes related
deaths is higher among Chinese than among whites.
These data are too limited to support any overall conclusions about
patterns of IHD risk among Chinese Americans. There does not appear to be
any striking evidence of excess IHD risk on the basis of these data; most
of the available data suggest less than average risk among
Chinese Americans compared to whites.
3.3 Filipino Americans
Other than the mortality data for Filipinos reported in section 2.0
above, the only relevant data identified specific to Filipino Americans was
from the California Hypertension Survey. Data from that survey for blood
pressure and smoking are noted below. No serum cholesterol data for
Filipino Americans have been identified at this writing.
3.3.1 Blood Pressure
Mean blood pressure levels among Filipino men in California in 1979
were estimated from the California Hypertension Survey data (24). Stavig
et al. note that the Filipino population of California tripled between 1970
and 1980. Estimates of elevated blood pressure prevalence (> or =140/90)
among California Filipino men and women were higher at all ages and
substantially higher than for whites in the age-sex groups with relatively
high prevalences: Filipino men 18-49, 29.5% vs. 15.0% for whites; Filpino
men ages 50+, 50.8% vs. 38.5% for whites; Filipino women 18-49, 6.5% vs.
4.8% for whites; Filipino women ages 50+, 61.3% vs. 36.4% for whites (24,
Table 1) (also see Table 9, section 3.4).
432
The influence of age, relative weight, and other predictors on blood
pressure levels of California Asian/Pacific Islanders was noted earlier in
the discussion of blood pressure levels of Japanese Americans. Filipinos
and other Asian-Pacific Islanders in California reported a greater
prevalence of excess weight (higher body mass index), higher average number
of alcoholic drinks per sitting, and fewer close friends, were less likely
to live in Asian neighborhoods and more likely to be foreign born than
Japanese and Chinese-_consistent with the higher prevalence of uncontrolled
hypertension in Filipinos vs. Chinese and Japanese. Educational attainment
was lower among Filipinos, particularly among Filipino men, vs. the general
population or Japanese American males.
In the more detailed report of the survey results, the prevalence of
hypertension (>140/90 or taking medication) among California
Filipino American men and women was as follows (from Table 4.3, ref. 23):
Filipino American men 18-49: 30.5% (vs. 29.5% with bp > or =140/90)
50+: 60.0% (vs. 50.8% with bp > or =140/90)
Filipino American women 18-49: 6.7% (vs. 6.5 % with bp > or =140/90)
50+: 65.2% (vs. 61.3% with bp > or =140/90)
The parenthetical data are repeated here to indicate the relative
percents of the populations who are hypertensive under control vs. those
whose blood pressures were elevated at the time surveyed, using the 140/90+
definition.
Levels of hypertension awareness among hypertensive Filipino men and
women ages 50 and older in California in 1979 were 67 to 91% in men (white
men 60-87%) and 49 to 83% in women (white women, 70-93%), depending on the
definition of hypertension used. Awareness levels among Filipino males
18-49 were 62 to 89% (white males 42-62%) (23, Table 4.4) (stable estimates
for women 18-49 were not possible).
Percentages under drug treatment were: 52 to 82% for Filipino men
18-49 (white men 15-38%); (no stable estimates for Filipino women aged
18-49); 43 to 76% for males ages 50 and over (white males 40-75%) and 39 to
82% for women ages 50 and over (white women 52-87%). Percentages of
hypertensives who were controlled were 3 to 38% for Filipino men ages 18-49
(white men 7-32%) and 15 to 60% for men ages 50 and over (white men 15-58%).
Six to 54% of Filipino women ages 50 and over (white women, 21-78%) were
controlled.
In summary, an excess prevalence of hypertension among Filipinos in
California is evident, a noteworthy departure from the picture seen in the
other Asian/Pacific Islander populations discussed in this review.
Awareness of hypertension was relatively high, particularly among the
younger Filipino men compared to white men in the same age-group.
Percentages of Filipino men under drug treatment and controlled were
comparable to or better than for white men. Among hypertensive Filipino
women over age 50, awareness, treatment, and control levels were lower than
for white women.
433
3.3.2 Smoking
Fewer Filipino than white men and women in the California survey were
smokers, in both the under 50 and 50 and over age-groups (as shown in Table
8). Among men and women who smoked, Filipino men and women smoked fewer
cigarettes per day. The estimates of percentages of Filipino smokers
wanting.to quit are not stable.
Table 8. Cigarette Smoking Variables among Filipino American
men and women in the California Hypertension Survey, 1979 (from
reference 23, Table 7.5) [comparison data for whites]
Men Men Women Women
18-49 50+ 18-49 50+
% current regular 30.7 21.2 12.4 16.1
smokers [ 34.6 30.5 36.5 25.9 ]
% current or 58.3 67.2 32.9 25.9
former smokers [ 58.0 72.6 52.2 48.7 ]
average cigarettes 18.2 17.2 15.0 1.1
per day among [ 26.5 28.3 23.4 23.2 ]
current smokers
% of current smokers 75.6 90.8* 67.6* 13.2*
who would like to quit [ 71.0 59.0 63.8 60.8 ]
* based on fewer than 20 cases
3.4 Other Asian/Pacific Islanders
CHD mortality data for Koreans in California are included in Table 1
(section 2.0). Blood pressure data for "other Asians" in the California
survey are shown in Table 9, below, with data for Caucasian, Japanese,
Chinese and Filipinos included for summary and comparison purposes.
434
(from reference 24; Table 1)
White Japanese Filipino Chinese Other
Asian/PI
MALES 18-49 15.0 19.2 29.5 11.8 28.5
weighted
% hypert
140/90+
MALES 50+ 38.5 29.1 50.8 45.0 45.2
140/90+
FEMALES 18-49 4.8 0.4 6.5 6.4 3.2
140/90+
FEMALES 50+
140/90+ 36.4 13.9 61.3 34.3 42.2
BOTH SEXES 20.2 12.5 24.5 15.7 20.1
18+
140/90+
BOTH SEXES
18+
160/95+ 6.6 4.3 9.9 5.8 8.2
The overall rate of hypertension for Asian/Pacific Islanders is 18.9%
compared to an overall rate of 19.3 for whites. However, this similarity
in rates is not a true reflection of the heterogeneous picture evident in
Table 9. The high rates of hypertension among the Filipino men and women,
the older Chinese men, and the younger Chinese women relative to whites in
the same sex-age-groups have been noted. Also, hypertension rates are
higher than those of whites among three of the four sex-age-groups of
"other" Asian/Pacific Islanders.
Additional relevant information is sparse but includes more detailed
data on "other Asians" from the California Survey (23), the Kraus et al.
analyses of CHD risk factors in several ethnic groups (data are for
Asian Americans, not further specified) (39), and data for Hawaiians
(Polynesians) from the Hawaii Cardiovascuar Study (33-36). The paucity of
data reflects the relatively small numbers of other Asians rather than a
lack of need for concern about significant levels of CHD risk.
435
4.0 CONCLUSION
In conclusion, the data on IHD risk among Asian/Pacific
Islanders as a group and especially for specific subgroups are
extremely limited. What data there are indicate that IHD risk
levels are generally lower than for whites, but with some
noteworthy exceptions. The extent of IHD risk appears to
parallel the degree of acculturation. Risks associated with
diet and lifestyle adaptations to the U.S. environment may be
important contributors to excess risks as they occur.
ACKNOWLEDGEMENTS
We gratefully acknowledge the editorial assistance of Sandra
J. Anderson and Elisabeth Pitt.
436
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441
Ischemic Heart Disease
Risk Factors in American
Indians and Alaska Natives
Shiriki K. Kumanyika, Ph.D., M.P.H.
Department of Epidemiology
Johns Hopkins School of Hygiene and Public Health
Baltimore, Maryland
Daniel D. Savage, M.D., Ph.D.
Medical Advisor
National Center for Health Statistics
Hyattsville, Maryland
TABLE OF CONTENTS
1.0 APPROACH
446
2.0 OVERALL PERSPECTIVE ON PREDISPOSITION TO ISCHEMIC HEART
DISEASE IN NATIVE AMERICANS ............. 447
2.1 Background Comments on the Native American Population
2.2 Heart Disease in the Mortality Profile of the Native American
Population
3.0 ISCHEMIC HEART DISEASE IN SPECIFIC INDIAN POPULATIONS . . . .453
3.1 Southwestern Indians
3.2 Indians outside of the Southwest
3.3 Summary
4.0 ISCHEMIC HEART DISEASE RISK FACTORS IN NATIVE AMERICANS . . .457
4.1 General Comments
4.2 Hypertension
4.3 Cholesterol
4.4 Smoking and Alcohol Use
5.0 MULTIVARIATE PERSPECTIVE .............. 466
.....467
6.0 IMPLICATIONS AND RECOMMENDATIONS .......
7.0 REFERENCES..................469
445
1.0 APPROACH
In general, ischemic heart disease (IHD) risk factor data sources for
the Native American population are in no sense comparable to those for the
other minority groups, due to the relatively greater emphasis on health
problems other than IHD in this population and to the general paucity of
data specific to the Native American subset of the U.S. non-white
population. The size of the Native American population is small compared
to the larger minority of black Americans. Numbers in research reports and
vital statistics categories relevant to cardiovascular risk are extremely
small due to the young age of the Native American population and to their
excess mortality from noncardiovascular causes (1,2). Rates and
percentages in this report should be interpreted with the small numbers in
mind.
The anthropological, socio-political, and cultural history of the
Native American population is unique and varies greatly among Indian
tribes. These factors have had a large influence on the amount and nature
of health and disease data available for this population. Related to this,
there is considerable redundancy in the authorship of cardiovascular
studies in Native American populations, a greater than desired reliance on
inherently biased data sources and anecdotal material, and relatively
little written about Native American health by Native American people.
Socioeconomic status of Native Americans is generally at the low end of
the continuum. Thus, it is difficult to separate genetic and cultural
factors from socioeconomic factors. Varying degrees of racial admixture
and inconsistencies in racial classification of Native Americans of mixed
ancestry (i.e., as Indian vs. white) also complicate the picture of Native
American-white differences in disease patterns.
A summary of selected background information on Native American
population and mortality characteristics has been included, to indicate our
perspective on IHD risk in this population group (section 2). Patterns of
IHD and IHD risk in specific Indian populations are then discussed
(sections 3 to 6).
A large portion of the literature pertinent to cardiovascular risk
factors relates to Indians in the Southwest and, in particular, to Pima
Indians, who are reported to have the "highest recorded prevalence of
diabetes in the world" (50% prevalence in Pima over age 35; almost
exclusively type II) (3, page 199). Pima or the closely-related Papago
Indians are a focus or sub-focus of a third of the papers identified as
relevant to this report 3,7,12-25). There are also several references
which provide information on Navajo or Apache Indians
(3 7,11,22-27,29-31,38). Papers on southwestern Indians include the above
groups as well as Hopi Indians and other tribes in the Arizona and New
Mexico area (3,7,22-24,29,30)
Papers from Minnesota (33,51) provide data primarily on Ojibwa
(Chippewa) Indians; small percentages of Sioux and Winnebago Indians are
also represented in the Minnesota Native American population. Other
446
relevant studies provide data on aspects of CHD risk among Crow and
Northern Cheyenne Indians in southeast Montana (34), Arapaho and Shoshone
Indians in Wyoming (35), Seminole Indians in Oklahoma and Florida (36),
Alaska Natives (37,50); Ojibwa Indians in Canada (38), Seneca Indians in
upstate New York (39,40), American Indian university students in Georgia
(41), and the Tarahumara Indians in Mexico (32,42).
The literature identified gives a less than complete picture of IHD risk
for the sub-groups listed above and leaves a substantial portion of the
Indian population uncovered (4,5). Published tables for the U.S. ^
population usually present Native American data in an aggregate "non-white
category along with data for black- and/or Hispanic- and/or Asian-Americans
(9,10). One tabulation of blood pressure levels of nonreservation Indians
was identified in an NCHS report from the National Health and Nutrition
Examination Survey, 1971-74 (43). Mortality data for some years were
obtained from Indian Health Service reports (2,6,8,44) for Indians and
Alaska Natives in reservation states.
2.0 OVERALL PERSPECTIVE ON PREDISPOSITION TO ISCHEMIC HEART
DISEASE IN NATIVE AMERICANS
2.1 Background Comments on the Native American Population
The census designation "Native American" includes American Indians,
Eskimos, and Aleuts. Native Americans were 0.6% of the United States
population in the 1980 census--l,418,000 of the 226,505 million Americans
counted (9, Table 1). In the 1970 census, Native Americans were 0.4% of the
population--793,000 of 203,212,000 Americans counted (10, Table 1). The
Native American population is disproportionately poor, has a lower
life expectancy and is younger than the U.S. population as a whole (median
age 18.4 vs. U.S. population median of 28.1 years in the 1970 census (3,8)
The Navajo, the largest of several hundred American Indian tribes
residing in the U.S., numbered approximately 150,000 in the mid-70's (3).
States with the largest Native American populations are Arizona, Oklahoma,
California, New Mexico (3), and North Carolina (45) but the federally
recognized Indian tribes are spread throughout more than 25 states (3,5).
Ninety percent of Indians lived on reservations prior to 1940. In
1970 and 1977, 40% and 51% of Indians lived off of reservations, primarily
in urban settings (45). Sievers and Fisher (3) point out that southwestern
Indians have remained more isolated and less racially mixed than Indians in
other regions. In recent decades however, social and environment changes
have been occurring, leading to reduced ethnicity. For example, whereas
60% or more of White Mountain Apaches lived in traditional tribal dwellings
in 1959, these "wickiups" have become rare. At the time the Sievers and
Fisher review was written, (1981 publication date) 6% of southwestern
Indians over age 15 vs. 20% of the population under age 15 were reported to
have some non-Indian admixture.
447
2.2 Heart Disease in the Mortality Profile of the Native American
Population
The mortality profile of Native Americans differs from that of the
overall U.S. population (Tables 1 and 2) and to some extent from that of
other racial minorities (Table 2). Age-adjusted total mortality
comparisons are not given in the 1979 Indian Health Service tables
available at this writing. Age-adjusted total mortality among Native
Americans was 1.3 times that for U.S., all races in 1975 (see Table 3 in
this report).
There were 19,474 deaths among Indians and Alaska Natives in 1979
(1,913,814 deaths among all races, U.S.). Table 1 indicates that, although
the majority of deaths are classified as due to heart disease in both the
general population and among Native Americans, the proportionate mortality
from heart disease in Native Americans is half that of the general
population (Note however, that proportionate mortality from heart disease
varies significantly by region. See Table 5 and accompanying text.) The
proportion of accidental deaths among Native Americans is nearly as high as
that due to heart disease and is more than three times as high as the
proportion of accidental deaths in the general population. The proportion
of Native American deaths associated with chronic liver disease or
cirrhosis is 3.8 times higher than in the general population.
Table 1. Leading causes of death among the U.S., all races 1979
and comparable data for Indians and Alaska Natives,
1978-1980 [taken from Table 4.1 in reference 2].
Percent Distribution
Causes of Death
Diseases of the heart
Malignant neoplasms
Cerebrovascular diseases
Accidents
COPD*
Pneumonia and influenza
Diabetes mellitus
Chronic liver disease & cirrhosis
Atherosclerosis
Suicide
All other
ALL CAUSES
* chronic obstructive pulmonary disease and associated conditions
** cirrhosis of the liver, 1978
# among Indians and Alaska Natives, "all other" includes 3.3% homicide, and
2.7 percent deaths attributed to "certain causes of mortality in early
infancy (1978)"
U.S. , Ind ians and
All Races Alas ka Natives
38.3 20.8
21.1 10.1
8.9 4.8
5.5 19.5
2.6 0.9
2.4 3.8
1.7 2.9
s** 1.6 6.0
1.5 0.7
1.4 2.6
15.1 28. 0#
100.0 100.0
448
The distinction between proportionate mortality from heart disease,
crude, and age-adjusted heart disease rates among Native Americans vs. U.S.
all races is critical due to the younger age and excess noncardiovascular
mortality in the Native American population. Disparities in age-adjusted
rates between Native Americans and whites are most pertinent for this
report. Unfortunately, of the data suitable for comparison purposes,
proportionate mortality data were more readily available than age-adjusted
rates [the Indian Health Service may have more specific recent tabulations
than those provided to date (2)].
As shown in Table 2, Native American rates of infant mortality and
mortality due to tuberculosis, gastrointestinal disease, accidents, and
alcoholism have decreased markedly since 1955. However, in 1980 Native
American mortality from tuberculosis, accidents, and alcoholism was still
disproportionately high when compared to the general population. Native
American mortality rates were more similar to mortality rates of other
non-whites in the population than to rates for whites. Native Americans
were at somewhat higher risk than other non-whites in 1979/1980 for all
mortality classes shown in Table 2 except infant mortality.
Table 2. Comparison of mortality rates for Indians and Alaska
Natives with those of the general population and other U.S. non
white populations in two time periods for selected causes @
CAUSE OF DEATH
CLASSIFICATION
Infant Mortality
Tuberculosis
Gastrointestinal
Disease
Accidents
Alcoholism
RATE
1955 62.7*
1979 14.6*
1955 57. 9//
1980 3.6//
1955 15.4**
1980 4. 0**
1955 184.0////
1980 107.3////
1969 56.6!
1980 41.3!
RATIO TO RATIO TO U.S.
S. ALL RACES OTHER NON-WHITES
2.4 1.5
1.1 0.7
6.9 2.4
6.0 1.5
4.3 2.3
1.3 1.3
3.3 2.6
2.5 2.1
7.4 not given
5.5
@ data for Indians and Alaska Natives are based on reservation states.
* deaths per 1000 live births; from reference 2, Table 3.3
// age-adjusted deaths per 100,000 population; from reference 2, Table 4.11
** age-adjusted deaths per 100,000 population; from reference 2, Table 4.13
//// age-adjusted deaths per 100,000 population; from reference 2, Table 4.7
! age-adjusted deaths per 100,000 population; from reference 2, Table 4.10
449
Data on heart disease mortality in the available Indian Health Service
tabulations covering the time period up to 1979 and 1980 (2) are limited in
detail. More detail is available in published IHS reports for the period
up to 1975 (6,8). Using these reports, Tables 3, 4 and 5 have been
constructed to show time trends in heart disease mortality among Native
Americans and their relationship to certain trends in other classes of
death, variations in mortality patterns by region, and age-specific
patterns vs. those of the total U.S. population.
Table 3. Percent change in age-adjusted mortality (rate per
100,000 population) between 1970 and 1975 for Indians
and Alaska Natives and the U.S., all races (from ref. 6)
Cause of Death Indians and U.S., ratio*
Alaska Natives^ All Races
All Causes - 7.3 -10.6 1.3
Disease of the Heart -12.7 -13.1 0.7
Cerebrovascular -20.9 -17.8 0.8
Arteriosclerosis -14.4 -21.4 1.5
Hypertension - 5.9 -34.5 0.8
Diabetes Mellitus -12.2 -17.7 2.1
Homicide + 19.4 +15.4 2.5
Suicide +45.3 + 6.8 2.1
Cirrhosis of the liver + 7.9 - 6.1 4.4
@ based on reservation states
* 1975 ratio of rate for Indians and Alaska Natives to rate
for U.S., all races.
Table 3 indicates a decrease in heart, cerebrovascular, and
arteriosclerosis mortality among Native Americans to an extent roughly
comparable to that for the general population during the period between
1970-75 but a substantially lesser decrease in deaths due to hypertension.
The disproportionate increase in deaths attributed to suicide and liver
cirrhosis among Native Americans influences interpretation of the decreases
in the other categories. Similar cardiovascular mortality may not
represent similar incidence of cardiovascular disease, (e.g.,if heart
disease mortality is pre-empted by competing causes of death).
450
Table 4. Age-specific death rates for cardiovascular diseases
and diabetes for Indians and Alaska Natives (1973-75
average) and U.S., all races (1974) in 25 reservation
states (deaths per 100,000 population) (from ref. 6)
Cause of Death 25-34 35-44 Age Group 45-54 55-64 65-74
Heart Ind US 19.6 9.4 65.0 55.7 192.4 215.5 451.0 590.8 1426.6 2758.4
Hyper-tension Ind US 0.3 1.3 0.9 2.8 2.0 9.2 4.3 9.8 26.3
Cerebro-vascular Ind US 4.8 3.6 17.2 13.3 47.4 35.3 123.8 99.6 492.7 869.0
Arterio-sclerosis Ind US 1.0 0 1.8 0.2 7.8 1.0 23.7 5.9 83.3 153.3
Diabetes Mellitus Ind US 3.8 1.9 15.5 4.3 35.1 11.4 86.4 31.7 171.6 132.6
Forty-three percent of the heart disease deaths among Native Americans
are due to myocardial infarction; 32% are due to chronic ischemic heart
disease (6). At all ages below age 35 (ages 1-24 not shown), the heart
disease death rate for Native Americans was approximately twice as high as
for U.S., all races. Above the age of 44, heart disease mortality
increases less steeply with age in Native Americans than in the general
population, and Native American rates are lower than U.S. rates for all age
groups over 45. This cross-over in heart disease mortality is hidden in
the overall 0.7 ratio of Native American to U.S., all races rates (Table 3),
since the numbers of deaths at the younger ages are quite small. A later
cross-over in arteriosclerosis and cerebrovascular disease death rates is
observed. Native American rates are similar or moderately higher than U.S.
rates at younger ages (under the age of 65), and substantially lower at
older ages (over age 65 years). It should be noted that heart disease
other than ischemic disease (i.e., congenital heart disease) makes up a
larger proportion of the heart disease under age 35 compared to the
proportion in older age-groups. Diabetes deaths are higher among Native
Americans at all ages over 25.
The differences in the proportion of mortality due to heart disease
among Native Americans in different regions of the country are shown in
Table 5. Since the rates for Indian Health Service service areas are not
age-adjusted, the percent of the population under one year and over 30
years of age is shown for reference in making comparisons. In 1977, 88% of
Indians lived in the states where the IHS had responsibility for providing
451
health services; 67.5% of the Indians living in these states lived within
the service unit boundaries (8). Among the Indians represented in the IHS
data for 1975-77, heart disease mortality is lowest in the Southwest.
Table 5. All cause and heart disease mortality and proportionate
mortality from heart disease in Indian Health Service
service areas, 1975-1977 (constructed from reference 8)
Service Area % < lyr % > 30 All Causes Heart % heart
old years old /100,000 /100,000 i
All areas 2.57 31.0 751.2 127.6 17.0
Tuscon 2.68 30.5 837.7 82.8 9.9
Aberdeen* 2.95 27.9 1,135.6 214.6 18. 9@
Bemidji** 2.31 30.0 918.2 252.7 27.5
Albuquerque// 2.67 30.3 648.1 56.3 8.7
Alaska 2.39 29.1 696.5 84.4 12.1
Billings//// 2.77 28.6 869.5 178.6 20.5
Oklahoma City 1.98 40.3 683.6 190.4 27.9
USET! 2.68 30.6 662.7 111.3 16.8
Phoenix!! 2.61 29.2 751.1 90.1 12.0
Portland+ 2.57 33.1 889.2 174.6 19.6
Navajo++ 3.07 25.1 613.8 49.8 8.1
* North and South Dakota, Nebraska, Iowa
** Minnesota, Wisconsin, Michigan
// Colorado, New Mexico
//// Montana, Wyoming
! North Carolina, Florida, Louisiana, Mississippi
!! Arizona,Nevada, Utah, California, Oregon, Idaho
+ Washington, Oregon, Idaho
++ Utah, Arizona, New Mexico
@ rate given in Table 18 (ref 8) is in error, but correct data
are shown elsewhere in Table 18 and in Table 20.
When the tabulations of mortality data are taken together, heart
disease appears to be a significant contributor to mortality in Native
Americans outside of the Southwest, except Alaska, but proportionately less
so than for the general population—apparently related to the mortality
contribution of noncardiovascular causes. The impression gained from
overall rates of heart disease mortality for the total Native American
population could be misleading if these two caveats are overlooked: 1) In
1975-77, Native American rates were lower than those of whites in older but
not younger age-groups; and 2) the proportion of deaths due to heart
disease was still relatively low among a large segment of the Indian
population.
452
3.0 ISCHEMIC HEART DISEASE IN SPECIFIC NATIVE AMERICAN POPULATIONS
3.1 Southwestern Indians
Review of older papers on coronary heart disease (CHD) in southwestern
Indians aids examination of the baseline from which increases or decreases
are judged. Although the data bases used have limitations (e.g.,
dependence on hospital cases, autopsy records), the methodologies and their
limitations are generally well-documented and data-based inferences
separated from impressions and opinions. Moreover, in many instances, the
magnitude of differences between Indian and white comparison populations is
often much larger than the probable error.
The clinical impression in the 1960's was of an absence of CHD among
the Navajo and Apache, based on the failure to observe CHD in Indian Health
Service hospitals for periods of several years (26,28,31). This impression
was supported by a prospective study conducted by Cornell Medical School
investigators in a rural, isolated, traditional Navajo community (Many
Farms) between 1956 and 1962 (31). With a very high probability that all
symptomatic CHD in Many Farms was identified during the study period, the
six year incidence was four in 508 persons. In a comparison with data from
Framingham (taking age and sex into account), the CHD incidence was
significantly less than expected in the Navajo men but not the women.
Prevalence of hypertension, ECG abnormalities and cigarette smoking were
also very low in this Navajo population.
ECG measurements on 70 male and 77 female White Mountain Apache Indians
ages 30 and over in 1957-58 found no records characteristic of coronary
disease (26). However, a 1957-1966 study of myocardial infarction in a
large southwestern Indian Health Service population suggests that CHD,
although of low occurrence, was definitely present to some extent in all
tribes (23). Rates were approximately one-fourth of Framingham-based
expected rates. One hundred and thirty-eight myocardial infarctions (Mis)
were identified in an estimated population of 15,905 Indian adults (over
age 30) at risk vs. 507 expected; only 56 of the 138 Mis were recent. The
Indian rate was 86 vs. 347.8 (per 100,000) estimated for Framingham
(estimate based on age and sex, not risk factors). The sex ratio for MI
was lower in the Indian populations (2.3:1 vs. 4.6:1 in Framingham),
possibly related to the high prevalence of diabetes among the Indian women.
MI rates were higher in the desert tribes (Pima, Papago, Colorado River)
than in the mountain or canyon tribes (Apache, Navajo, and others).
Cigarette smoking patterns paralleled the MI patterns. In reporting these
data Sievers emphasizes that no tribal group is immune from CHD, as had
been implied in some earlier reports.
More recent studies among the southwestern Indians suggest that CHD
is increasingly less rare, particularly when diabetes is present (3).
However, a 1976 report points out that CHD incidence in both diabetic and
nondiabetic Pima Indians was lower than among white comparison populations
(ECG data (Q wave changes) on 85% of half to full-blooded Pimas on the Gila
River Reservation (46)). Sievers (47), as noted below, describes
increasing rates of ischemic heart disease in Indians. In contrast, Kunitz
453
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Table 6. Comparison of rates of acute myocardial infarction
during 1957-66 vs. 1975-78 in three sub-groups of southwestern
Indians (taken from 3,47)
rate per 100,000 per year
1957-66 1975-78 % increase
Piman 50 74 48%
(Pima and Papago)
Athapascan 18 53 194%
(Navajo and Apache)
Other 33 97 194%
Southwestern*
In the text accompanying these data, the authors note that
35% percent of the infarctions in this category were among
Hopi Indians, who are only 19% of this group
3.2 Indians Outside the Southwest
Mayberry and Lindeman examined cardiovascular disease death rates
among Seminole Indians integrated into the Seminole County, Oklahoma
population vs. those of whites in the same county (36). The authors note
that in addition to other limitations of death certificate data,
mixed-heritage Indians may have been recorded as either Indian or white on
death certificates. The percent of mortality attributed to coronary artery
disease (using data for persons age 25 and over) was less among the
Seminoles than among whites (15.5 vs. 31.0% for men; 11.1 vs. 20.7% for
women) (36, table III). Coronary artery disease (CAD) death rates
calculated from Table III are as follows: Seminole males 15.5/1000; white
males 37.5/1000; Seminole women 8.4/1000; white women 14.1/1000.
Tabulations of death rates for male Indians aged 25 and over in other
Oklahoma counties showed proportionate CAD mortality ranging from 12 to 33%
(36, table IV), varying with the overall mortality pattern for the Seminole
men in the different counties. These data demonstrate higher CAD mortality
among Seminoles than among southwestern Indians at approximately the same
time period.
Pinkerton and Badke (34) retrospectively determined the incidence of
myocardial infarction (MI) among Crow and Cheyenne Indians admitted to Crow
Hospital (Crow Agency, Montana) during the 14-year period from 1956 to
1970. The study methodology was designed for comparability with the
14-year Framingham data, to the extent possible. Of the CHD categories
ascertained, the authors were most confident of the completeness of the MI
data (compared to angina pectoris, for example, which may have been treated
primarily on an outpatient basis). Therefore, the authors base their
455
conclusions on the MI data. In calculating denominators for MI rates,
off-reservation Indians who lived too far away to be in the hospital
service population were excluded. Otherwise, maximum estimates of
populations of Crow and Cheyenne men and women at risk were used so that
the rates calculated would be conservative (i.e., if in error the rates
would underestimate rather than overestimate the incidence of MI. The
racial criterion in the tribal census was one-quarter or more Crow (this
may also have applied to the Cheyenne).
Equivalent or higher MI rates for Crow men and both Crow and Cheyenne
women vs. rates for Framingham age-sex counterparts (10-year age-groups
between 30 and 59) were reported. Indian women had MI rates at least twice
as high as Framingham wo-nen at all ages, and had rates six times higher in
the 45-54 year age-group.
Rates for Cheyenne men were substantially lower than those of the Crow
and Framingham men. When maximum Framingham rates were calculated assuming
that all persons excluded at the first exam due to known CHD had had
infarctions during the subsequent 14 years, Framingham MI rates for men
were significantly higher than for both Crow and Cheyenne men. Rates among
women were not significantly different using the upper limit Framingham
rates. As noted above for the Seminole Indians, rates for Crow and
Cheyenne Indians were higher than those reported for southwestern Indians.
Pinkerton and Badke point out that their findings were contrary to the
clinical impression of the Crow hospital staff that infarction was rare
among Crow and Cheyenne Indians.
Gillum et al. (33) report that cardiovascular disease was the leading
cause of death among Minnesota Indians (primarily Chippewa) between 1968
and 1973 with rates comparable to those for Minnesota whites (age-adjusted
rates for heart disease and stroke combined: 448.7/100,000 for Indians
455.2/100,000 for all races; proportionate mortality 26% among Indians).
These authors draw attention to the similarity in heart disease and stroke
mortality rates between Indians and whites vs. the substantially higher
age-adjusted total mortality for the Indians (due to excesses in other
categories. Thus, this is an example of similar cause-specific rates but
lower proportionate mortality. Fifty-six percent of Minnesota Indians
lived in urban areas in 1970. Rates in reservation and urban areas were
similar.
3.3 Summary
These studies of CHD in specific populations, although neither
comprehensive nor up-to-date, confirm the general impression that CHD is
lower among Indians in the Southwest than among Indians elsewhere and that
patterns for Indians elsewhere are similar to those of whites in the same
areas. Also, the higher heart disease death rates among Indians in IHS
health service areas in 1973-75 vs. the U.S. general population through age
45 may suggest higher risk in younger cohorts (Table 4). However, the
proportions of ischemic vs. other forms of heart disease at the younger
ages are not clear.
456
Due to marked differences in the risk of death from other causes
among Native Americans and whites, proportionate mortality figures, which
are relative, tend to minimize the potential importance of heart disease
risk. The overall impression of lower heart disease mortality among Native
Americans (1975 ratio to U.S., all races = 0.7) may be influenced downward
by the lower rates in the Southwest where the majority of Indians live.
The CHD picture for Indians outside of the Southwest may be less favorable.
There are many as yet unresolved issues related to CHD in Indians.
Those encountered most often are issues of measurement (e.g., appropriate
interpretation of ECG findings (46)); risk factor-disease associations
(e.g., obesity and diabetes on CHD (13,20); consequences of hypertension
(45)); and heredity-environment interactions (20,25).
4.0 ISCHEMIC HEART DISEASE RISK FACTORS AMONG NATIVE AMERICANS
4.1 General Comments
Lifestyle-related risk factors appear to have increased substantially
in Native American communities in the last 50 years with increasing
urbanization and acculturation (3,33,45). However, in the absence of
systematic risk factor surveys among most Indian populations,
quantification of these risk factor changes is difficult. Some apparent
increases are possibly due to increased screening efforts (45).
In addition to personal and environmental factors which affect IHD risk
factor trends in the general population, risk factor changes of Native
Americans vary with tribe (both hereditary and cultural factors), extent of
admixture for Indians who are not full-heritage, extent and duration of
acculturation to white society, and regional factors (e.g., origins in the
Southwest vs. in Seattle, Minnesota, or upstate New York (3,45)). The
picture is further complicated by the differential rates of change of the
admixture and acculturation variables in different Indian communities and
by the different socioeconomic and quality of health care patterns for on
and off-reservation Indians (45). The variation is both qualitative and
quantitative; summary statements about IHD risk in Native Americans can
only be made within groups with similar origins and experiences.
4.2 Hypertension
Mortality attributed to hypertension and stroke was lower than that
for heart disease in the IHS health service areas in 1973-75 (Table 4).
However, between ages 25 and 64 years, rates among Indians were similar to or
higher than those for the general population. Thus, hypertension is not
inconsequential in the Native American population and it may increase in
importance as other causes of mortality decline.
At the 1977 conference on hypertension control in Native American
communities, Maurice Sievers, M.D., Director of Research for the Phoenix
Indian Health Service Area presented an historical overview (and critique)
of reports of hypertension among American Indians and Alaskan Natives (45,
457
pp.77-82). Dr. Sievers notes the inadequacy of the "numerous bits of
information" on this subject. Several speakers at this 1977 conference
noted that the extent of the problem of hypertension among Native Americans
was not at all well-documented. Dr. Sievers points out that the data which
are available are often difficult to identify; they are buried within
studies of diabetes or other aspects of Indian disease. He also points out
that there are major tribal differences in cardiovascular disease,
including a higher prevalence of congenital cardiovascular abnormalities in
the Athapascans (Navajo and Apache) than in other tribes.
Highlights of Dr. Sievers' summary follow--grouped by tribe and region
to the extent possible. The talk by Sievers (45) is reported without
citations. Reference 48 is a documented version of this text. Where the
study described was recognized as one included in the bibliography for this
report, a notation to this effect has been made in parentheses and the
impression conveyed in Sievers' report verified by examination of the
primary data.
Regarding southwestern Indians:
- a rate of hypertension among Navajo Indians less than one-fourth
the white rate was reported in 1948-52;
- 6.2% of the men and 3.7% of the women ages 30 and over in the
Cornell-Navajo 1956-62 study at Many Farms Arizona (reference 31)
were hypertensive;
- a 1970 report indicated that migration to an urban environment was
associated with higher blood pressures among Navajo men (49);
- 1.4% of admissions to the Phoenix Indian Medical Center in 1953 had
primary hypertension (based on one, unstandardized casual blood
pressure reading);
- hypertension-related morbidity among Phoenix-area outpatients in
1952 was 7 per 1,000 for Papagos, 4 per 1,000 for Pimas, and 2 per
1,000 for Apaches vs. 25 per 1,000 for whites. Two-fifths of the MI
cases identified in a 10-year study (1957-66) (23) were hypertensive;
- an analysis of computerized clinic records of more than 4,000 Papago
Indians for the period 1969-1972 yielded a hypertension prevalence rate of
20% (Sievers notes, however, that the methodology used has rather serious
limitations); the prevalence of hypertension and complications was greater
in hypertensives who also had diabetes;
- blood pressures of Pima Indians studied by Ingelfinger
(46) were lower compared to whites but were higher in diabetic
vs. nondiabetic Pimas;
458
- Leo observed a 34% prevalence of diastolic blood pressure greater than 95
mmHg among White Mountain Apache men and a 29% prevalence among the women
(28) in a 1958 study of 110 men and 110 women volunteers;
- Clifford et al. also noted a high prevalence of hypertension among 327
White Mountain Apaches studied in 1963 (26% in men, 23% in women) (26);
examination of the Clifford et al. data indicates particularly high
hypertension prevalence (BP >160/95) in Apache men ages 30-49 (43-47% vs.
rates of 12-23% among older men). Highest rates among Apache women were in
the 50-59 year old group (Figure 1 in reference 26)).
Regarding Indians outside of the Southwest:
- a systematic study of blood pressure found a very low rate of
hypertension (1 in 200 Indians over age 20) in a northwestern coastal
village;
- A blood pressure survey of Seminole Indians in Seminole County, Oklahoma,
Seminoles on a reservation in Florida, and Seminole County whites indicated
similar blood pressure levels among the three groups (36);
- no differences in blood pressure levels were observed among Sioux and
white admissions to a South Dakota hospital (50 consecutive admissions of
each race) in spite of the fact that 50% of the Sioux vs. 10% of the whites
were diabetic (and most of the Indians were overweight).
Regarding Eskimos and Alaska Natives:
- 2.6% of 842 Eskimo men surveyed by Scott et al. (50) in 1958 had a mean
blood pressure of 125; blood pressures were similar to those in a large
group of U.S. men.
Sievers' account of hypertension studies gives an adequate impression
of the patterns of hypertension among Native Americans to the limited
degree that these had been documented up to the mid 1970's. Hypertension
has previously been relatively infrequent in southwestern Indians-- White
Mountain Apaches excepted. No striking excess prevalence of hypertension
in Indians outside of the Southwest (vs. whites in the same areas) has
been reported.
Sievers notes that the Indian Health Service age-adjusted death
rate for hypertension for Native Americans in 1971 was lower than the rate
for white Americans by only 10% (45). NCHS estimates of mean blood
pressure levels for American Indians (off-reservation only) in 1971-74 do
not show a consistent pattern of differences from blood pressure levels of
whites (see Tables 7 and 8). However, given earlier statements about the
intertribal differences and the substantial proportion (60%) of Indians
still on reservations in 1970 (45) the value of the NHANES data may be
limited to showing that there were no large differences in off-reservation
Native American vs. white blood pressure distributions in 1971-74.
459
Table 7. Systolic and diastolic blood pressure levels of American
Indian men, with comparison values for white men,
U.S., 1971-1974. (from reference 43)
Systolic
Indian* White
Diastolic
Indian* White
Age (mill
Group
18-24 121.2 123.7
25-34 128.0 125.2
35-44 127.7 127.0
45-54 130.9 134.7
55-64 139.4 139.6
65-74 139.9 146.0
(millimeters of Hg)
77.7 76.4
76.5 80.8
84.9 84.2
89.8 87.5
85.4 86.4
84.9 84.9
examinees who identified themselves as American Indians and
were not living on a reservation or in an institution at the
time of the survey
Table 8. Systolic and diastolic blood pressure levels of American
Indian women, with comparison values for white women,
U.S., 1971-1974. (from reference 43)
Systol ic
Indian* White
Women Women
Age (mill
Group
18-24 114.9 115.1
25-34 119.0 116.2
35-44 117.4 122.6
45-54 138.9 131.1
55-64 144.3 143.0
65-74 145.0 151.6
Diastolic
Indian* White
Women Women
73.8 71.3
75.0 74.6
77.6 79.3
80.1 82.6
88.6 86.2
81.5 85.4
examinees who identified themselves as American Indians and
were not living on a reservation or in an institution at the
time of the survey
460
Only three recent reports of hypertension surveys in Indian
populations were identified--two from Minnesota (33,51) and one among
Navajo (27).
The Navajo survey reported blood pressure data from 1977 clinic-based
screenings of Navajo people ages 20 years and older at Fort Defiance,
Arizona and Crownpoint, New Mexico—two demographically similar Navajo
communities (n=640) (27). The populations were relatively diverse but were
not randomly selected. Blood pressure levels of the Navajo women showed a
linear increase with age. There was no age trend in either systolic or
diastolic blood pressure among the Navajo men, but their blood pressure
levels and hypertension prevalence were greater than among Navajo women.
The prevalence of DBP >=90 was higher among the Navajo men ages 20 to 59
(24 to 28%) than among the small number of men aged 60 years and older
(16%). The pattern was similar among the women. Prevalence of DBP >=95
was 9,16,8,and 11% in the 10-year age-groups of Navajo men between 20 and
59 years of age; 0,8,3, and 10% among the women. One hundred and ten of
the Navajo screened had DBP >=90, of whom 57 reported a prior knowledge of
having high blood pressure. Eighty and 72 percent of the Navajo men and
women on medication had DBP less than 95 mmHg. The authors note that the
estimates of hypertension are based on one casual reading and are thus
probably overestimates.
In an analysis of determinants of blood pressure levels in these Navajo
subjects, male sex, obesity and alcohol were found to be important
variables (alcohol use was measured only as yes or no). Overweight was a
statistically significant hypertension risk factor for both men and women.
Relative risks were estimated as 3.0, 3.6, and 9.0 for overweight females,
normal weight males, and overweight males if normal weight females were
assigned a value of 1.0. The highest reported use of alcohol was among the
younger men (43% of men under age 40 vs. 22% of those over 40). The
prevalence of DBP >=90 was significantly higher among the men who used
alcohol. Very few Navajo smoke and smoking was not a determinant of
hypertension. An index of acculturation was not significantly related to
blood pressure levels (this index included ratings on alcohol use and
smoking).
In their discussion, DeStefano et al. (27) compare the Navajo blood
pressure levels in 1977 with levels in the 1956-62 Many Farms Study (31)
for an impression of changes in blood pressure over time. Blood pressures
of Navajo females were essentially the same at both points in time. Blood
pressures of the younger Navajo men measured in 1977 were higher than those
of the men measured in 1956-62 at Many Farms. The authors suggest that a
trend towards increasing hypertension may be present in the younger cohort
of men. The 1977 data were also compared with blood pressure levels of
black and white men in a 1973-75 study of one million Americans. Again,
the trend towards hypertension in the young Navajo men was apparent.
Systolic and diastolic blood pressure levels and the prevalence of DBP >=90
were equal to or greater than levels of young black and white males in the
mid 70's. Although this trend in the younger cohort of Navajo men is
presumably associated with some aspect of acculturation, the nature of such
an acculturation factor was not evident from the measures used in this
461
study. Alcohol use may be an important factor. Blood pressures of the
Navajo women are lower than those of women in the comparison populations.
Gillum et al. reported on a blood pressure survey of essentially all
first, second, and third grade children in the Minneapolis Public Schools
(who were not absent from school on the day concerned) during the spring of
1978 (51). The population of 10,640 6- to 9-year old children surveyed
included 307 Native American children. Analyses of the blood pressure data
indicated higher systolic (by 1-3 mmHg) and lower 4th and 5th phase
diastolic (by 2-5 mmHg) blood pressures (and higher pulse pressures) among
the Native American vs. the white children. The systolic blood pressure
differences were statistically explained by higher body mass index of the
Native American children. No good explanation for the lower diastolic
blood pressure among Native American children could be uncovered. Several
methodological explanations were tested and ruled out (51).
Gillum et al. have also reported on a blood pressure survey among
adult Indians in Minneapolis in 1980-81. Two populations of Indians were
reached—one in an Indian housing project (n=173) and the other through
community screenings (n=295) during American Indian Week (33). Comparison
data for whites were taken from the Minnesota Heart Survey (probability
sample) (clinic measurements; n=1950).
Self-reported prevalence of hypertension was somewhat higher among
Indians than whites (33% vs. 27%), but unlike whites who reported a
positive history, the Indians with a positive history were more likely than
whites with such a history to have blood presssures in the normal range.
This discrepancy was not fully accounted for by the proportions of Indians
and whites on medications. The prevalence of hypertension (defined as
diastolic blood pressure >=90 mm Hg or diastolic blood pressure <90 but
taking blood pressure medication) was 13-17% among the Indians and 14% in
whites. Levels of control among Indians and whites on medication were
similar. A smaller proportion of Indians than whites with a history of
high blood pressure were on medication; a larger proportion were on special
diets (33).
Ten percent of Indians reporting a history of high blood pressure also
reported a history of diabetes. Diabetes, smoking, and obesity were more
prevalent among Indians than whites. Systolic and diastolic blood pressure
were significantly correlated with the body mass index (coefficients were
0.33 and 0.36 (33) in the Indians). The overall impression was that blood
pressure levels of Indians and whites were similar, but that associated
risks were higher in Indians due to higher prevalences of obesity, smoking
and diabetes.
These later studies add to the evidence that
obesity- and diabetes-related hypertension is an important health problem
in Indians and suggest the need for more systematic and careful studies of
blood presssure levels and trends in different Indian communities.
Attention to trends in younger cohorts seems particularly important
(26,27). The workshop summaries in the 1977 conference report (45) do not
contain data on hypertension prevalence (except in references to various
462
studies). However, this report is a useful point of reference for issues
of Native American health services in general and hypertension control
issues in particular. Many of the relevant research and data needs have
already been identified and attention to some of these needs may already be
underway. However, the picture obtained from literature identified in
conjunction with the present report does not appear to have changed much
from that reported at the 1977 conference.
4.3 Cholesterol
Comparisons of cholesterol levels of Native Americans vs. whites
indicate lower or similar levels in Native Americans. In a 1968 report of
cholesterol levels of 746 southwestern Indians compared with 70
nonsouthwestern Indians and 163 whites, Sievers observed lower levels in
both groups of Indians compared to whites, no increase in cholesterol
levels with age, and no sex differences (peak levels between ages 30-44)
(29). Cholesterol determinations were for Phoenix Public Health Service
hospital patients over the age 15 during the period July, 1963 through
December, 1965. The lowest levels were observed among Pima and Papago
Indians. Pima and Papago Indians had lower cholesterol levels than Apache
and Navajo, in spite of greater obesity among the Pimans. In a separate
report, Sievers also comments on the paradox of lower cholesterol levels
among the Pimans vs. Navajo and Apache in light of the higher frequency of
myocardial infarction among Pimas (23).
Cholesterol levels for nonsouthwestern Indians were slightly higher
than for southwestern Indians but still lower than those of whites (29).
For example, among 45-59 year old men in the study, mean cholesterol level
was 193.7 for southwestern Indians; 214.7 for nonsouthwestern Indians;
302.8 for whites (levels for whites were duplicated in outside laboratories
because they seemed unusually high; however, the levels of the Indians
would have been significantly lower even if the levels for whites had been
substantially overestimated).
Hamman et al., in a 1975 report (52) noted similar cholesterol levels
in 148 pre-menopausal (ages 35-54) and 75 age-matched post-menopausal Pima
women. Similar pre- and post-menopausal cholesterol levels in women were
also observed in 65 women followed longitudinally. The findings were not
affected by the presence of diabetes. Cholesterol levels of males were
also measured in the cross-sectional survey. The levels of Pima males and
females were 20-30% lower than those of Caucasians and did not rise with
age. A 1976 report of serum cholesterol levels in Pima children and adults
indicates that levels of Pima and white children are similar at birth but
that levels among the Pima remain low and do not rise with age in adulthood
(17).
Ingelfinger et al. (46) reported mean cholesterol levels of 189 and 188
mg/dl for nondiabetic Pima men and women over age 40 and slightly higher,
but still low, levels for diabetic Pimas (197 and 198 mg/dl for men and
women), with no age-related changes in either group. The most recent
report of cholesterol levels in Pimas (from the same laboratories) presents
data collected between 1979 and 1982 (14). Although levels in Pimas are
463
lower than those of the Lipid Research Clinic whites, the finding of an
increase in plasma cholesterol with age in Pima women is a departure from
the previous findings that no such rise occurred. It is not clear whether
this is due to sample factors or to a "westernization" of cholesterol
levels among the Pima women. Levels in men peaked in the 45-54 year age
group and then tapered off. HDL cholesterol levels were similar in Pima
males and women. The lack of a gender difference was not explained by
obesity although obesity and HDL levels were negatively correlated.
The fat content of the traditional Pima diet is primarily animal fat
(from beef and pork). Meat consumption (and thus the percentage of fat
calories) in the traditional Pima diet was relatively low compared to
typical U.S. diets (29). However, Savage notes that the cholesterol levels
of Pima remained lower than those of whites at a point when the usual Pima
diet had become quite similar to that of the general population (17).
Metabolic studies in Pima volunteers suggest that there are significant
differences in apoprotein and lipoprotein metabolism which may account for
the different lipid profiles of Pima Indians (15,24). The high prevalence
of gallstones among southwestern Indians, including the Pima, has been
suggested as a possible explanation for the lower blood cholesterol levels
(3,11); however, this view is not widely supported.
The 1956-62 Many Farms Study among the Navajo indicated relatively low
cholesterol values in 89 and 113 randomly-selected men and women for whom
cholesterol determinations were made (31). The authors were reluctant to
generalize to the Navajo as a whole, partly because of their belief that
the Navajo diet was high in saturated fat. In fact, the study was
motivated by what appeared to be a paradox of high fat intake and low CHD
in this population. Although fat from mutton or lard is an important part
of traditional Navajo food, other authors, including Keys (25,26) have
pointed out that the total percent fat in the Navajo diet was around 24%,
much lower than the 40% typical of Americans in general. Also, dairy fat
is not common in the Navajo diet (26).
Two studies among the White Mountain Apache (26,28) indicated low
cholesterol levels in this group (in the range of 185 to 200 mg/dl)
compared to whites. However, Clifford et al. noted a lower percentage of
cholesterol levels under 225 mg/dl among younger Apache men ages 25-44 vs.
45-64 year old men (72% vs. 86%) and commented that cholesterol patterns in
the younger Apache men might be changing (26).
In the study of Seminole Indians in Oklahoma (36), the prevalences of
serum cholesterol >260 mg/dl were 9.1% and 5.4% in Seminole men and women
vs. 15.6 and 9.1% in white men and women. The authors attribute most of
this difference to the younger ages of the Seminoles in their sample and
state that the overall serum cholesterol distributions were similar.
The Minnesota study (33) is the only recent report of cholesterol
levels among Indians other than Pimas which could be identified. Total
cholesterol levels of the Minneapolis Indians were similar to those of
whites under age 55 and lower after age 55. HDL cholesterol levels of
Indian and white men were simliar; lower HDL levels among the Indian vs.
464
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men under age 40 compared to 22% over age 40 reported using alcohol in the
1977 study. The authors noted that this may have indicated a trend towards
higher alcohol use in the younger cohort. Ingelfinger reported that only
2.5% of Pima males and no Pima females smoked more than one pack of
cigarettes per day (46).
In contrast, smoking was highly prevalent among the Minneapolis
Indians surveyed by Gillum et al. in 1980 (33). However, this probably
does not represent a trend towards increased smoking among the Chippewa.
According to the authors, smoking has been highly valued in traditional
Chippewa culture. Seventy-seven and sixty-seven percent of the Indian men
and women surveyed were current smokers; 45% smoked more than 20 cigarettes
per day (there was no sex difference in number smoked per day). Of those
who smoked, only 25% reported wanting to stop smoking, although most had
tried to quit. Reported alcohol intake in the Minnesota population was
low. Forty-eight percent reported abstinence; those who drank reported
consumption of alcohol at least two days per week.
Cigarette and alcohol use of 76 Native American students in the
University System of Georgia were ascertained in a 1972 study of 20,547
students (41). Reported cigarette use among the Native American students
was highest of all the ethnic groups (white, black, Asian, other) and
reported alcohol use was second highest. A 1973 study of drug use patterns
among American Indian and white high school students in Wyoming reported
more favorable attitudes towards drug use among the Indian students, but
alcohol was not among the drugs specifically queried (35). In a survey of
students between 10 and 20 years of age in Anchorage Alaska, Native
American students (5.7% of 15,634 respondents) were less likely than white
students to be nonusers of any drugs and more likely than any of the other
ethnic groups to have tried drugs in addition to alcohol or tobacco (37).
The association of cigarette and alcohol use with IHD risk among
Native Americans has apparently not been explored, although the social and
other health consequences of heavy alcohol use in Indian populations have
received great attention in the Native American literature (3,53).
Insufficient data are available to draw any conclusions about trends in
these variables or their contributions to IHD patterns.
5.0 MULTIVARIATE PERSPECTIVE
A discussion of obesity and diabetes among Native Americans is beyond
the scope of this paper. However, it is appropriate to draw attention to
the apparently large public health importance of these two conditions in
most Native American populations and to their enhancement of what might be
(for many tribes) an otherwise relatively benign IHD risk profile. A
greater prevalence of obesity in American Indians vs. whites was mentioned
in the majority of papers reviewed (7,11,12,20,23,26,27,30,31,33,36,39,40,
45,46,48,49,51) and in others not noted above (54-57). Two papers (39,40)
note the excess prevalence of obesity among Seneca Indians--a group for
466
whom other papers related to IHD risk were not identified. The mortality
risk associated with obesity among Pima Indians does not appear to be the
same as for the general population (20).
The excess risk of diabetes among Native Americans is evident in the
mortality data. The Pima Indians have an unusually high prevalence of
diabetes, but an excess of glucose intolerance prevalence is apparently
typical of many adult Indian populations (3,12,13,20,33,36,39,40,46). The
absence of diabetes among the leading causes of death for the Navajo (11) is
consistent with a low or moderate prevalence of diabetes among some
Athapascan tribes (Navajo and Apache)(3,23). Diabetes is reportedly common
in Apache tribes in Oklahoma (3).
From a multivariate perspective, Native Americans are at high
potential IHD risk. With the exception of elevated cholesterol and
smoking, standard risk factors and predisposing co-morbid conditions are
equivalent or higher in American Indian populations where comparisons have
been made. This suggests that the future of IHD risk may become worse for
American Indians at a time when the picture is improving for large segments
of the general population.
6.0 IMPLICATIONS AND RECOMMENDATIONS
To draw conclusions about current IHD risk perspectives among Native
Americans on the basis of the limited data available would be
inappropriate. Probably there is no one conclusion that will apply to all
Native American people; there are at least two distinct patterns implied.
Indians in the Southwest have lower overall IHD risk than Indians in other
parts of the country. However, Native Americans in all parts of the
country may have excess IHD risk associated with excess obesity and
diabetes. In some areas of the country Native Americans are at excess IHD
risk due to lifestyle factors (cigarette use). Although the risk of
hypercholesterolemia among Native Americans may be lower than in the
general population, in no sense does this result in "immunity" to IHD.
In spite of an impression from available literature that IHD is not an
important contributor to overall Native American-white mortality
disparities (due to extreme disparities in certain other mortality
classes), the fact that heart disease is the leading cause of death among
Native Americans must be kept in mind. Moreover, there is evidence of
excess heart disease mortality among Native Americans at younger ages.
In conclusion, the following recommendations are put forth:
--systematic data collection is needed, if not tribe-specific
then at least specific to major subgroups which show different
risk patterns (e.g., Southwest vs non-Southwest);
467
--more of the Indian Health Service data should be included
in frequently used publications of health statistics;
--intervention on those risk factors already identified is indicated,
particularly prevention of obesity and diabetes; the disparities
in this area are huge and are bound to result in increasing
health problems for Native Americans as their life span increases
and deaths from other causes are reduced.
ACKNOWLEDGEMENTS
We gratefully acknowledge the editorial assistance of Sandra
J. Anderson and Elisabeth Pitt.
468
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3. Sievers ML, Fisher JR. Disease of North American Indians.
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New York: Academic Press, 1981, Chapter 8, pp. 191-252.
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5. Taylor TW. The States and Their Indian Citizens. United
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11. Kunitz SJ. Disease Change and the Role of Medicine. The
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13. Howard BV, Lisse JR, Knowler WC, Davis MP, Pettitt DJ,
Bennett PH. Diabetes and atherosclerosis in the Pima Indians.
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Plasma and lipoprotein cholesterol and triglceride concen-
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15. Howard BV, Zech L, Davis M, Bennion LJ, Savage PJ, Nagulesparan
M, Bilheimer D, Bennett PH, Grundy SM. Studies of very
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population with low plasma lipids. Lack of influence of
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T, Nikkila EA. Characterization of lipase activities in
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PH. Serum cholesterol levels in American (Pima) Indian
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20. Pettitt DJ, Lisse JR, Knowler WC, Bennett PH. Mortality
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R, Casdorph HR. The plasma lipids, lipoproteins, and diet
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33. Gillum RF, Gillum BS, Smith N. Cardiovascular risk factors
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34. Pinkerton RE, Badke FR. Coronary heart disease. An epidemi-
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36. Mayberry RH, Lindeman RD. A survey of chronic disease
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heart disease in Pima Indians. Electrocardiographic findings
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with a high prevalence of diabetes mellitus. Diabetes
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of urban Native American school children. Hypertension
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on serum cholesterol in American (Pima) Indian women.
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NB, Miller M. Hyperinsulinemia and hypoinsulinemia. Insulin
responses to oral carbohydrate over a wide spectrum of
glucose tolerance. Diabetes 1975;24:362-368.
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473
Stroke Report
Lewis H. Kuller, M.D., Dr.P.H.
Chairman, Department of Epidemiology
Graduate School of Public Health
University of Pittsburgh
Pittsburgh, Pennsylvania
MORTALITY
Stroke is a major cause of death and disability in the United States.
In 1981 there were 163,504 stroke deaths (Table 1), including 9,429 among
non-white men and 11,310 non-white women. Most of these deaths, 8,760
in men, and 10,656 were among black men and women.
Age adjusted stroke death rates are approximately two times as high
in the all other or black men and 1.8 times as high in black women than
for white v. mien who have the lowest death rates (Table 1).
Age specific stroke death rates increase substantially with age
(Table 2). Approximately doubling with each increase in 5 year age group
(Table 2). Stroke death rates are much higher in the younger and middle
aged blacks than whites (Table 2). The mortality rate is generally over
3-fold higher through age 65 (Table 3). Stroke is estimated to reduce
life expectancy at age 45 for non-white men by 12.3 years and for non-
white women by 14.7 years (Manton and Baum, STROKE 1984;15:451-457).
Stroke accounts for about seven percent of all deaths in 1981,
including about 10% among black women (Table 4). Stroke is also an
important contributing cause of death on the death certificate, that is
not listed as the underlying cause (Table 5).
In 1976-1978, the last year in which current data is available,
stroke was the underlying cause for 31,368 deaths among black men and
contributed to another 19,216 based on the death certificate listings
and for women it was the underlying cause in 35,864 and in 21,313 a contri-
buting cause. Previous studies have shown that when stroke is the under-
lying cause of death, the individual has usually died from the acute
complications of stroke usually within the first several months after
the stroke. However, many other individuals who survive the initial
stroke event may subsequently die of a stroke or related cause without
any mention of this on the death certificate.
There is a very substantial variation in stroke mortality by
geographic area. These differences have persisted for many years. In
1969-1971 (Table 6), stroke death rates were 10 times higher for black
men in Savannah, Georgia than for white men in Baltimore, Maryland aged
45~54. In 1978 stroke death rates aged 45~54 were still four times higher
in Georgia for black men than for white men and 3.5 times higher for
black than white women. Rates were still substantially higher in Georgia
and other areas of the southeast than in the Great Plains or Rocky Mountain
areas (Tables 7 end 8).
Previous studies have clearly demonstrated a marked socioeconomic
gradient in stroke mortality for both black men and women (Table 9).
There are also marked variations in stroke mortality within a state such
as North Carolina (Table 10). A recent study in Allegheny County,
Pennsylvania, for white men continues to demonstrate a considerable socio-
economic gradient in stroke mortality. These observations are consistent
with a greater prevalence of risk factors especially hypertension in
lower socioeconomic and less educated populations and also poor control
of these risk factors.
477
High stroke death rates among blacks are not limited to the United
States. Stroke is reported to be increasing and common in Africa. A
recent WHO report noted stroke rates in Cape Verde Islands (Table 11),
similar to those of blacks in the United States. Unfortunately mortality
statistics for other countries in Africa with predominantly black
populations are not available. However, clinical studies suggest an
increase stroke mortality associated with hypertension especially in
urban areas. In the March, 1983 report of the East Africa Medical Journal,
Daresi, et al., noted that cerebral vascular disease was becoming a major
cause of mortality and morbidity. One hundred eighty stroke cases and
180 age and sex matched controls were studies over a two year period in
Lagos, Nigeria. The stroke patients had a much higher prevalence of
systolic and diastolic hypertension, diabetes mellitus and obesity.
In Lagos University Teaching Hospital, cerebrovascular accidents
were the second most common of all neurological admissions between 1962
and 1967, the most common being tetanns. Evidence from the Stroke Registry
in Ibadan, Nigeria, has shown that the incidence of stroke was 26/100,000.
Daresi, et. al., East Africa Medical Journal, March 1983.
The prevalence of cerebro atherosclerosis increases in Nigeria with
age and with the presence of a history of hypertension (Table 12). The
prevalence is not as high as in U.S. populations (Table 12). Therefore,
the current evidence from Africa suggest that stroke is becoming
increasingly prevalent, that it is related to hypertension and perhaps
diabetes, and that cerebral atherosclerotic disease is increasing especially
among hypertensives. Coronary artery disease and myocardial infarction
is still very uncommon. The picture in Africa especially in urban west
Africa is probably a replication of changes in risk factors and stroke
that occurred many years ago in the United States.
Blacks in the United States are also reported to have a higher
prevalence of both intracranial and extracranial pathology as compared
to whites (Tables 13-14).
Stroke death rates are not elevated among the Chinese, Japanese,
Koreans and Philippino's compared with U.S. whites in the United States
(Tables 15-17). There also does not appear to be an excess stroke
mortality among Hispanics in Southern Texas (Table 18) as compared to
whites. There may be a slight excess of stroke mortality among Puerto
Ricans in New York especially in the younger age groups as compared to
whites (Table 19). The apparent absence of an increase in stroke death
rates among Mexican-American populations may be of particular importance.
This population is generally of lower socioeconomic status, has a very
high prevalence of obesity especially among women, and diabetes, but
little increase in hypertension. The failure to note an apparent increase
in hypertension with acculturation may be due to genetic factors or diet.
Further investigation of this population should be done especially in
search of possible protective constituents in the diet or selected genetic
factors.
Stroke death rates among American Indians appear to be slightly
higher than the rest of the United States population, but lower than
those for U.S. blacks. Stroke death rates also appear to be declining
among American Indians (Tables 20-21).
478
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MORBIDITY
Information pertaining to stroke morbidity as compared to mortality
is more difficult to identify especially as related to specific minority
groups. The 1972 National Health Interview Survey estimated the prevalence
of stroke as 7.2/1,000 among whites and 9.1/1,000 among all others.
The prevalence of stroke reported in the Evans County, Georgia study
in 1967-1969 was 53.2/1,000 for white males, 15.0 for white women, 58.6
for black men and 43.4 for black women age adjusted (Table 32).
Among participants eligible for randomization in the Hypertension
Detection and Prevention Trial, the prevalence of stroke was much higher
in blacks than whites.
The data on the prevalence of stroke among whites has been provided
by previous national stroke surveys, but no data for blacks was included
in that report or for other minority groups. The need for including
larger numbers of minorities in future prevalence surveys is obvious if
good prevalence data is to be obtained.
The prevalence of stroke among Japanese in Hawaii and California
was much lower than for Japanese in Japan (Table 33).
There were 806,000 stroke hospital discharges in which stroke was
the first listed diagnosis in 1981 in the United States including 100,000
among non-whites (Table 34). The average length of stay was slightly
longer for other racial groups than for whites. Based on these data,
there were approximately 1.4 million hospital days directly related to
stroke care among non-whites.
The estimated annual medical care cost of stroke in 1980 was 5.1
billion dollars, half of which was for hospital care. Non-whites accounted
for about 1/8 of the hospital days or a minimum of 300 million dollars
for their hospital care alone. The total cost of stroke care for both
whites and non-whites in the United States is very substantial (Table
35).
Data on the incidence of stroke among several minority groups is
available. The southern Alabama study is the most recent and most complete
(Table 36). The age adjusted incidence is higher in blacks than whites
especially for black women.
The risk of stroke was also substantially higher among black men
and women in the Hypertension Detection and Follow-up Program clinical
trial for both the stepped and referred care populations (Table 37).
Stroke incidence has also been measured among blacks in Ibadan,
Nigeria (Table 38). Stroke rates in Ibadan appear to be in the same
range as those noted in the southern Alabama study. For example, age
specific incidence per 100,000 in Ibadan, ages 50-59, is 440/100,000 as
compared to a rate of 642/100,000 aged 55-64 in southern Alabama. It is
unclear however, whether the Ibadan rates are from one or three years.
It is also unclear what percentage of stroke cases are actually ascertained
480
in Ibadan as compared to the southern Alabama study. The high stroke
incidence rates may not be limited to the U.S. black population.
Stroke incidence is comparable among Japanese living in Hawaii and
the U.S. white population. Stroke incidence is much lower among the
Japanese in Hawaii than for the Japanese in Japan (Table 39). There is
no evidence for increased stroke death rates among Chinese in the United
States. Chinese in Taiwan have the highest stroke death rates reported
(Table 31). Stroke death rates are declining in Taiwan even though there
is no apparent well-organized hypertension control program (Table 31).
Prophylactic approaches to hypertensive diseases (Y. Yamori, Raven Press,
New York 1979). A stroke registry in part of Taipei in 1975 reported a
stroke incidence rate aged 55~64 substantially higher than in the United
States whites, 11.6/100,000 in men, as compared to 2.7/100,000 in Southern
Alabama (Table 40). The remarkable apparent decrease in stroke among
both Chinese and Japanese migrants to the United States certainly requires
further evaluation especially as it does not appear to be directly related
to changes in blood pressure levels.
Stroke is not a single disease but rather a group of related
diagnoses. Many investigators believe that blacks and Japanese have
more intracranial and more hemorrhagic disease than whites. Few studies
have documented the specific types of stroke based on good clinical and
laboratory-diagnostic evaluations.
The stroke study in Southern Alabama included a detailed review of
the specific types of stroke based on careful clinical evaluations. Most
strokes in both blacks and whites were due to infarction rather than
hemorrhage (Table 41). Thromboembolic stroke also predominants among
Japanese in Japan as well as among Japanese in Hawaii (Tables 42-43).
Further evaluation of the specific types of strokes will be possible
with the development of new technology for evaluating stroke diagnosis
such as CT scan and NMR, etc. The availability of improved diagnostic
methods may provide a better understanding of the interrelationship of
some of the key risk factors for stroke especially the relationships if
any between the types of hypertensive disease and specific clinical-
pathology of stroke.
RISK FACTORS
Hypertension is the major risk factor for stroke. Diabetes, alcohol
intake, high hematocrit or hemoglobin and lipoprotein abnormalities may
also be important risk factors.
Other cardiovascular disease, specific electrocardiographic
abnormalities especially signs of left ventricular hypertrophy, as well
as other manifestations of increased left ventricular mass such as an
increased left ventricular wall mass by echocardiography and cardiac
arrhythmias including atrial fibrillation are major risk factors for
stroke.
Both systolic and diastolic blood pressures are higher in blacks
than whites (Table 44).
481
The prevalence of elevated blood pressure increases substantially
with increasing age among both blacks and whites (Table 45). The decline
in the prevalence of elevated blood pressure, as noted in Table 45, is
apparently primarily due to the treatment of hypertension which has
substantially improved over time.
Blood pressure increased with age among Mexican Americans. Blood
pressure levels appear to be similar among Mexican American and U.S.
whites (Table 46).
Blood pressure among American Indians in Minnesota were similar to
those of U.S. whites (Table 47). No data could be obtained on the blood
pressure distribution of Indians living on the reservations in the south-
western United States.
Blood pressures are higher among Japanese in the United States than
among Japanese in Japan (Table 48). This is surprising because of the
much higher stroke death rates among Japanese in Japan than those in the
United States. The blood pressures of Japanese in Hawaii and California
are similar to those of the U.S. whites. Part of the difference in blood
pressure between Japanese in Japan and Hawaii may be related to a greater
prevalence of obesity among U.S. Japanese. However, obesity adjusted
blood pressures are either similar or slightly higher among U.S. Japanese
than those in Japan (Table 49). Similar studies of blood pressure
distribution of Chinese in Taiwan fail to demonstrate any higher levels
as compared to other populations inspite of the much higher stroke death
rates (Table 50).
The prevalence of hypertension is also higher among Japanese in the
United States (Table 51). The prevalence of electrocardiographic evidence
of left ventricular hypertrophy and hypertensive heart disease is however
much higher among Japanese in Japan than in Hawaii or California (Table
52). This is also true even when comparing electrocardiographic
abnormalities among Japanese in Japan working for the NTT Telephone
Company versus U.S. telephone workers (Table 53). There is also a
relationship between the high R-waves on the electrocardiograph and
elevated blood pressure in both of these populations. There is evidence
from studies both in Japan and in Hawaii that these electrocardiographic
abnormalities may be an independent predictor of stroke incidence and
mortality. The higher prevalence of left ventricular hypertrophy in
relationship to hypertension has been noted in Chinese in Taiwan (see
ref. Fig. 50).
The prevalence of electrocardiographic abnormalities was also noted
to be much higher among blacks even after controlling for the degree of
hypertension. This has been noted most recently in both the Multiple
Risk Factor Intervention Trial (MRFIT) (Table 54) and the Hypertension
Detection and Follow-up Program (HDFP).
There have been numerous surveys of selected population groups in
Africa. Few of the studies represent true population samples or comparable
methods of measurement. The studies were reviewed by Adenounmu (Clinical
and Experimental Hypertension, 1981;3(4):597-621). He noted that blood
pressure increases with age and is higher in urban than rural men in
482
Africa (Table 55). The blood pressure levels are similar to those in
the Carribean Islands but lower than in the U.S. or south Africian blacks.
Stroke, congestive heart failure and renal diseases are the major
complications of hypertension. Coronary artery disease remains very
rare.
Earlier studies such as from Evans County, Georgia (Table 56) suggested
relatively little difference in the risk of stroke in relationship to
blood pressure level among blacks and whites. More recent studies, however,
suggest that black hypertensives may be at greater risk of stroke than
white hypertensives. The estimated incidence of stroke in the referred
care group for blacks in the Hypertension Detection and Follow-up Program
was 35.3/1,000 as compared to 24.2/1,000 for whites. There was a
substantial decrease in stroke morbidity and mortality in the special
care as compared to the referred care for all four race, sex groups (Table
57).
In the Multiple Risk Factor Intervention Trial the ineligible
screenees were followed initially for five years. Among the screenees
there were 23,490, black men between the ages of 35~57. The incidence
of stroke, was 1.3/1,000 among black men and 0.5/1,000 for white men
(Table 58). The risk of stroke death increased with level of diastolic
blood pressure (Table 59). At most, levels of diastolic blood pressure
the stroke rates were higher in blacks than whites.
The logistic regression coefficient for the risk of stroke death
was greater for black men than white men (Table 60) suggesting that at a
given level of blood pressure the risk of stroke death is greater for
blacks than whites. However, part of this difference could be due to
differential subsequent treatment for hypertension.
The risk of stroke was increased among individuals with electro-
cardiographic abnormalities in the Evans County Study, this was true for
all four race/sex groups but especially for men (Table 61). In the HDFP
trial the mortality rates including stroke were increased among men with
electrocardiographic abnormalities based on the "Minnesota Code" (Table
62-63).
Stroke incidence is also directly related to blood pressure levels
among Japanese men in Hawaii (Table 64). The increased risk appears to
be related to both intracranial hemorrhage and thromboembolic disease
(Table 64). It appears that at higher levels of systolic blood pressure
the Japanese in Japan have a greater risk of stroke than Japanese in
Hawaii (Table 65).
Surveys in Taipai also demonstrate a striking association between
hypertension and stroke, as well as the high prevalence of left ventricular
hypertrophy (Table 66).
The relationship between lipoprotein levels and risk of stroke is
equivocal. In the Evans County Study there was no consistent relationship
between the serum cholesterol level and risk of stroke among blacks or
whites (Table 67).
483
In the MRFIT screenees there was also no consistent relationship
between the serum cholesterol level and risk of stroke death for either
black or white men (Table 68). None of the regression coefficients related
to serum cholesterol and risk of stroke were significant (Table 69).
Prior studies in Japan had suggested a possible inverse relationship
between stroke and serum cholesterol levels. Studies of Japanese in
Hawaii are consistent in demonstrating a possible inverse relationship
between serum cholesterol levels and cerebral hemorrhage but not for
cerebral thrombosis or infarction (Table 70).
More recent studies from Japan (Table 71) do not demonstrate a
consistent relationship between the serum cholesterol level and stroke
except for a lower cholesterol levels among the small number of individuals
with cerebral hemorrhage. These initial studies however do demonstrate
that lower animal protein and very low saturated fat intake may be a
risk factor for stroke (Tables 72-73).
A further analysis of the Japanese in Hawaii based on post-mortem
measurement of cerebrovascular disease again demonstrated a slightly
lower cholesterol level among deaths with cerebral hemorrhage and higher
cholesterol for those found with a brain infarction. Animal protein
intake was decreased only for deaths with cerebral hemorrhage.
This data set further demonstrated a relationship between cerebral
and aortic atherosclerosis and brain infarction and also a high prevalence
of prior myocardial infarction among those also found to have brain
infarction by post-mortem examination (Tables 73~74). The results of
these studies therefore suggest that the relationship between lipoproteins,
dietary factors and stroke may be different for those who have cerebral
thromboembolic disease as compared to cerebral hemorrhage.
Cerebral thromboembolic disease secondary to atherosclerosis is by
far the most common stroke disorder in the U.S. black and white population
as well as among the Japanese in Hawaii and California. The primary
emphasis should obviously be placed on the risk factors for this disorder.
On the other hand, the relationships between low protein intake and
cerebral hemorrhage especially animal protein may be a clue to the
apparent sharp decline in cerebral hemorrhage over the past 20 and 30
years associated with improved diet and lifestyle including a probable
increase in animal protein intake.
The prevalence of diabetes is also substantially higher among blacks
as compared to whites (Table 75). Diabetes is also very prevalent among
several American Indian tribes and among Mexican Americans in the
southwestern United States.
Diabetes is an important risk factor for stroke. Blacks have a
higher prevalence of diabetes than whites. In the Three-Area Study of
Stroke Risk Factors, blacks had higher blood sugars and history of diabetes
than whites especially in the southeastern United States (Table 76).
Diabetes is clearly associated with an increase in cerebro atherosclerosis
(Table 77). Prospective studies such as the American Cancer Society
Followup Study, (Table 78) or the Framingham Study (Table 79) have noted
the increase risk of stroke among diabetics.
484
A study in the 1960's demonstrated that diabetes was a frequent
contributing cause of death on a death certificate in which stroke was
the underlying cause especially among black women (Table 80). Studies
in the late 1960's (Table 81) showed that diabetes was listed on about
16% of all stroke hospital discharges. A more recent, unpublished study,
from Pennsylvania showed that stroke was listed as a secondary diagnosis
on 2.7% of hospital discharges for diabetes among blacks and 4.8% among
whites, and in 5.2% of the records among blacks when diabetes was listed
as a secondary diagnosis on the hospital discharge record.
A followup study of a diabetic cohort in Rochester, Minnesota
suggested that the increased risk of stroke among diabetics may be limited
to those with concurrent hypertension (Table 82). This observation could
explain the lower rates of stroke inspite of the high prevalence of
diabetes among Hispanics and Mexican Americans due to their apparent
lower prevalence of hypertension as compared to U.S. blacks.
The prospective Honolulu Heart Study has further documented an
increased risk of stroke especially thromboembolic associated with
increasing levels of blood sugar (Table 83). In multivariate analysis,
the blood sugar levels remained an independent predictor of thromboembolic
stroke but not hemorrhage.
OTHER RISK FACTORS
Alcohol Consumption
Alcohol consumption has been identified as an independent predictor
of stroke as well as a possible risk factor for elevated blood pressure.
Among Japanese in Hawaii, there was a direct relationship between alcohol
consumption and cerebral hemorrhage but not cerebral thrombosis (Table
84, 85). Alcohol consumption and hypertension may be an especially lethal
combination for cerebral hemorrhage. A major effort must be made to
treat hypertension among alcohol consumers, as well as reducing prevalence
of alcoholism.
Cigarette Smoking
The relationship between cigarette smoking and stroke is uncertain.
Among Japanese in Hawaii, there was a statistically non-significant greater
number of cigarettes smoked among subsequent cerebral hemorrhage or thrombosis
cases than non-strokes. In the MRFIT trial screenees, the risk of stroke
appeared to increase up to 26-35 cigarettes per day and then decrease
among black men (Table 86). Cigarette smoking has an important effect
on platelets and thrombogenesis. It is possible that smoking could be
an important precipitant of stroke among individuals with a high risk of
cerebro thromboembolism especially those with carotid artery stenosis,
heart disease and cardiac arrhythmias.
485
Hematocrit and Hemoglobin
Many studies such as the "Framingham Heart Study", have shown a
direct relationship between hematocrit or hemoglobin levels and risk of
stroke. The relationship may be due to an association of elevated hemo-
globin or hematocrit with blood pressure to greater viscosity of the
blood or to other unknown pathophysiological changes associated with the
level of hematocrit or hemoglobin. In the Evans County Study, there
appeared to be an increased risk of stroke among both blacks and whites
with increasing hematocrit levels (Table 87). These studies may have
important implications for defining ideal hematocrit or hemoglobin levels
especially among women. It is possible that the lower levels of hemoglobin
or hematocrit in women secondary to recurrent menstrual bleeding offer
some protection against thromboembolic disease. Attempts to raise these
levels could increase the risk of stroke or other thromboembolic diseases.
Sickle cell anemia is an important cause of stroke especially in
the younger age groups. There is no evidence however that sickle cell
trait or other hemoglobin disorders are associated with a substantial
increased risk of stroke.
COMBINATION OF RISK FACTORS
A combination of these risk factors such as in the Hawaii Heart
Study of Japanese men (Table 88) can identify a high risk of stroke.
The combination of several of these risk factors plus hypertension (Table
88) defines a much higher risk group. Many of these risk factors are
clearly ameanable to preventive efforts.
DISCUSSION AND IMPLICATIONS
The death rates due to stroke have continued their long-term decline.
The slope of the decline accentuated in the raid 1970's most likely due
to an improvement in the treatment and control of hypertension. The
changes in awareness, treatment and control of hypertension as noted in
the "Impact Study" (Table 89) have resulted in a decrease in the
prevalence of elevated diastolic blood pressure. Blood pressure remains
substantially higher among blacks than whites. Improvement in the control
of hypertension has also occurred among Mexican Americans (Table 90) and
probably among Japanese and other minority groups in Hawaii and California.
Inspite of these good efforts the stroke death rates and incidence
still remain much higher among blacks than whites. There is little
evidence that other minority groups such as Hispanics, Chinese, Japanese,
Koreans or native Americans are at substantially higher risk of stroke
than whites. The risk may be elevated among Puerto Ricans in New York.
No data could be obtained for Cubans in the southeast or for Vietnamese
or other Asian groups.
The risks of stroke are related primarily to hypertension. Prevention
and treatment of hypertension remains the cornerstone of any stroke control
program. The increased prevalence of hypertension among blacks is probably
486
a combination of genetic and environmental factors. Clinical and
epidemiological studies have identified differences in renin, sodium,
lithium counter transport, the ability to excrete a salt load and urinary
kallikrein excretion between blacks and whites. Elevated blood pressure
is clearly not due to any one single factor. The type of blood pressure
elevation and relationship to outcome may vary in relationship to the
key risk factors.
Obesity is the most important risk factor for elevated blood pressure
in the United States. However, obesity related hypertension may be a
different type of disease than non-obesity hypertension especially in
relation to specific hypertensive outcomes, such as, cerebral hemorrhage,
intracranial vascular disease, renal disease, and retinopathy. Obesity
hypertension may be a more important factor for atherosclerotic disease
including myocardial infarction. The decline in stroke that occurred
from the 1920's and 1930's may be related to this non-obesity related
hypertension. A recent report from the Hypertension Detection and
Followup Program noted a substantially higher mortality among those with
non-obese, as compared to obesity hypertension (Table 91). Other
hypertensive studies have shown similar results.
The origins of non-obesity hypertension is unknown but low protein
intake, high intake of salt and low consumption of potassium and calcium
may be playing important roles. There is also most likely an important
genetic component. It is important to reiterate that both obese and
non-obese hypertension must be treated in order to reduce the specific
hypertensive complications especially stroke. The lower the blood pressure
the greater the decrease in hypertensive complications especially stroke
and congestive heart failure. The only issue perhaps that still remains
is the interaction between the treatment of hypertension and atherosclerotic
complications especially myocardial infarction.
The highest rates of hypertension and stroke among blacks are found
in the southeast, in lower socioeconomic groups and among less educated
individuals. Key environmental factors appear to play an important role
in these geographic and socioeconomic variations including obesity, sodium,
potassium, and calcium intake, possibly stress and "hostility", alcohol
intake and health care especially as related to the treatment of
hypertension and its complications.
The control of diabetes and hypertension especially the combination
of diabetes and hypertension among black women may be associated with an
exceptionally high risk of stroke. The joint prevalence of hypertension
and diabetes may both be primarily related to nutritional factors especially
the development of obesity.
The future accentuation of the rapid reduction of stroke mortality
and morbidity especially among blacks will require efforts focused at
identifying the high risk individuals and communities in the United States,
and aggressive control of hypertension and other risk factors in these
high risk communities. Such communities can be easily identified by
monitoring the high stroke death rates. Such communities should be candidates
for aggressive hypertension treatment programs and careful monitoring to
determine a consistent reduction in stroke mortality. The stroke death
487
rates in general reflect the acute stroke case fatality which is generally
at least 20-30%. Mortality rates reflect the trends in the incidence of
stroke and are the easiest and best endpoint to monitor in hypertension
control programs. The reduction in stroke mortality especially among
younger blacks, i.e., 35~64, is probably the most important medical factor
in decreasing the black-white difference in mortality rates among adults.
Major efforts should be continued to reduce the prevalence of elevated
blood pressure by control of risk factors for hypertension. The ultimate
control of this epidemic of hypertension and stroke will depend on primary
prevention. Much of the health habits which lead to the elevated risk
factors are learned early in life and therefore may be ameanable to modifi-
cation. Nutrition and genetic factors are probably the key elements.
The role of diabetes and hyperlipoproteinemia in the etiology of
stroke especially among blacks needs further investigation. It is unclear
whether elevated levels of HDL cholesterol or its subfractions are associated
with a reduced risk of stroke especially thromboembolic stroke as well
as heart attack. There is little evidence that treatment of non-insulin
dependent diabetes with either oral hypoglycemic agents or insulin reduces
the risk of stroke. There is a strong genetic component to diabetes, as
well as a clear relationship to dietary factors especially obesity and
perhaps a low fiber intake. Prevention of diabetes and a better
understanding of its pathophysiology and improved methods of treatment
offer the best potential for the prevention of the complications of this
disease including stroke.
Treatment of stroke may have improved in recent years. There is
some evidence for reduction in the case fatality. Diagnostic methods
have certainly improved substantially. Early detection and treatment of
potential strokes may be of substantial value especially the identification
of transient ischemic attacks and the possible treatment with antiplatelet
agents or surgical correction of underlying carotid artery disease or
identification of carotid artery bruit and asymptomatic stenosis and
occlusion.
There is also a strong association between vascular disease at other
sites especially coronary artery disease and subsequent risk of stroke.
Patients who have had a myocardial infarctions or other manifestations
of coronary artery disease are ideal candidates for preventive efforts
to reduce the subsequent risk of stroke. Furthermore, there appears to
be a strong association between certain electrocardiographic and
echocardiographic abnormalities, and subsequent risk of stroke. The
identification of such high risk individuals and effective treatment may
also be important in reducing the risk of stroke. There is strong evidence
that blacks, as well as Japanese may have more intracranial and less
extracranial disease than whites (Tables 92-93) and therefore such approaches
as carotid artery surgery, antiplatelet drugs may be less effective in
black populations. The major effort to reduce stroke mortality should
continue to emphasize identification, treatment and control of hypertension.
The risk factors for stroke are identifiable and can be controlled effectively.
488
TABLE 1
Age Adjusted Death Rates Due to Cerebrovascular
Disease (430-438) 1981—United States by Race and Sex
Number of Deaths Rate/100,000
Total 163,504 38.1
Men 66,429 41.7
Women 97,075 35.4
White Men 57,000 38.9
White Women 85,765 33.1
All Other Men 9,429 65.6
All Other Women 11,310 53.2
Black Men 8,760 72.7
Black Women 10,656 58.1
Monthly Vital Statistics Reports. National Center for
Health Statistics, Vol. 33, No. 3, Supplement, June, 1984.
Ratio to
White Women
1, .1
1, ,3
1. ,1
1. ,2
1
2. ,0
1. 6
2. 2
1. 8
489
TABLE 2
Death rates for cerebrovascular diseases, according to race, sex, and age: United States,
selected years 1950-82
(Data are based on the National Vital Statistics System)
Race, sex, and age
1950J
Total3
All ages, age adjusted ......... 88.8
All ages, crude................. 104.0
Under 1 year.......................... 5.1
1 -4 years............................. 0.9
5-14 years............................ 0-5
15-24 years........................... 1-6
25-34 years........................... 4-2
35-44 years........................... 18.7
45-54 years........................... 70«!
55-64 years........................... 195-3
65-74 years........................... 549-7
75-84 years........................... 1,499.6
85 years and over..................... 2,990.1
Year
1960J
1970
1975
1979
1980
1981'
Number of deaths per 100,000 resident population
1982'
79.7 66.3 53.7 41.6 40.8 38.3 36.1
108.0 101.9 90.1 75.5 75.1 71.3 68.9
4.1 5.0 5.0 4.6 4.4 3.6 3.8
0.8 1.0 0.8 0.3 Ml 0.2 0.2
0.7 0.7 0.5 0.3 0.3'
1.8 1.6 1.4 0.9 1.0 0.9 1.0
4.7 4.5 3.4 2.6 2.6 2.6 2.3
14.7 15.6 11.7 9.1 8.5 8.1 7.9
49.2 147.3 41.6 115.8 32.3 90.4 26.4 68.1 25.2 65.2 26.3 64.5 24.2 57.2
469.2 384.1 302.2 226.9 219.5 209.8 195.3
1,491.3 1,254.2 1,028.8 793.8 788.6 702.6 678.6
3,680.5 3,234.6 2,736.4 2,264.9 2,288.9 2,119.8 2,056.4
White male
4
All ages, age adjusted ...........
All ages, crude...................
Under 1 year..........................
1-4 years.............................
5-14 years............................
15-24 years...........................
25-34 years...........................
35-44 years.....................*.....
45-54 years...........................
55-64 years...........................
65-74 years...........................
75-84 years........................... *
85 years and over..................... 3
87.0 80.3 68.8 56.7 42.9 41.9
100.5 102.7 93.5 80.2 64.2 63.3
5.9 4.3 4.5 4.6 3.6 3.8
1.1 0.8 1.2 0.9 0.3 0.4
0.5 0.7 0.8 0.5 0.3 0.2
1.6 1.7 1.6 1.4 0.9 1.0
3.4 3.5 3.2 2.6 2.2 2.0
13.1 11.3 11.8 8.7 6.8 6.5
53.7 40.9 35.6 27.6 22.2 21.7
182.2 139.0 119.9 93.8 68.0 64.2
569.7 501.0 420.0 339.4 249.5 240.4
,556.3 1,564.8 1,361.6 1,134.9 867.0 854.8
,127.1 3,734.8 3,317.6 2,807.4 2,224.5 2,236.9
White female
All ages, age adjusted ...........
All ages, crude...................
Under 1 year..........................
1-4 years.............................
5-14 years............................
15-24 years...........................
25-34 years...........................
35-44 years...........................
45-54 years...........................
55-64 years...........................
65-74 years........................... .
75-84 years........................... *■
85 years and over..................... J
See footnotes at end of table.
79.7 68.7 56.2 46.1 35.9 35.2
103.3 110.1 109.8 101.6 88.5 88.8
2.9 2.6 3.2 3.9 3.3 3.3
0.6 0.5 0.6 0.7 0.3 0.4
0.4 0.6 0.6 .0.5 0.3 0.3
1.2 1.4 1.1 1.1 0.7 0.7
2.9 3.4 3.4 3.0 2.0 2.0
13.6 10.1 11.5 9.3 7.0 6.7
55.0 33.8 30.5 25.0 20.1 18.7
156.9 103.0 78.1 64.5 50.6 48.7
498.1 383.3 303.2 233.6 179.2 172.8
,471.3 1,444.7 1,176.8 966.2 739.3 730.3
,017.9 3,795.7 3,316.1 2,794.9 2,335.7 2,367.8
Health-United States, 1983.
490
TABLE 2 (cont.)
Death rates fqr cerebrovascular diseases, according to race, sex, and age: United States,
selected years 1950-82--Continued
(Data are based on the National Vital Statistics System)
Race, sex, and age
1950'
Black male
4
All ages, age adjusted ...........
All ages, crude...................
Under 1 year..........................>
1-4 years..............................
5-14 years............................
15-24 years...........................
25-34 years...........................
35-44 years...........................
45-54 years...........................
55-64 years...........................
65-74 years...........................
75-84 years...........................j
85 years and over.....................\
146.2
122.0
2.5
0.7
3.3
12.0
59.3
211.9
522.8
783.6
1,504.9
Year
1960J
1970
1975
1979
1980
1981'
1982'
Number of deaths per 100,000 resident population
141.2
122.9
8.5
1.9
*0.9
3.7
12.8
47.4
166.1
439.9
899.2
1,475.2
2,700.0
124.2
108.7
95.0
87.8
12.2 9.1
•1.4 1.1
0.8 0.7
3.0 2.5
14.6 9.4
52.7 36.9
136.2 98.0
343.4 253.7
780.0 626.9
1,442.6 1,123.0
2.315.4 2.115.2
77.9
73.8
12.7
0.5
0.3
1.4
7.3
34.4
88.8
204.0
470.9
963.9
1,840.4
77.5
73.1
11.2
0.6
0.5
2.1
7.7
29.2
82.1
189.8
472.8
1,067.6
1,873.2
Black female
4
All ages, age adjusted .
All ages, crude.........
Under 1 year...............
1-4 years..................
5-14 years.................
15-24 years................
25-34 years................
35-44 years................
45-54 years................
55-64 years................
65-74 years................
75-84 years................
85 years and over..........
155.6
128.3
2.8
0.6
4.2
15.9
75.0
248.9
567.7
754.4
1,496.7
139
127
*6.7
*1.3
1.0
3.4
17.4
57.4
166.2
452.0
830.5
1,413.1
2,578.9
107.9
112.1
9.1 8.
*1.4 0.
0.8 0.
3.0 1,
14.3 8,
49.1 31.
119.4 81.
272.5 187
673.4 502
1.337.8 998
2,504.8 2,126
78.6
91.4
60.
76.
9.
0,
0
1
6
21
62
133
373
865
1.881
61.7
77.9
6.4
0.5
0.3
1.7
7.0
21.6
61.9
138.7
362.2
918.6
1,896.3
includes deaths of nonresidents of the United States.
^Provisional data.
WXTJll byC"/dfrect me^oV'to the total population of the United States as enumerated in 1940, using 11 age groups.
N0TE: For the data years shown^ «-0«-?h.--SS SSll^TSr'^aSirf'SriJS. Vin^^^^1^r^K.,"3Sc^i*3S,;0?-
SiJ£^!^?1^th to'"». «iS>» u2^^*«« States. „os.'430-438; and for .979-82. the Ninth Revision. Nos.
430-438!
, , *„ uaaith statistics- Vital statistics of the United States, Vol. II, 1950-80. Public Health
SOURCES: National Center for Health Statistici. mai >tat st f bWth deaths marriages, and divorces, United
Service. Washington U.>,^erment■>"«£%*f™' TiVff DHHS Pub. No. (PHS) 83-1120. Public Health Service
States, 1982. Monthly V •a\nSff ^"CuK^'by the Division of Analysis from data compiled by the Division of Vital
Hyattsville, Md., Sept. 27, J^i. Data £3"? °yes™-mates and projections. Current Population Reports. Series P-25. No.
Statistics; U.S. Bureau of the Census POP"1*1;00^^. 1950 Nonwhite Population by Race. Special Report P-E, No. 38.
310. Washington. U.S. Government Printingi Officej ^nyy* population characteristics, United States sugary. 1960 and
^n^V^^ Wl)-Bl. ««"1"9ton. U.S. Government Printing Office. 1961
and 1971:
491
TABLE 3
Ratio of Stroke Mortality By Age 1980: Black and White
Black Men/ Black Women/
White Men White Women
25-34 3.5 3.5
35-44 4.5 3.2
45-54 3.8 3.3
55-64 3.0 2.8
65-74 2.0 2.1
75-84 1.1 1.3
85 + 0.8 0.8
Total 1.8 1.8
Monthly Vital Statistics Reports. National Center for
Health Statistics, Vol. 33, No. 3, Supplement, June, 1984.
492
TABLE 4
Percentage of Deaths Due to
White Men
White Women
Black Men
Black Women
Total
Monthly Vital Statistics
Health Statistics, Vol. :
Stroke By Race and Sex 1981
Percent
5.3
8.2
7.2
9.7
6.7
Reports. National Center for
3, No. 3, Supplement, June, 1984.
493
TABLE 5
NUMBER OF DEATHS
1968 - 1970
Stroke as Stroke as Stroke Hot
Underlying Associated Mentioned
Cause Cause
WM 246,313 145,496 2,447,487
WF 299,625 160,170 1,756,574
NM 38,042 20,653 348,661
NF 41,691 21,940 246,305
625,671
348,259
4,799,027
NUMBER OF DEATHS
1976 - 1978
Stroke as Underlying Cause Stroke as Associated Cause Stroke Hot Mentioned
WM 200,429 138,515 2,416,466
WF 278,924 166,131 1,834,235
NM 31,368 19,216 351,681
NF 35,864 21,313 248,673
546,585
345,175
4,851,055
Personal communication from Herb Baum,
494
TABLE 6
Age-Race-Sex Specific Death Rates Due to Stroke
Baltimore, Maryland and Savannah, Georgia
(1969-71/100,000)
45-54 55-64 65-74
Baltimore, Maryland
White Males
White Females
Black Males
Black Females
Savannah, Georgia
White Males
White Females
Black Males
Black Females
34
26
137
109
52
53
379
260
106
64
237
168
142
96
657
710
355
252
567
429
551
400
1266
1195
963
790
952
913
1600
1207
1599
1355
Computed from Vital Statistics of United States.
TABLE 7
Age Specific Stroke Death Rates: 1978 for
Selected States by Race and Sex/100,000
Age 45-54
Georgia Pennsylvania Colorado Mississippi All
White Women 26 22 16 18 22
White Men 35 24 21 28 23
Black Women 97 53 — 65 58
Black Men 143 92 — 116 81
Data provided by the National Center for Health Statistics.
496
TABLE 8
Age Adusted Stroke Death Rates By
Geographic Area 1978/100,000 Ages (35-74)
Colorado
Kansas
Utah
New York
Maryland
South Carolina
Georgia
Mississippi
North Carolina
White White Black Black
Men Women Men Women
43 38
50 43
38 47
48 39 91 75
47 38 115 73
79 54 231 173
82 59 283 158
77 45 169 103
70 47 197 145
Data provided by National Center for Health Statistics
497
TABLE 9
Age-adjusted death rates per 100,000 {age 4(H)9)
for cerebrovascular disease in Baltimore based
on multiple-cause tabulation of 1960 death
certificates by socioeconomic status:
based on combination distribution of
socioeconomic areas in whites and
non-whites*
Socioeconomic status
Race & sex Upper half Lower half
No. deaths Rate No. deaths Rate Unknown
WM 85 129 78 189 1
WF 73 90 77 174 2
NM 26 280 108 422 2
NF 43 410 124 472 2
•Excludes 30 deaths in state hospitals out-
side Baltimore City.
Kuller L, Seltser R: Cerebrovascular Disease Mortality in Maryland.
Am J Epidemiol 1967;86:442-450.
498
TABLE 10
560r
Mountain
I I PwJmonl
■I Plains
HH Coastal
tfnife Males White Femoies Block Moies Slock fero*>
Age-adjusted mortality rates (per 100.000) for stroke
(ICu 430 to 438) in North Carolina in 1969 according to region o'
state and sex-race groups (all entries). The numbers within each bo'
indicate the number of stroke deaths for that region.
Heyman A, Tyroler HA, et al: Geographic Differences in Mortality
From Stroke in North Carolina. Stroke 1976;7:41-45.
499
TABLE 11
Stroke Mortality By Age and Sex: Cape Verde Islands (1980)
Stroke U.S. Blacks
Sex Deaths Rate/100,000 1980
Age 45-54 M 10 128 82
F 12 131 62
55-64 M 13 158 190
F 9 94 139
65-74 M 23 424 472
F 21 338 362
WHO.Statistics Annual 1983.
500
TABLE 12
100
80
_ 60
c
0J
U
Vw
QJ
40
20
0
O—O Hypertensives
■—•"■ Normotensives
D Hypertensives
Normotensives
Percent of Nigerian and Minnesota subjects with cerebral
atherosclerosis in the presence or absence of hypertension. Note the
similarity in percent of Nigerian hypertensive subjects and nor-
motensive Minnesota subjects.
Williams 0, Loewenson RB, et al: Cerebral Atherosclerosis and Its
Relationship to Selected Diseases in Nigerians: A Pathological
Study. Stroke 1975;6:395-401.
501
TABLE 13
Carotid Arteries
100
90
80
ro
60
50H
40
30H
20
10
Itoqro-Main
• si
»i*^ «r* i* i*1 i—p-i—r»i
Ntgro-Ftmaltt
» ■ »
* *■
| ,0°
| *H
^ 80
§ 70H
* 60
50H
40
30
20 H
iO
Whitt-Moin
*• • •
"»"-»t—i—i**i—r»i—i—r—«t—i
20 30 40 50 60 70
WhilfFtmoiti
20 30 40 50 60 70
Age
Percentage ot iutimal surface involved with raised atherosclerotic lesions in carotid arteries
oi autopsied N'ew Orleans inon and women, basal group of cases. Each point represents a case; the
triangle represents the mean of the age group.
Solberg LA, McGarry PA: Cerebral Atherosclerosis in Negroes and
Caucasians. Atherosclerosis 1972;16:141-145.
502
TABLE 14
Intracranial Arteries
100
90H
BO
70
60 H
50
40
30 H
20
ioH
90
BO
70H
GO
50
40
30H
20
10
Ncqro-Malt*
• :7
• • • /
rN^fO* rtflU i*n
m S
• ^%«^d*v: • •• V*
Whitt-IKain
■■yt—i
Or'+rfr
•••
Whltt-Fwwlt*
20 30 40 50 60 70
20 30 40 50 60 70
Age
Percentage of intimal surface involved with raised atherosclerotic lesions in intracranial
arteries of autopsied New Orleans men and women, basal group of cases. Each point represents a
case; the triangle represents the mean of the age group.
Solberg LA, McGarry PA: Cerebral Atherosclerosis in Negroes and
Caucasians. Atherosclerosis 1972;16:141-145.
503
TABLE 15
Age- and sex-adjusted mortality rates, by ethnicity, Los Angeles County, 1980
Age- and sex-adjustedf mortality rates per 100,000 population
Asians and Pacific Islanders
Los Angeles
Cause of death County White Black Hispanicf Japanese Chinese Filipino Korean
All causes 819.9 870.2 1038.3 814.8 482.5 362.8 137.2 421.8
Major cardiovascular diseases 409.4 429.5 472.0 390.6 255.3 157.0 84.2 143.8
Diseases of heart 313.4 331.2 353.4 307.8 161.7 99.2 57.8 82.1
Total IHD 194.0 207.7 192.5 177.7 106.9 47.4 31.4 63.9
MI and other acute IHD 90.9 97.9 88.3 82.3 55.4 28.1 18.8 13.1
Chronic IHD 103.1 109.8 104.3 95.4 51.4 19.3 12.6 50.9
Hypertensive disease 21.0 19.5 47.4 — — — — —
Cerebrovascular diseases 74.3 75.8 94.2 63.5 79.6 48.7 19.7 48.3
IHD - Ischemic heart disease; MI «■ myocardial infarction.
'From Chapman J, Frerichs Ft, Maes R: Cardiovascular diseases in Los Angeles, 1980. Los Angeles, 1983, American Heart Association, Greater Los Angeles
Affiliate, Inc.
t Direct method of adjustment with Los Angeles County population, 1980, as standard.
{Census tracts in which 75r< or more of the population are persons of Spanish-Hispanic origin or descent.
Haywood LJ: -Issues in the natural history and treatment
of coronary heart disease in black populations: Medical
management. Am Heart J 1984;108:683-687.
504
TABLE 16
181.7
■ MALE
E3 FEMALE
( ) RATIO MALE:FEMALE
JAPAN HAWAII
JAPANESE JAPANESE
(1.4) (1.3)
HAWAII U.S.
WHITES WHITES
(.94) (1.0)
Age-adjusted stroke mortality
(1970).
Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke
Incidence in Hawaii Japanese Men. The Honolulu Heart
Study. Stroke 1980;11:14-21.
505
TABLE 17
Ratio of age-adjusted Chinese-White death rates by sex,
for leading causes of death: United States, 1969-71
8
Heart disease
Cancer
Stroke
Accidents
Influenza Et pneumonia
Diabetes
Cirrhosis
Suicide
Homicide
Heart disease
Cancer
Stroke
Accidents
Influenza & pneumonia
Diabetes
Cirrhosis
Suicide
Homicide
Male
Female
W////////////////////////A -50
V///////////////////////////////////////A -74
V//////////////////////////////////77777A .73
V7/////////////////////////A -so
Y/////////////////////////////A .57
W////////////////////////////////A -64
W/////////////A .30
V////////////////////////////////////W^ 1 -42
1__________I__________L
0
.2
.4
.6
.8
1.0
1.2
1.4
Ratio of age-adjusted death rates
SOURCE: National Center for Health Statistics
Rice DP: Figures and Tables for "Health of the Chinese in America". Handout at Conference
on Health Problems Related to the Chinese in America. Department of Health and Human Services.
May 23, 1982, San Francisco, CA.
TABLE 18
O
_i
Q.
O
0.
o
o
o
o"
o
a:
ui
o.
>-
cr.
O
o
IS
(7)
D
-a
O
<
I
Ui
<
400 -i
300-
200-
100
80
40-
20-
10-
SScr"
0W9
0Wor»
-------ss
1970
1971
1972
1974
1975
—i
1976
1973
YEARS
Secular trends in age-adjusted cerebrovascular
disease mortality (ICDA codes 430-8) in Bexar County,
Texas, from 1970-1976 by sex and ethnic group.
Stern MP, Gaskill SP: Secular Trends in Ischemic Heart Disease and
Stroke Mortality from 1970 to 1976 in Spanish-surnamed and Other White
Individuals in Bexar County, Texas. Circulation 1978;58:537-543.
SS=Spanish Surname
507
TABLE 19
Average Annual Death Rate3 from Selected Leading Causes of f>ath:
Puerto RIcan-Born and White Non-Puerto RIcan-Born by Age and Sex:
New York City, 1969-71 (number of deaths per 100,000 population)
Males Females Ratio of Rater; ol Puerto Rican Rnm to Nnn PijpMo Riran While
Aqe (yenrs) Puerto nican Non-Puerto Rican White Puerlo Non Rican Rica -Puerto n While Mains F ornalns
Heart Disease (ICDA* 390-98. 402. 404-29)
25-34 19 10 9 6 1 77 1 A')
35-44 05 94 30 27 0 90 1 to
45-54 265 378 117 111 0 70 1 nri
55-64 616 995 393 347 0 0? i 1:1
65-74 1.610 2.166 1.01 T 1.102 0 74 0 92
75 and over 2.713 5,197 3.037 4.578 052 Ofifi
Malignant Neoplasms (ICDA 140-209)
25-34 13 16 11 17 079 0 66
35-44 48 52 53 75 0.9? 0 7(1
45-54 143 184 148 210 0.78 0 70
55-64 414 510 276 383 0.81 0 72
65-74 726 1.102 570 588 O.fifi D.Q7
75 and over 1.529 1,768 886 1.062 0.86 0.03
Cerebrovnscul; lr Disease (ICDA 430-38)
25-34 6 3 4 3 2.21 1.10
35-44 21 10 16 10 2.11 1.65
45-54 44 29 36 25 1.52 1.45
55-64 97 80 92 59 1.21 1.r)H
65-74 216 267 302 196 0.81 1.5S
75 and over 495 918 771 974 0.54 0.79
Diabetes Mellitus (ICDA 250)
25-34 2 2 2 2 0 82 O.G0
35-44 7 6 4 4 1.12 n/m
45-54 19 15 17 10 1-31 1.73
55-64 52 35 72 71 1.47 2-60
Rosenwaike I: Mortality Among the Puerto Rican Born in New York
City. Social Science Quarterly 1983;64:375-385.
508
Age-specific daath rates for selected causes, Indian and Alaska Native population in 25 reservation states, 3-year
average (1973-1975) and U.S. All Races, 1974: rates per 100,000 population
Under 1 year 1-4 years 5-14 years 15-24 years 25-34 years 35-44 years 45-54 years 55-64 years 65 Years and over
All Causes Indian ..................... 2,342.3 1,755.7 127.1 48.3 32.2 7.5 94.9 40.9 49.2 28.4 42.4 22.0 6.8 5.1 0.0 1.7 3.8 239.0 86.9 0.5 1.7 1.1 15.3 2.8 150.2 73.9 80.7 29.2 35.8 9.9 44.9 19.3 5.4 2.9 4.6 2.0 0.0 0.8 0.8 5.4 5.9 11.7 4.7 0.1 0.4 0.1 0.4 0.4 63.6 38.2 40.4 18.4 19.2 8.7 21.2 9.7 2.9 1.7 1.7 0.9 0.0 1.1 0.6 0.2 0.0 4.0 5.2 2.2 1.3 0.2 0.1 0.2 376.2 121.7 230.5 61.6 160.5 40.5 70.0 21.1 6.9 4.5 4.5 2.8 0.0 1.5 1.4 0.9 0.0 7.1 6.9 2.6 1.7 0.6 0.5 3.4 0.4 0.4 0.4 578.0 146.8 245.1 45.4 155.5 25.3 89.6 20.0 25.4 14.0 19.6 9.4 0.3 4.8 3.6 1.0 0.0 12.7 15.0 10.0 2.5 3.8 1.9 60.8 4.2 0.7 0.4 773.1 278.6 202.0 40.0 105.6 19.0 96.4 21.0 84.4 72.0 65.0 55.7 1.3 0.9 17.2 13.3 1.8 0.2 37.1 55.1 26.5 5.7 15.5 4.3 139.7 18.6 1.8 1.7 1,150.7 675.0 208.1 43.5 97.6 18.3 110.4 25.2 251.6 259.8 192.4 215.5 2.8 2.0 47.4 35.3 7.8 1.0 101.5 183.8 49.6 11.1 35.1 11.4 179.0 38.7 2.8 7.0 1,729.7 1,549.2 188.0 51.2 86.4 19.5 101.7 31.7 607.6 720.9 451.0 590.8 9.2 4.3 123.8 99.6 23.7 5.9 269.0 437.0 64.2 26.6 86.4 31.7 123.8 50.9 14.5 27.3 4,6402
All Races ................... 6.172.9
Accidents Indian...................... All Races ................... 267.2 125.0
Motor Vehicle Accidents Indian ................... All Races ................ 90.7 27.9
All Other Accidents All Races ................ 174.0 97.1
Major Cardiovascular Diseases All Races .................... 2.0639 3.096.5
Diseases of the Heart Indian ................... 1.426.6
All RAces................ 2,758.4
Hypertension 9.8
26.3
Cerebrovascular Diseases 492.7
All Races ................ 869.0
Arteriosclerosis 83.3
153.3
Malignant Neoplasms 683.9
1.040.4
Influenza and Pneumonia 304.0
200.9
Diabetes Mellitus 171.6
132.6
Cirrhosis of Liver 68.6
42.1
Bronchitis, Emphysema and Asthma 31.9
94.7
Indian Health Trends and Services. U.S. Department of Health, Education
and Welfare. Public Health Service, Health Services Administration.
Publication No. 78-12009.
509
TABLE 21
Age adjusted mortality rates for selected causes among Indians and Alaska Natives in reservation states and the U.S.
All Races population, 1970 to 1975
INDIAN AND ALASKA NATIVE
Cause of death Number of deaths in: Rate per 100,000 Populat ion
1975 1970 1975 1974 1973 1972 1971 1970
All causes................. 5.774 1,335 965 291 70 9 1,256 704 552 508 355 281 145 64 27 185 180 5,268 1.340 933 326 71 10 1,116 595 521 421 276 314 143 63 33 125 105 824.8 202.5 147.4 43.5 10.1 1.6 170.5 94.1 76.4 79.8 61.4 36.1 23.8 9.9 3.7 26.5 26.0 872.6 235.6 169.5 50.1 12.9 3.0 163.2 86.7 76.5 88.4 66.7 30.7 24.4 9.8 4.3 31.7 21.8 968.8 237.0 167.7 53.0 13.4 2.9 202.7 117.1 85.6 81.6 66.0 49.9 28.4 9.1 6.9 31.7 22.9 881.6 229.3 165.4 490 6.8 2.7 185.1 107.1 78.0 81.3 60.5 39.0 29.3 10.7 2.8 25.7 20.6 935.5 251.1 182.6 32.8 12.0 2.6 183.0 96.5 86.5 84.4 66.8 41.6 31.7 10.6 6.6 26.4 21.8 889.6
Major Cardiovascular Diseases ................ 237.2
Diseases of the Heart....................... 168.8
Cerebrovascular diseases.................... 55.0
Arteriosclerosis.............................. 11.8
Hypertension................................ 1.7
Accidents.................................... 181.8
Motor Vehicle.............................. 98.5
All Other .•.................................. 83.3
Malignant Neoplasms.......................... 79.5
Cirrhosis of the Liver.......................... 56.9
Influenza and Pneumonia..................... 46.7
Diabetes Mellitus............................. 27.1
Tuberculosis, all forms........................ 11.4
Bronchitis, Emphysema and Asthma........... 5.7
Homicide..................................... 22.2
17.9
Indian Health Trends and Services. U.S. Department of Health, Education
and Welfare, Public Health Service, Health Services Administration.
Publication No. 78-12009.
510
TABLE 22
i0° t"
to :
40
to
iob
4
600
I»ii0 m>o txo
—r—i iii i;
40
to
DIPHTHERIA
I HAT 6 UNCtA«QUAH»|
8.
o
S .0
-1
3 *
X
I
ItOQ IfcQ littQ HM l»40
l>00 IttO 1920 ISM 1*40
IT
, SCARLET FEVER
; i*AU UAOW 10YIAASI
4
400
too
100
to
40
too
400
it 00
. WHOOPING COUGH
. IhAlC UhOfcft KOUAtttl
■»---1---1---1---1 t I---HH---h
TUBERCULOSIS (ALL formsl
J—I t t I t---1—HH---*
8 *
I
i—I I I I I, I t I »
£ . - DIARRHEA AND ENTERITIS.
(fCM UMOUVt ttfllHtl
too
400
100
i* 100
=*—1---1 I I---►—»----•---r—♦;
E PNEUMONIA lALL FORMS) 5
to
40
DISEASES OF THE HEART
(ALL FORMS)
-t-H—i—lit!—t ■■ t t
«00t INTRACRANIAL LESIONS
OF VASCULAR ORIGIN
1001-
100
to
-I- I I I I___I I I, I 1
3 *o
© to
* too
►- too
a
x tO
3*
H--> I «--1--H-*---1--HH-
I SYPHILIS (ALLFORMS)-
+-H—I—hH—till—*■
NEPHRITIS(ALL FORMS)
l i l
J___I---LI -L
a—I—h—1—I i t t I—r
I"
56 40
«
M
>
5 •
rt
4
I
I
400
COO
: DIABETES MELLITUS :
^—i—I I t i—i—|—i—r-j
ACUTE RHEUMATIC
FEVER
* i i—i i l i I i i
. CANCER
100-
to-
J--1___I___L
ttOO 1*0
l»«0 i»W i»*0
UA*
rtOO UtO HiO imO i»40
?»AA
l»00 IttO
t I I ■ ■ I x
t»iO i»*0
UAH
itio
Course of mortality for selected causes of death in the
expanding death registration States (logarithmic scale),
1900-1945.
Moriyama IM, Gover M. Statistical studies of heart diseases
U.S. Public Health Service, April 23, 1948.
511
TA&LE 23
AGE ADJUSTED DEATH RATES (AGE 45-74) FOR CEREBROVASCULAR DISEASE
(UNDERLYING AND CONTRIBUTING) BY RACE AND SEX
EACH DECADE BALTIMORE AND MEMPHIS*
IOOO-
900-
800H
700
600
500-
400
O
o
o
o"
2 300-
UI
<
200-
100
NM-NF
NM
— Baltimore
—— Memphis
'Age adjusted to the estimated I960 Baltimore population.
1930
31
1940
1
41
—, ,
1948 I960
1 1
49 61
Kuller L, Seltser R, Paffenbarger RS, Krueger DE. Trends in
cerebrovascular disease mortality based on multiple cause
tabulation of death certificates 1930-1960. Am J Epidemiol
1969;88:307-317.
512
TABLE 24
Age Adjusted Annual Decrease in Stroke Mortality
1968-1978 By Race and Sex in Percentage
White White Black Black
Women Men Women Men
1968-1978 5.0 4.6 5.5 6.8
1968-1973 2.0 2.3 3.1 3.6
1974=1978 7.8 6.8 6.7 8.8
Arteriosclerosis 1981, Vol. 2. U.S. Department
of Health and Human Services, PHS NIH # 82-2035.
513
Table 25
Trends of Mortality Rates from Cerebrovascular Diseases (ICD 430-438),
Age-Adjusted, Persons Age 35 to 74 by Sex-Color,
United States, 1968-78
White White Nonwhite Nonwhite
Year Men Women Men Women All
1968 155.4 110.8 340.2 292.1 148.1
1969 150.3 106.8 317.1 274.3 142.2
1970 146.8 105.8 304.0 261.9 139.3
1971 143.8 100.7 292.9 248.6 134.2
1972 144.8 99.7 280.4 249.8 133.6
1973 137.4 96.8 282.0 239.8 128.7
1974 129.4 91.3 260.8 216.6 120.7
1975 117.8 83.7 233.7 190.1 109.7
1976 108.9 78.5 216.6 176.9 102.2
1977 100.9 72.4 202.2 162.4 94.6
1978 93.9 68.7 194.7 148.6 88.7
Change 196fi i-78 -62.1 -42.1 -145.5 -143.5 -59.4
Percent Change -40.0 -38.0 -42.8 -49.1 -40.1
Slope 1968- •73 -0.0174 -0.0190 -0.0348 -0.0359 -0.0288
Standard Error 0.0035 0.0036 0.0049 0.0048 0.0032
Slope 1973- 78 -0.0789 -0.0707 -0.0769 -0.0951 -0.0761
Standard Error 0.0017 0.0021 0.0054 0.0041 0.0020
Report of the Working Group on Arteriosclerosis of the National
Heart, Lung and Blood Institute. Arteriosclerosis 1981.
Volume 2.
514
TABLE 26
Average
annual
incidence
rates
300
200
1<
70 r
60
so
10
Men
Women ^^ ^*"***
1945-49 1955-59 1965-69 1975-79
1950-54 1960-64 1970-74
Calendar years
Five-year average annual incidence rates per
100,000 population for all first episodes of stroke in men and
women in Rochester. Minnesota, age adjusted to I960 US white
population.
Whisnant JP: The Decline of Stroke. Stroke 1984;15:160-168
515
TABLE 2
7
Trends in Age Specific Stroke Mortality in Georgia and
Pennsylvania, and U.S. by Race and Sex 1968-1978
Age 45-54
Georgia Pennsylvania
Year White Women White Men Black Women Black Men White Women White Men Black Women Black Men
1968 33 53 234 302 35 38 101 105
1969 36 50 216 271 28 38 95 127
1970 45 47 158 301 35 39 96 103
1971 34 49 227 259 29 36 101 111
1972 39 48 181 313 31 34 111 131
1973 41 31 182 229 30 36 79 123
1974 26 35 140 201 23 28 91 93 i
1975 29 42 140 148 25 32 56 81
1976 31 40 143 162 24 24 62 56
1977 22 30 113 137 22 27 60 74
1978 1 26 35 97 143 21 24 53 92
Data provided by National Center for Health Statistics.
TABLE 28
Trends in Stroke Mortality 1974-1978 By State: In
Percent, Annual Change, Age Adjusted (35-74)
White White Black Black
Women Men Women Men
6.6 6.7
9.2 6.0
10.0 11.0 18.2 -1.0
6.9 8.2 11.2 6.1
4.8 9.1 10.9 7.3
6.8 8.4 9.0 8.3
6.7 6.1 10.4 6.1
5.8 10.9 6.4 6.6
5.0 10.0 9.9 5.3
Center for Health Statistics.
Colorado
Connecticut
Massachusetts
Maryland
North Carolina
Pennsylvania
Georgia
South Carolina
Mississippi
National
517
TABLE 29
Changes in Cerebrovascular Disease Death Rates by
Country for Men Ages 55-64, 1970 and 1980, per 100,000
Country 1970 1980 Change % Change
Japan 444 204 240 54
U.S. Black 343 190 153 45
Australia 175 120 55 31
Canada 105 67 38 36
England and Wales 155 114 41 26
West Germany 160 111 49 31
U.S. Whites 120 64 56 47
New Zealand 137 112 25 18
Sweden 87 72 15 17
Poland 85 125 40 47
WHO Annual Report.
TABLE 30
Percentage Decline in Stroke Mortality
By Age, Race and Sex 1970-1980
WM WW BM BW
35-44 44.9 41.7 44.6 56.0
45-54 39.0 38.7 39.8 48.2
55-64 47.6 37.6 44.8 48.9
65-74 42.9 43.0 39.3 46.2
7 5-84 37.2 37.9 26.0 31.3
Health United States, 1983.
519
TABLE 31
L
i ' « »_________i_________i________i_________i________i_________i_________i_________' * «.....■ ■
1955 196C 196S 1970 1975
Mortality from cerebrovascular disease in population aged 55-64, (1955-1974).
Tseng WP, Epidemiological study of hypertension and stroke in
Taiwan. In: Prophylatic Approach to Hypertensive Diseases,
Y. Yamori et al. (eds.), Raven Press, New York, 1979.
520
TABLE 32
Age-Specific Prevalence Rates of Stroke (per 1,000) Found in Examination, 1967 Through 1969
Age White Men White Women Black Men Black Women
First Exam-ination, yr Population Examined No. of Cases Rata Population Examined No. of Cases Rate i-Population Examined No. of Cases Rate Population Examined No. of Cases Rate
_i34 198 *» 196 1 5.1 82 110
35-44 152 3 19.7 175 63 2 31.7 93 2 21.5
45-54 223 9 40.4 221 2 9.0 133 9 67.6 147 7 47.6
55-64 138 7 50.7 161 5 31.0 61 5 82.0 109 2 18.3
>65' 60 9 150.0 102 3 29.4 47 2 42.6 59 7 118.6
Total _S35 yr 573 28 659 10 304 18 408 18
All ages 771 28 855 11 386 18 518 18
Age-adjusted rate <35 53.2 15.0 58.6 43.4
All ages 40.9 12.7 45.0 33.4
• Only 11 persons were greater than 75 years of age. two of whom had cerebrovascular disease.
Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the
Biracial Population of Evans County, Georgia. Arch Intern Med 1971;128:949-955
521
TABLE 33
Prevalence of stroke in examined cohorts as determined by neurologists
Japan" Hawaii* 1 California' Significance level"
Age group N Rate/1.000 /V Rate/1,000 N Rate/1,000
Definite cases only
45-49 0 - 0 - 2 2.7 NS
50-54 5 20.3 14 4.9 4 7.6 <0.02
55-59 16 41.3 12 6.2 2 7.4 <0.001
60-64 19 49.5 25 19.2 3 18.1 <0.01
65-69 28 72.4 29 34.2 3 19.4 <0.01
Total 68 46.6 80 10.7 14 7.6
Age-adjusted 35.4 10.7 10.4
rate' Definite and possible cases
45-49 0 — 1 2.0 4 5.5 NS
50-54 7 28.5 21 7.3 5 9.6 <0.01
55-59 17 43.9 18 9.3 3 11.0 <0.001
60-64 23 59.9 31 23.8 3 18.1 <0.01
65-69 33 85.3 41 48.4 4 25.8 <0.01
Total 80 549 112 15.0 19 10.3
Age-adjusted 42.5 15.0 13.0
rate'
"In Japan,-85% of definite and possible stroke cases were seen by the neurologist.
Remaining cases diagnosed by neurologist from review of clinic records and occasionally
from hospital records.
* In Hawaii. 62% of definite and possible stroke cases were seen by the neurologist.
Remaining cases diagnosed by neurologist from review of clinic and hospitalization
records. The latter were usually available.
r In California, 74% of definite and possible stroke cases were seen by the neurologist.
Remaining cases were classified as definite stroke or no stroke on the basis of the screen-
ing test results.
"Chi square test with two degrees of freedom.
' Age-adjusted by direct method to age structure of Hawaii cohort.
Kagan A, Popper J, Rhoads GG, et al: Epidemiologic studies
of coronary heart disease and stroke in Japanese men living
in Japan, Hawaii, and California: Prevalence of stroke.
Cerebrovascular Diseases, edited by P. Scheinberg, Raven
Press,-New York, 1976.
522
TABLE 34
Number of Hospital Discharges* for Stroke
By Race and Average Length of Stay 1981
Discharges Average Length of Stay
______________________(in 1, OOP's)________________(DaVs) ______.
White 707
All Others 100
Total 806
*First Level Diagnosis Only
National Center for Health Statistics,
12.2
14.2
12.4
Hospital Discharge Survey.
523
TABLE 35
Stroke Economic Costs (1980)
Total $5.1 Billion
Hospital 52%
Nursing Home 35%
Professional Ser. 11%
Drugs 2%
Per Capita
<65 Men $8
Women $7 _„
>65 Men $128
Women $147
Total
Per Capita <65 Men $627
Women $791
>65 Men $2,278
Women $2,667
Health Care Financing, Summer, 1984.
524
TABLE 36
Swniur «'/ ("i.M. and liuidctuv" Kttln tor Slmkc. .S<»i.//» .\Uihmim Study /'cpuluiiim. l9ir«tkc*« Female number of Mr« »kes Total number of strokes
As_c All l-irv| Incidence rates All Hirvt Incidence rales All First Incidence rales
211-54 5 4 4V 4 3 35 9 7 42
55- 64 5 5 274 6 s 233 II 10 252
65-74 K 7 541 6 6 365 l-l 13 442
75 + II It) 1.3X5 8 K 719 19 18 981
All uecs 29 2ft 24 •>■> 53 48
Crude rate 136 107 121
Ape-adjusted ratc+ 139 88 109
Black
Male number of stroke* Female number of strokes Total number of strokes
Age All Kirsl Incidence rates All First Incidence rates All First Incidence rates
20-54 7 3 32 9 8 64 16 II 50
55-64 14 13 566 19 18 712 33 31 642
65-74 16 14 1.106 19. 16 957 35 30 1.021
75 + 5* 3 482 IK 16 1.824 23 19 1.268
All aces 42 33 65 58 107 91
Crude rate 110 174 144
Ace-adjusted rate* 172 236 208
'Rate of initial strokes per 100.000 persons.
tAgc-adjustcd rates based on the NINCDS National Survey of Stroke, indirect method.
?0nc case had unknown jxior stroke history in each of these categories.
Gross CR, Kase CS, et al: Stroke in South Alabama: Incidence
and Diagnostic Features—A Population Based Study. Stroke 1984-
15:249-255.
525
TABLE 37
Ftva-yaar incidanca of fatal and nonfatal atroke by race and aax for Slopped Care
(SC) and Rata.rod Care (RC) participanta. Data are adtualad for *o« and entry dieatoilc
blood proaaura. Shaded portion indicalaa fatal atroke; white portion, nonfatal atroke.
a
a
2.9
m
'RC
i
t a
7"
Ksc
34 6%
37
i
RC
I Ifl2% ,---,
y 33
3.1
'SC4
1
RQ<
_■_•_■
'46 6%
i.a
F77
2.6
VA
1
1.6
7""
40.0%
2.3
W>
[ 3C
30.4%
i.a
sc
All tiucfc Man Buck WomM Wlwia Man ww» Woman
Five-Year Findings of the Hypertension Detection and Follow-up
Program. III. Reduction in Stroke Incidence Among Persons
with High Blood Pressure. JAMA 1982;247:633-638.
526
TABLE 38
Stroke Registry in Vxuian 197.1-76 Incidence Rales________________
Malta ____________Females
No. of Incitlrnoe
patients per l.(KX)
0 —
1 0.01
3 0.01
8 0.08
16 0.4
25 1.4
27 2*1
4 l.:i
5 2.1
RO 0 1 i
No. of Incidence
Age io yra patieola per 1.000
0-0 0 —
10-10 4 0.03
20 20 r, 0.01
;io no 18 0.12
40-40 64 0.0
m-u\ 66 2.6
li»l *M 50 6.4
70-70 2H 7.8
WJ 6 220 2.0
0.26
Osuntokun BO, Bademosi 0, Akinkugbe 00, et al: Incidence of Stroke
an African City: Results from the Stroke Registry at Ibadan, Nigeria,
1973-1975. Stroke 1979;10:205-207.
TABLE 39
u .•.«.*•«• Animal Ituidnu c of Dt funic and Pa>.\ihh' Sin ike per HMK) by Aft'
Japan I972-78 Haw aii l9o5-73
No. «i| No. of No. of No. of
Age subjects cases Ratet subjects cases Kate Test+t
45-49 54 0 0.0 1825 II 1.0 NS
50-54 239 7 7.3 2766 39 2.3 * *
55-59 J67 11 7.5 1569 21 2.2 ***
60-64 357 17 11.9 1306 37 4.7 ***
65-69 349 27 19.3 429 18 7.0 . *«
Total 1366 62 11.3 7895 126 2.7
Age adjusted raict+t 7.4 2.7 .*«
^Annual Incidence rate is calculated as follows: Japan: (No. of cases/No. of subjects)'4 (Years follow-up). Hawaii:
(No. of cases,No. of subjects.,6 i Years follow-upl
■f*X2 lcsl of ,xvo ra,C;> between two cohorts NS: /> > 0.10. •: p < 0.05. *•: p <»0.0I. ***: p < 0.001
t+^Calculated by the indirect method wiih Hawaii as standard
Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii
and California: Incidence of Stroke in Japan and Hawaii.
Stroke 1984;15:15-23.
528
TABLE 40
Incidence rate, death rate, and prevalence rate of stroke per 1,000 per annum, by age and
sex, Taipei, 1975
Age and
sex
Male
<54
55-64
65+
Total
Female
<54
55-64
65+
Total
No. of
subjects
23,632
1,467
892
25,991
21,832
1,268
1,069
24,169
Incidence
No. %
13
17
23
53
2
8
20
30
0.6
11.6
25.8
2.0
0.1
6.3
18.7
1.2
4
11
12
27
2
7
15
24
Death
No.
%
0.2
7.5
13.5
1.0
0.1
5.5
14.0
1.0
Prevalence
No.
28
31
66
125
6
17
46
69
%
1.2
21.1
74.0
4.8
0.3
13.4
43.0
2.9
Tseng WP. Epidemiological study of hypertension and stroke in Taiwan.
In: Prophylactic Approach to Hypertensive Diseases, Y. Yamori et al.
(eds.), Raven Press, New York, 1979.
TABLE 41
0\
trail Incidence Rates* for Stroke by Diagnostic Category. Rate and Sex South Alabama Study Population, 19H0
Diacnosis
Total"!
Athcro-
ihrombotic
infarction
Unspecified
origin
infarction
Embolic
infarction
Lacunar
infarction
Parenchy-
matous
hemorrhage
Subarachnoid
hemorrhaec
All cases 160(1001$ 9(6) 64(40) 42(26) 20(13) 13(8) 9(6)
crude rate 282.4 15.9 113.0 74.1 35 J 22.9 15.9
White
male number 29( 100) 0 9(31) 12(41) 5(17) 2(7) 0
rate 242.7 0 75.3 100.4 41.8 16.7 0
female number 24(100) 0 10(42) 6(25) 2(8) 1(4) 3(13)
rate 177.3 0 73.9 44.3 14.8 7.4 22.2
Black
male number 42(100) 5(12) 13(31) 15(36) 4(10) 5(12) 0
rate 307.5 36.6 95.2 109.8 29.3 36.6 0
female number 65(100) 4(6) 32(49) 9(14) 9(14) 5(8) 6(9)
rate 371.2 22.8 182.8 51.4 51.4 28.6 34.3
•All strokes per 100.000 persons aged 20 and over.
^Includes 139 initial stroke cases. 19 recurrent stroke cases. 2 cases with unknown CVD history. Three cases which had other stroke
diagnoses arc in the total but not listed by diagnosis.
.Numbers in parentheses are the piuponions of cases in each diagnostic category.
Gross CR, Kase CS, et al: Stroke in South Alabama
and Diagnostic Features—A Population Based Study.
15:249-255.
Incidence
Stroke 1984;
530
TABLE 42
Xuinbcr of Stroke Cases by Subiypr and Certainty
Diagnosis — Japan and Hawaii
Japan Huwaii
Defi- Pos- Defi- Pos-
Subt\pc Total nite sible Total nite sible
Tolal 62 38 24 126 71 55
ICH 18 12 6 34 26 S
T-E 44 26 18 74 42 32
Unknown 0 0 0 18 3 15
Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii
and California: Incidence of Stroke in Japan and Hawaii.
Stroke 1984;15:15-23.
531
TABLE 43
Average Annual Stroke Incidence Per 1000 by Age and Subtype — Definite Cases Only__________________________
Total Intracranial hemorrhage Thromboembolic stroke
Japan Hawaii Japan Hawaii Japan
Age No. of cases Rate No. of cases Rate No. of cases Rate No. of cases Rate No. of cases Rate No. of cases Rale
45-49 0 0.0 6 0.55 0 0.0 2 0.18 0 0.0 3 0.27
50-54 6 6.3 22 1.3 4 4.2 10 0.60 •» 2.1 II 0.66
55-59 7 4.8 13 1.4 2 1.4 3 0.32 5 3.4 10 I.l
60-64 II 7.7 21 2.7 i 1.4 9 i.l 9 6.3 12 1.5
65-69 14 10.0 9 3.5 4 2.9 ■> 0.77 10 7.: 6 2.3
Total 38 7.0 71 1.5 12 2.2 26 0.55 26 4.S 42 0.S9
Age ad-
juslcd
rate 4.7 1.5 1.7 0.55 _____JJ)
Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii
and California: Incidence of Stroke in Japan and Hawaii.
Stroke 1984;15:15-23.
532
Risk factor
and r_)ce-sex
group_______
TABLE 44
Mean systolic and diastolic blood pressure and mean serum cholesterol
of adults 25-74 years by race, sex and survey period showing standard
errors and age-adjusted* means: United States, 1971-75 and 1976-80.
1971-75
Mean
Standard
error
1976-80
Mean
Standard
error
1971-75
Age-adjusted*
mean
Standard
error
1976-80
Age-adjusted* Standard
mean error
Systolic blood pressure
(mmHg)
White men 132.8 0.5 130.5 0.6 132.8 0.5 130.6 0.7
White women 130.1 0.5 125.6 0.7 129.4 0.4 125.1 0.7
Black men 140.0 1.6 133.2 1.1 140.4 1.7 133.7 1.1
Black women 137.8 1.4 130.6 1.2 138.6 1.4 131.7 1.1
Diastolic blood pressure
(mm Hg)
White men 83.7 0.3 82.3 0.5 83.6 0.3 82.2 0.5
White women 80.4 0.4 78.1 0.5 80.1 0.3 78.0 0.5
Black men 89.9 1.0 85.3 0.8 89.8 1.0 85.5 0.8
Black women 87.0 0.9 82.3 0.6 87.1 0.8 82.6 0.6
Serum cholesterol
(mg/dl)
White men 218.0 1.1 216.7 1.2 217.5 1.0 216.7 1.1
White women 222.8 1.1 220.7 1.2 221.4 1.0 219.9 1.2
Black men 225.5 4.5 214.7 3.1 225.7 4.9 214.9 2.8
Black women 219.4 2.9 216.9 3.0 221.2 2.6 219.0 2.6
*Age-adjusted by direct method to the total U.S. population as estimated at the midpoint of the 1976-80 National
Health and Nutrition Examination Survey.
SOtBCE: Division of Health Examination Statistics, National Center for Health Statistics: Data from the National
Health ahd Nutrition Examination Survey.
Rowland ML, Fulwood R: Coronary "Heart Disease Risk Factor Trends in Blacks Between the First and Second
National Health and Nutrition Surveys, United States, 1971-1980. Presented at American Heart Association
c.vmmm iimi on rnrmv.rv llrirl l.i,ci .r> in R1 1 r l- Pnnnlil ii.n«-- Mirrli S 1Q81
TABLE 45
Prevalence rates of elevated blood pressure levels* for black persons
25-74 years by sex and age: United States, 1971-75 and
1976-80.
Sex and Age
Men
Age-adjusted* rate for 25-74 years,
25-34 years..........................■
45-44 years..........................■
45-54 years..........................-
55-64 years..........................
65-74 years...............•..........
Women
Age-adjusted* rate for 25-74 years
25-34 years.....................
35-44 years.....................
45-54 years.....................
55-64 years.....................
65-74 years.....................
Elevated blood pressure*
1971-75
Standard
1976-80
Standard
Rate
error
Rate
error
Per 100 population
35.7
3.7
23.1
1.8
16.4 5.7 11.7 2.4
37.7 8.8 22.3 4.4
34.7 6.8 23.0 5.7
59.9 6.5 39.2 4.5
43.7 8.0 27.5 3.0
30.5
2.7
24.4
2.4
..... 12.4 5.1 5.7 5.4 7.4 6.7 4.3 17.6 37.3 36.4 43.4 l.S
..... 23.9 4.1
..... 39.4 5.6
..... 46.0 6.2
..... 46.7 5.8
* Systolic blood pressure of at least 160 mm Hg and/or diastolic blood pressure of
at least 95 mm Hg.
♦ Ase adiusted by direct method to the total U.S. population as estimated at the
midpoint of the 1976-80 National Health and Nutrition Examination Survey.
SOURCE- Division of Health Examination Statistics, National Center for Health
Statistics: Data from the National Health and Nutrition Examination Survey,
Rowland ML, Fulwood R: Coronary Heart Disease Risk Factor
Trends in Blacks Between the Firsthand Second National
Health and Nutrition Examination Surveys, United States, 1971-80.
Presented at American Heart Association Symposium on Coronary
Heart Disease in Black Populations, March 5, 1983.
534
TABLE 46
Mean systolic blood pressure ( zSD) in Laredo Project participants and HANES I subjects, by sex
:e n Laredo HANES 1(1)
Ag "Spa nish- US US
(years) __to ject Mexican white black
American"
Men
35- ■44 18* 129.2 £ 19.1 124.7 £ 12.8 127.0 = 14.8 136.7 £ 18.8
45- -54 37 134.4 £ 18.1 140.1 £ 15.0 134.7 £ 19.7 141.7 £ 28.2
55- -64 42 132.1 r 25.7 139.9 r 19.9 139.6 £ 20.4 144.2 £ 23.0
65- -74 30 150.3 .t 29.2 146.0 £ 19.4 146.0 = 24.1 156.6 £ 28.3
Women
35- -44 34* 119.2 _c 20.6 122.4 £ 19.8 122.6 £ 18.7 130.5 £ 21.4
45- -54 93 126.9 £ 18.3 130.0 r 17.5 131.1 £ 22.2 150.8 £ 35.1
55- -64 70 134.8 r 21.6 144.8 ~ 28.0 143.0 £ 25.2 153.4 r 27.4
65- -74 65 155.7 £ 25.5 150.1 £ 21.2 151.6 £ 24.7 161.3 r 28.7
Mean diastolic blood pressure (±SD) in Laredo Project participants and
HANES I subjects, by sex
Men
35-44 18* 89.6 £ 13.3 81.8 £ 9.7 84.2 £ 11.3 91.2 £ 12.1
45-54 37 88.3 £ 10.6 86.5 £ 9.3 87.5 £ 12.7 91.9 £ 16.5
55-64 42 82.6 £ 12.6 86.8 £ 7.3 86.4 £ 12.0 93.4 r 14.1
65-74 30 84.5 £ 11.5 82.4 £ 10.6 Women 84.9 £ 13.0 90.9 _= 14.0
35-44 34* 79.2 £ 13.0 78.3 £ 11.8 79.3 £ 12.0 86.9 £ 13.7
45-54 93 80.5 £ 9.3 83.7 £ 10.5 82.6 £ 13.1 93.5 r lo.o
55-64 70 80.9 £ 10.3 85.8 £ 9.9 86.2 £ 12.4 90.6 £ 13.9
65-74 65 77.5 £ 12.4 81.6 £ 10.8 85.4 £ 12.5 90.4 = 15.9
♦ Age range 40-44 years for Laredo Project participants.
Stern MP, Gaskill SP, Allen CR, et al: Cardiovascular Risk Factors in
Mexican Americans in Laredo, Texas. Am J Epidemiol 1981;113:556-562.
535
TABLE 47
Systolic blood pressure levels by age and sex among Minneapolis American Indians and Twin Cities whites
Clinical screenings (whites)
Little Earth Other site screenings Average
Average second/ Average second/ second/
First SBP third SBP First SBP ' third SBP First SBP third SBP
n X (SD) X (SD) a X (SD) X (SD) n X (SD) X (SD)
Men 15-24 13 119.5 (15.8) 117.5 (14.3) 36 121.7 (11.6) 120.6 (13.1)
25-34 11 121.5 (13.3) 120.4 (13.3) 49 125.2 (13.8) 125.3 (13.2) 265 117.7 (11-5) 117.7 (U.l)
35-54 13 138.2 (17.8) 139.4 (18.9) 32 127.1 (11.7) 126.8 (11.7) 419 121.4 (13.9) 121.4 (13.5)
55-34 8 136.8 (19.0) L31.5 (15.8) 10 138.0 (19.1) 141.2 (17.3) 235t 131.1 (17.6) 131.0 (17.1)
All ages 45* 128.5 (18.1) 127.2 (17.9) 127* 125.7 (13.7) 125.6 (14.0) 919 122.8 (15.3) 122.8 (14.9)
Women
15-24 34 114.3 (10.3) 113.2 (10.2) 35 113.7 (12.6) 112.8 (12.2) —
25-34 33 112.9 (10.6) 113.8 (11.0) 42 115.4 ( 9.2) 117.0 (13.0) 343 108.5 (11.3) 103.5 (11.0)
35-54 25 122.9 (17.1) 123.4 (18.6) 46 122.9 (12.0) 122.9 (13.7) 451 116.1 (14.9) 116.0 (14.8)
55-34 13 129.1 (10.1) 129.7 ( 8.2) 15 132.1 (21.2) 133.3 (18.9) 237t 134.3 (19.5) 133.6 (19.0)
AH a,;es 105* 117.7 (13.6) 117.8 (13.9) 138* 119.3 (13.8) 119.6 (15.0) 1031 117.8 (13.4) 117.6 (18.0)
SBP = systolic blood pressure
'Excludes participants with missing age. sex, or blood pressure data.
Twin Cities whites, 55 to 74 years old.
Gillum RF, Gillum BS, et al: Cardiovascular risk factors among urban
American Indians: Blood pressure, serum lipids, smoking, diabetes, health
knowledge, and behavior. Am Heart J 1984;107:765-777.
536
TABLE 48
Systolic Blood Pressure Medians by
Age, Area, and Generation
mmHg
150
120 JAPAN'/ ...
•' CALIF ISSEI
45-49 50-54 55-59 60-64 05-69
AGE
Winkelstein W, Kagan A, Kato H, Sacks S: Epidemiological
Studies of Coronary Heart Disease and Stroke in Japanese
Men Living in Japan, Hawaii and California: Blood Pressure
Distributions. Presented at 101st Annual Meeting,
American Public Health Association, San Francisco, California,
November, 1973.
537
TABLE 48 (cont.)
Diastolic Blood Pressure Medians by
Age, A rea, and Generation
mm Hg
100
CALIF NISEI
90
z
<
~ 80
CALIF ISSEI
PQ
Q
70
45-49 50-54 55-59 60-64 65-69
AGE
Winkelstein W, Kagan A, Kato H, Sacks S: Epidemiological
Studies of Coronary Heart Disease and Stroke in Japanese
Men Living in Japan, Hawaii and California: Blood Pressure
Distributions. Presented at 101st Annual Meeting,
American Public Health Association, San Francisco, California,
November, 1973.
538
TABLE 49
Systolic Blood Pressure Msdians* Adjusted to Relative
Weight Differences by Age, Area and Generation:
Japan, Hawaii and California
(Unadjusted medians shown in parentheses)
Age
45 - 49
50 - 54
55 - 59
GO - 64
65 - 69
Japan Hawaii Califo rnia
Issei Nisei Issei Nisei
123 124** 122 119** 129
j (120) (122) (128) (118) (130)
127 125 124 127 132
(128) (128) (130) (128) (136)
131 130 126 132 141
(130) (132) (132) (140) (140)
138 130 132 140 134
(138) (134) (136) (114) (140)
142 134 136 146 135
(HO) (140) (138) (146) (142)
• Median = mean of medians fiom the rclatixe weight groups:
< 90,90-100.100-110. 110-120. 120-130, > 130.
•* Values based on n < 30.
Winkelstein W, Kagan A, Kato H, Sacks S: Epidemiological
Studies of Coronary Heart Disease and Stroke in Japanese
Men Living in Japan, Hawaii and California: Blood Pressure
Distributions. Presented at 101st Annual Meeting,
American Public Health Association, San Francisco, California,
November, 1973.
539
TABLE 50
180
MEN
-----US. 1960-62
—— Framingham. Mass
—— Taipei. Taiwan
Japanese
Nutrition
Taiwan, 1976
en
I
140
K
3
w.
__
a.
-a
o
o
m
SYSTOLIC
100
601-
........ _—^ ^
DIASTOLIC
L
20 30 40 50 60
Age (in years)
7d
60
Mean blood pressure, by.age for men: five surveys.
Tseng WP. Epidemiological study of hypertension and
stroke in Taiwan. In: Prophylactic Approach to Hypertensive
Diseases, Y. Yamori et al. (eds.) , Raven Press, New York, 1979
540
TABLE 51
Prevalence of Hypertension for Japanese Males
by Age and Geographical Location
Age Japan Hawaii California Definite Hypertension (Prevalence/1000) Japan Hawaii California Borderline Hypertension (Prevalence/1000)
45-49 139 142 234 163 222 306
50-54 194 183 286 203 221 280
55-59 255 199 263 199 252 253
60-64 280 247 384 239 236 292
65-69 318 352 423 278 288 245
Age-Adjusted Rate 223 194 315 215 235 285
No. of men 2127 7998 1795 2127 7998 1795
Winkelstein W: Cooperative studies of blood pressure in
Japanese in Japan, Hawaii and the United States. In:
Epidemiology and Control of Hypertension, edited by
Oglesby Paul, Stratton Intercontinental Medical Book
Corporation, 1975.
541
TABLE 52
Prevalence of left-ventricutar toyfwrwaffcy tad hypawwivt n«__n liiwi— anwug Jap__»
mm rmi. br geographical loom*.
Af*a__juswd provaiancsMOOO
a*-* lasaA to-2127) Hawaii to - 7991) California to-1795)
LaA-venincuUr hypertrophy • Hypertensive heart tiitmn * 144 5.1 4.1 44
■ Uft-vcmricular hypertrophy - Mmimmu Cartes 3-4 »*_» 4-1, 4-2 or 4-3 piuc 5-1. 5-2 or
• Definite hypertension (sy«ohc > M» wwwi95 mm Hg and Screen 2 DBP >90 rain Hg by Color
Abnormality
Q-QS
ST Depression (A.1-4.3)
Negative T Waves (5.1-5.3)
A-V Conduction Defects (6.1-6.3)
Ventricular Conduction Defects
(7.1-7.8)
Rhythm (8.1-8.6)
Low QRS (9.1)
ST Elevation (9.2)
Lai'c Axis deviation (£30°)
Rifcht Axis deviation (>+120°)
liigh R - left (3.1)
High R - right (3.2)
Hi£h R (3.3)
5.1-5.3^ or left axis deviation
^-20°, or 3.1 or 3.3
.Any Abnormality
Non- black
Black (..=623) (N -6367) Total No. (N-6995)
No. Percent No. Percent Percent
18 2.9 95 1.5 113 1.6
20 3.2 168 2.6 188 2.7
60 9.6 304 4.8 364 5.2
11 1.8 74 1.2 85 1.2
24 3.8 423 6.6 447 6.4
27 4.3 242 3.8 269 3.9
0 0.0 2 0.0 2 0.0
56 8.9 70 1.1 126 1.8
17 2.7 208 3.3 225 3.2
1 0.2 7 0.1 8 0.1
81 12.9 248 3.9 329 4.7
0 0.0 0 0.0 0 0.0
150 23.0 430 6.C 580 8.3
275 43.8 1096 17.2 1371 19.6
328 52.3 1769 27.8 2097 30.0
MRFIT Study, Unpublished Data.
544
150
140 H
~ 130-1
X
| 120
T 110
in
8 100 H
S 90
o
CD
80
70 -I
60
TABLE 55
Males
..o
Urban •-
Rural o
i i i " t i » i i i
15- 20- 25- 30- 35- 40- 45- 50- 55-
Age in years
Mean systolic and diastolic l)lood pressure of
urban and rural males.
160
150
140
a»
x 130 -I
E
1 120 ^
S 110
* 100 i
CO
80
70
60
Females
Diastolic
^-°
Urban
Rural o<
15- 20- 25- 30- 35- 40- 45- 50- 55-
Age in years
Mean systolic and diastolic blood pressure of
urban and rural females.
Oviasu VO, Okupa FE. Occupational factors in hypertension
in the Nigerian African. J Epidemiol Community Health 19 79;
JJ.2/4-2A8,
545
TABLE 56
<, .59/ <, Mmm. Hg
16O-179/95-109
>ieo/ >no
BM BW
Risk of stroke or ischemic heart dis-
ease according to blood pressure on entry—age-
adjusted. In this figure and in the subsequent
ones, the numbers within each bar indicate the
population at risk in the denominator and the
subjects developing either stroke or ischemic
**art disease in the numerator.
Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the
128?949-955PUlati°n °f ***** C°Unty' GeorSia« ^ Intern Med 1971;
546
TABLE 57
Total Fetal and Nonfatal Stroke**
(fatal Hortmtal Total
Group • 8_Mt 6Uo* aa Mwt aa Strot •a
SC RC 6C RC 8C RC «C RC
Blaofc man 1.064(42) 1.084(70) 7 14 26 28 32 40
Biaa* mommn 1.344 (CM) 1.364(91) 8 18 18 27 24 46
-Vtirta man 1.692(60) 1.881(130) 9 12 18 36 27 47
WrtMt# woman (.186(80) 1.168(124) 6 a 14 18 IS IS
Total biacka 2.406(00) 2.438(161) 16 32 41 63 68 88
Total «*ft*«a 3.077(149) 3.017(264) 14 20 32 63 48 73
Total 6.486(246) 6,466(416) 29 62 73 toe 102 166
'Data lor Slapped Cera (SC) an* RetarraO Cera (RC) participant* during *»■ yaar foHowup. by
raca-aam groupe
fMumbara to parentheeea tndtoata untuwna In whom nonfatal atrofca lno.8__.tn mi not
setamwneo.
Five-Year Findings of the Hypertension Detection and Follow-up
Program. III. Reduction in Stroke Incidence Among Persons
with High Blood Pressure. JAMA 1982;247:633-638.
547
TABLE 58
Number of Deaths by Cause for MRFIT Black and White Men
Black Men
White Men
Cause of Death
(ICD 9th Revision)
Total With Death Certificates
All Cardiovascular Diseases
Cerebrovascular Diseases
(430-438)
Myocardial Infarction (410)
Other Ischemic Heart
Disease (411-414)
Hypertensive Heart Disease
(402)
Other Hypertensive Disease
(401,403-405)
Other Cardiovascular Disease
(390-459 Exclusive of
above)
All Non-cardiovascular Diseases
Genitourinary Diseases
(580-629) '
Diabetes Mellitus (250)
Neoplastic Diseases (140-239)
Gastrointestinal Diseases
(520-579)
Respiratory Diseases (460-519)
Infectious Diseases (001-139)
Accidents, Suicides and
Homicides (800-999)
Other Disease
Rate/ +
No, 1000 Percent
450 19.2 100.0
203 8.6 45.1
30 1.3 6.7
17 0.7
0.0
3.8
0.2
48 2.0 10.7
Rate/ +
No. 1000 Percent
4602 14.1 100.0
2226 6.8 48.4
152 0.5 3.3
78 3.3 17.3 1225 3.8 26.6
29 1.2 6.4 483 1.5 10.5
26 0.1
0.0
333 1.0
0.6
0.1
7.2
247 10.5 54.9 2376 7.3 51.6
0 0.0 0.0 14 0.0 0.3
5 0.2 1.1 37 0.1 0.8
128 5.4 28.4 1440 4.4 31.3
15 0.6 3.3 155 0.5 3.4
12 0.5 2.7 124 0.4 2.7
4 0.2 0.9 16 0.0 0.3
63 2.7 14.0 455 1.4 9.9
20
0.9
4.4
135
0.4
2.9
♦ Percent of total number of deaths in race group.
Neaton JD, Kuller LH, Wentworth D: Total and Cardiovascular
Mortality in Relation to Cigarette Smoking, Serum Cholesterol
M^X?,™^™?}^ B1°°d ?ressure Among Black and
White Men Followed 5 Years.
548
TABLE 59
"O
cd *_»
(/) 73
5<
I? O)
3 <
O W
o o
o> a
O q)
cd
>
in
cd
cd
91)
7,491
66.322
Neaton JD, Kuller LH, Wentworth D: Total arid Cardiovascular Mortality in Relation to Cigarette
Smoking, Serum Cholesterol Concentration and Diastolic Blood Pressure Among Black and White Men
Followed Five Years.
Table 60
Comparison of Logistic Regression Coefficients'1' For Diastolic Blood
Pressure For All Cause and Cause Specific Mortality for Each Race Group
Bl_ tck Whit :e Difference In Coeff
Coeff SE Coeff SE SE
All Cause (1) .0195 .0033 .0170 .0013 .0025 .0035
Mortality (2) .0202 .0035 .0171 .0013 .0031 .0037
CVD Death (1) .0261 .0051 ,0301 .0019 -.0040 .0054
(2) .0299 .0055 .0322 .0020 -.0023 .0058
CHD Death (1) .0188 .0072 .0263 .0021 -.0075 .0075
(2) .0244 .0078 .0289 .0024 -.0045 .0082
Death From (1) .0623 .0105 .0372 .0068 .0251* .0125
Cerebrovascular Disease (2) .0624 .0109 .0324 .0072 .0300* .0131
(1) All Participants in Race Group.
(2) Excludes Those Participants Who Reported Previous Hospitalization
for a Heart Attack or Taking Medication for Diabetes.
+ Estimated for Fixed Age, Serum Cholesterol and Cigarettes per Day.
* P < .05
Neaton JD, Kuller LH, Wentworth D: To'al and Cardiovascular
Mortality in Relation to Cigarette Smoking, Serum Cholesterol
Concentration, and Diastolic Blood Pressure Among Black and
White Men Followed 5 Years.
550
TABLE 61
no
BO
70
50
30
I 10
a
a
_.
S 110
1 *
70
30
18
5T6
____.
-I
II
-1
| No ECG Abnormality
I ECG Abnormality
Stroke
T?t?B
II
io
_Tf
11
t i-
m
He«n Oismm
11
]__.___.
ii
WM WW BM BW
Risk of stroke or ischemic heart dis-
ease according to ECG abnormalities on en-
try—age-adjusted.
Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the
Biracial Population of Evans County, Georgia. Arch Intern Med 1971;
128:949-955.
551
TAULE bl
Five year mortality per 1000 in the absence of ECG abnormalities: HDFP participants with entry DBPof 90 io 104 mm
Hg who were not on antihypertensive medication and were free of specific end organ damage at baseline*
White men White women Black men Black women Total
SC RC SC RC SC RC SC RC SC RC
Sample size (n) 777 745 401 408 189 169 237 284 1604 1606
No. of deaths
All causes 22 29 12 14 14 17 6 16 54 76
CVD 11 12 5 4 4 6 2 11 22 33
CHD 8 11 3 4 3 5 2 5 16 25
Mortality rate
All causes 28.3 38.9 29.9 34.3 74.1 100.6 25.3 56.3 33.7 47.3
CVD 14.2 16.1 12.5 9.8 21.2 35.5 8.4 38.7 13.7 20.5
CHD 10.3 14.8 7.5 9.8 15.9 29.6 8.4 17.6 10.0 15.6
95% Confidence
intervals for
(SC-RC) rate
All causes (-28.7, 7.5) (-28.7, 19.9) (-85.3, 32.2) (-64.5, 2.4) (-27.3, 0.0)
CVD (-14.2. 10.3) (-11.8, 17.1) (-49.0, 20.3) (-55.6, -5.0) (-15.8, 2.1)
CHD (-15.7, 6.7) (-15.1, 10.4) (-44.9. 17.4) (-28.4, 10.1) (-13.4, 2.2)
CHD = coronary heart disease; CVD = cardiovascular disease; SC = stepped care; RC = referred care.
''End organ damage includes history of definite myocardial infarction, stroke, intermittent claudication, angina pectoris, or
elevated serum creatinine (^ 1.70 mg/dl).
Five year mortality per 1000 io the presence of ECG abnormalities: HDFP participants with entry DBP of 90 to 104 mm
Hg who were not on antihypertensive medication and were free of specific end organ damage at baseline*
White men White women Black men Black women Total
SC RC SC RC SC RC SC RC SC RC
Sample size (n) 313 318 168 198 232 298 220 216 933 1030
No. of deaths All causes CVD CHD 21 14 11 23 12 7 7 3 2 11 8 2 18 4 4 28 15 8 8 5 3 16 5 1 54 26 20 78 40 18
Mortality rate All causes CVD CHD 67.1 44.7 35.1 72.3 37.7 22.0 41.7 17.9 11.9 55.6 40.4 10.1 77.6 17.2 17.2 94.0 50.3 26.8 36.4 22.7 13.6 74.1 23.1 4.6 57.9 27.9 21.4 75.7 38.8 17.5
95% Confidence
intervals for
(SC-RC) rates All causes CVD CHD (-45.0, (-24.0, (-12.9, 34.5) 38.0) 39.1) (-57.8, (-56.5, (-19.7, 30.1) 11.4) 23.3) (-64.1, (-63.0, (-34.5, 31.4) -3.1) 15.2) (-80.5, (-28.5, (-8.8, 5.1) 27.7) 26.8) (-39.9, (-26.8, (-8.3, 4.2) 4.9) 16.2)
CHD = coronary heart disease; CVD = cardiovascular disease; SC = stepped care; RC = referred care.
AEnd organ damage includes history of definite myocardial infarction, stroke, intermittent claudication, angina pectoris, or
elevated serum creatinine (2:1.70 mg/dl).
The Hypertension Detection and Follow-up Program Cooperative
Research Group. The effect of antihypertensive drug treatment
on mortality in the presence of resting electrocardiographic
abnormalities at baseline: The HDFP experience. Circulation
1984:70:996-1003.
552
TABLE 63
Five-year mortality rates in black and white males by education and presence of LVH at baseline for all
HDFP stratum I participants and those not receiving medication at baseline: Referred-care males ages 40 to 69 years,
with entry diastolic blood pressure of 90 to 104 mm Hg*
% Mortality
(Deaths) N Crude Age-adjusted^
LVH-t LVH+ LVH- LVH+ LVH- LVH+
All stratum I participants
WM > HS (18) 446
WM - HS (26) 402
WM < HS (42) 335
BM < HS (56) 344
Participants not receiving medication at baseline
WM > HS (13) 347
WM - HS (21) 315
WM < HS (22) 260
BM < HS (41) 268
( 1) 8 4.0 12.5 4.5 10.2
( 2) 10 6.5 20.0 7.0 21.9
( 7) 16 12.5 43.8 10.6 28.6
(11) 32 16.3 34.4 15.4 32.3
me ( 1) 8 3.8 12.5 4.4 10.2
( 0) 7 6.7 0.0 7.4 0.0
( 5) 12 8.5 41.7 7.2 12.4
( 6) 18 15.3 33.3 14.9 33.2
WM - White males; BM - black male*; HS - high school education completed.
•From Tyroler HA: Race, education, and 5-year morulity in HDFP stratum I referred-care males. In Gross F, Strasser T, editors: Mild hypertension:
Recent advances. New York, 1983, Raven Press.
tAge-adjusted rates by direct method. Standard population is age decade distribution of all white males aged 40 to 69 years with entry diastolic blood
pressure of 90 to 104 mm Hg.
JLVH determined by ECG. LVH+ defined as major LVH by. Minnesou Code; LVH- defined as all others.
Tyroler HA: Overview of risk factorsAfo^™ary
heart disease in black populations. Am Heart J
1984;108:658-660.
553
TABLE 64
STROKE INCIDENCE
6r
<
UJ
o
o
o
UJ
o
z
UJ
Q
O
s
~^\ THROMBO-EMBOUC
HEMORRHAGIC
ill
<\2\
122-134 135-149
150+
SYSTOLIC BLOOD PRESSURE (mmHg)
Incidence of stroke by quartile of systolic blood
pressure.
Kagan A, Popper JS, Rhoads GG: • Factors Related to Stroke
Incidence in Hawaii Japanese Men. The Honolulu Heart
Study. Stroke 1980;11:14-21.
554
TABLE 65
TEST
<»30 1-0- 140- 160 180'
139 159 W9
SYSTOLIC 8LO0
Stmpto 0*fr«wl>on l%l
JA'AN n3 13.0 339 13.1 • <
HA»»A • 2(3 36 7 23 1 ■ ft 35
T-«
Relative risk of i/ilnu nmial firm-
orrhage ami thromboembolic stroke by systolic
blood pressure ami country.
130- uo-
139 IM
ISO-
179
•» <0O5 St* 0 06 < * < 0 10
NS » 0 10
Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii
and California: Incidence of Stroke in Japan and Hawaii.
Stroke 1984;15:15-23.
555
TABLE 66
CTs
Table 3. Mortality from cerebrovascular disease (CVD) in persons aged 15 and over during
19-year period according to the level of blood pressure at entry
Normotensive
Borderline
Hypertensive
Total
Male
Female
Total
Total CVD
Total CVD
Total
No. %
No. %
5923
1179
738
7840
71
42
126
239
1.2
3.6
17.1
3.0
CVD
No.
%
7 282 41 0.6 13205 112 0.8
1 603 35 2.2 2 782 77 2.8
1228 108 8.8 1966 234 11.9
10 113 184 1.8 17 953 423 2.4
Tseng WP. Epidemiological study of hypertension and stroke in Taiwan.
In: Primary Health Care in the Making, U. Laaser, R. Senault, H. Viefhues
(eds.), Springer-Verlag, Berlin, 1985.
TABLE 67
Stroke
Risk of stroke or ischemic heart
disease according to level of serum cho-
lesterol on entry—age-adjusted.
Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the
Biracial Population of Evans County, Georgia. Arch Intern Med 1971;
128:949-955.
557
TABLE 68
00
•a
(1) 0)
CO (0
a) 1
0)
en u
Q < 1
k_ 01
cd O)
~i <
o v—.*
Ui o
as o
> o 1— o
-Q _-.
a> 0)
__ oj a
O a>
_- CO
ca 0) GC
>- _c
•«-•
m c0
a>
Q
• Black Men
o White Men
(<182)
No. Black Men: 5,947
No. White Men: 62,614
III IV
(182-202) (203-220) (221-244)
Serum Cholesterol Quintile (mg/dl)
4,835
65,222
4.214
64,277
4,117
66,011
V
(>244)
4,377
67,260
Neaton JD, Kuller LH, Wentworth D: Total and Cardiovascular Mortality in Relation
to Cigarette Smoking, Serum Cholesterol Concentration and Diastolic Blood Pressure
Among Black and White Men Followed 5 Years.
TABLE 69
Comparison of Logistic Regression Coefficients'*' For
Serum Cholesterol Concentration For all Cause and Cause Specific
Mortalilty For Each Race Group
Bl_ tck Whit :e Difference In Coeff
Coeff SE Coeff SE SE
All Cause (1) .0016 .0010 .0028 .0003 -.0012 .0010
Mortality (2) .0013 .0011 .0024 .0004 -.0011 .0011
CVD Death (1) .0054 .0014 .0072 .0004 -.0018 .0014
(2) .0059 .0015 .0073 .0005 -.0014 .0015
CHD Death (1) .0071 .0017 .0079 .0005 -.0008 .0018
(2) .0079 .0017 .0082 .0005 -.0003 .0018
Death From (1) -.0034 .0046 .0023 .0020 -.0057 .0050
Cerebrovascular Disease (2) -.0032 .0047 .0021 .0021 -.0053 .0051
(1) All Participants in Race Group
(2) Excludes Those Participants vho Reported Previous Hospitalization
for a Heart Attack or Taking Medication for Diabetes.
+ Estimated for Fixed Age, Diastolic Blood Pressure and Cigarettes
per Day
Neaton JD, Kuller LH, Wentworth D: Total and Cardiovascular
Mortality in Relation to Cigarette Smoking, Serum Cholesterol
Concentration, and Diastolic Blood Pressure Among Black and
White Men Followed 5 Years.
559
TABLE 70
STROKE INCIDENCE
6r
a:
<
UJ
>-
o
o
o
UJ
o
z
UJ
Q
O
^] THROMBO-EMBOUC
■H HEMORRHAGIC
< 193 194-216 217-241
242+
CHOLESTEROL (mg/dl)
Figure 7. Incidence of stroke by quartile of serum
iholcslcrot.
Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke
Incidence in Hawaii Japanese Men. The Honolulu Heart
Study. Stroke 1980;11:14-21.
560
TABLE 71
Cerebral Hemorrhage*
3- 2.53 0.35
2 1.98
1 - 0.89
0.63
0 - I
129 130 159 160 199 200 / 229 230
Serum Cholesterol (mg/100ml)
3-
2-
1 -
0-1
Cerebral Infarction
1.43
1.04 1.00 1.12
0.59
Standardized morbidity ratio for
stroke by the level of serum cholesterol at entry
(both sexes, _> 40 years of age at entry, 10-year
follow-up, Taisho. Japan).
130 160 200 230
. 1 . . .
129 159 199 229
Serum Cholesterol (mg/100ml)
• The decreasing trend (slope) is significantly different
from zero at the p < 0.05 level.
Tanaka H, Ueda Y, Hayashi M, et al: Risk factors for cerebral
hemorrhage and cerebral infarction in a Japanese rural
community. Stroke 1983;13(1):62-73.
561
TABLE 72
Axe-adjusted* Mean* of Selected Variables \iilh ami \\llhontStroke — Definite and Passible Cases
Japan
Hawaii
Non- Non-
Variable strokc ICH T-E stroke ICH T-_:
Systolic MikkJ pressure (mm Hg) 135.2 163.4**" IM 4— I3S.X 148.9" 154.1*"
Diastolic blood pressure (mm Hg) 84.4 Y7.2** ^C.}— 81.9 92.5*** 88.8***
Serum cholesterol dug.'100 ml I 190.8 1X3.7 isio 217.1 207.4 Sug. 218.5
Hematocrit (CJ) 43.3 44.2 44Z 44.5 44.2 44.6
Relative body weight (CJ) 101.7 108.7 107 7 III.8 115.8 111.7
Cigarette/day 13.7 10.3 18.5*** 9.6 12.1 11.7
Calorie 2251 2144 20.^ Sue 2177 2020 2063
Animal protein (g) 42.2 28.1 3?.ir 66.9 54.3** 57.4**
Vegetable protein (g) 38.0 44.7 36 S 23.3 24.9 21.9
Saturated fat (g) 17.7 10.9 9.0* 55.1 41.1*** 53.3
Unsaturated fat (g) 22.1 20.7 19.4 24.5 29.6 20.7*
Simple carbohydrate (g) 63.0 67.0 55* 86.9 74.1 86.4
Complex carbohydrate (g) 283.9 270.0 2si: 166.7 170.9 159.0
Alcohol (g) 31.1 40.6 24 7 12.2 13.0 14.2
Calorics'body weight (kg) 41.0 38.0 »$•« 35.6 31.8 33.7
*Agc adjustment constants
Japan Hawaii
45-54 0.216 45-49 0.120
55-59 0.267 50-54 0.233
60-64 0.262 55-59 0.211
65-69 0.255 60-64 0.256
Sug.:/. < 0.10 65-69 0.180
*: p < 0.05
**: p < 0.01
•••:/» < 0.001
Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii
and California: Incidence of Stroke in Japan and Hawaii
Stroke 1984;15:15-23. u"
562
TABLE 73
Standanlized Multiple b»xi\iic Function Coefficients — Definite and Possible Stroke Cases
Standardized coefficient Absolute coeflicienl
Variable Japan Hawaii Japan Hawaii Tcst+
Systolic MikhJ pressure (mm Hg» 0.73* 0.45* 0.030 0.021 NS
Serum cholesterol (mg/l(X) ml) -0.12 -0.06 - 0.003 -0.1X12 NS
Relative body weight (r/f) -0.01 -0.12 -0.001 -0.001 NS
Hematocrit (CJ-) 0.24 Sug. -0.06 0.066 -0.019 NS
Proteinuria 0.19 Sug. 0.14* 0.384 1.046 NS
LVH in l-XG -0.08 0.26* -0.401 0.880 *
Alcohol (g) -0.11 0.12 -0.002 0.005 NS
Saturated fat (g) -0.22 0.02 -0.041 0.002 NS
Animal protein (g) -0.27 Sug. -0.27* -0.077 -0.062 NS
Cigarettes per day 0.14 -0.12 0.012 0.009 NS
Calorics/body weight (kg) -0.22 -0.17* -0.019 -0.013 NS
Age 0.39* 0.30* 0.069 0.053 NS
tTcsts for difference of absolute coefficient between two countries
NS:/» > 0.10
Sug.: p < 0.10
*: p < 0.05
Takeya Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan,, Hawaii
and California: Incidence of Stroke in Japan and Hawaii.
Stroke 1984;15:15-23.
563
TABLE 74A
C/V.V Disease i \. \o CXS Disease at Autopsy
Age adjusted me ;ths
No disease (191) Brain infarction (57) Hemonhage
(Examination variables
BMI (wt/hn 23.5 24.5 23.7
Cigarcttcs/day 12.9 11.7 19.8*
Scrum cholesterol 216 235+ 202
Scrum triglyceride 246 220 214
Scrum uric acid 6.2 6.1 6.7
1-hr. pp. glucose 178 199 156
Hematocrit 44.7 45.8* 44.1
FVC 3.1 2.93 3.29
Systolic BP 139 146 153+
Diastolic BP 83 87* 95*
Diet variables
Calories 2311 2032* 2322
Alcohol (g/d) 20.3 13.5 29.1
Animal protein (g) 69.4 67.7 59.6
Vegetable protein (g) 23.0 20.4 22.7
Saturated fat (g) 59.6 53.3 51.2
Unsaturated fat (g) 23.9 23.5 27.9
Starch (g) 167 136* 148
Cholesterol (mg) 565 512 463
Cf Calorics, protein 16.2 17.7* 14.9
Ct Calorics, fat 32.6 33.3 30.6
<57> (22)
Examination variables
Body mass index 23.9 24.5 23.8
Cigarcttcs/day 9.7 12.4 20.5*
Serum cholesterol 218 233+ 202*
Scrum triglyceride 234 237 221
Uric acid 596 6.15 6.78+
Glucose 158 196$ 153
Hematocrit (Ct) 44.7 46.0* 44.3
FVC 3.25 2.99? 3.36
Systolic BP 133 144* 1528
Diastolic BP 82 87+ 958
Diet variables
Calories 2301 2091* 2394
Diet alcohol (g/d) 12.9 13.8 29.9+
Animal protein 71.6 70.1 62.4
Vegetable protein 23.7 20.4* 22.9
Saturated fat 60.1 56.3 54.2
Unsaturated fat 26.5 23.7 28.7
Starch 164 139+ 150
Sugar 46.1 38.4 52.2
Cholesterol 549 537 478
Cfc Calorics, protein 16.7 17.7 14.9*
He Calorics, fat 33.5 34 31.2
tt Calories. CHO 46.3 44.3 45.5
Ic Calorics, alcohol 3.57 3.94 7.98+
Sodium 2914 2586 2646
*p sJ 0.05. +/> *J 0.01. %p *J 0.001. Ip *J 0.0001. Signifi-
cance tests are based on the contrast to the living group.
Stemmermann GN, Hayashi T, Resch JA, et al: Risk Factors
Related to Ischemic and Hemorrhagic Cerebrovascular Disease
at Autopsy: The Honolulu Heart Study. Stroke 1984;15:23-28
565
TABLE 75
Percent of the United States population with diabetes, 1976-80*
Age (Years)
20-74 20-44 45-54 55-64 65-74
White 6.2 1.7 8.2 11.9 16.9
Male 5.3 1.0 7.7 9.1 18.1
Female 7.0 2.2 8.5 14.5 16.1
Black 9.6 3.1 12.9 20.8 25.9
Male 8.5 2.8 11.1 14.4 29.4
Female 10.5 3.5 14.5 25.4 23.1
*Sum of percent of persons with a physician-diagnosed medical history of diabetes and of
undiagnosed diabetes using NDD6 criteria.
SOURCE: Hadden, WC, and Ml Harris. Prevalence of diabetes and Impaired glucose tolerance and
plasma glucose In the United States population, NCHS Vital and Health Statistics,
Series 11, In preparation.
Diabetes in America, Diabetes Data Compiled 1984. U.S.
Department of Health and Human Services, NIH Publication
No. 85-1468, August, 1985.
566
TABLE 76
25Cr
OHAGcflSTOWN
EZ_ SAVANNAH
WHITE WHITE BLACK
MALES FEMALES MALES
BLACK
FEMALES
ALL
GROUPS
Men* cholesterol and blood giucxxs*
determinations and 95% confidence limits (±1.96
standard error) by color and sex for each city.
1972-1974
Stolley PD, Kuller LH, Nefzger MD, Tonascia S, et al: Three-Area
Epidemiological Study of Geographic Differences in Stroke Mortality
II. Results. Stroke 1977;8:551-557.
567
TABLE 77
Diob«l«s
Median Vessel Scores al Given Age
40 ■
5 30
20 ■
10
« • 0-_UI«_ \ _.
» • NS OiObfllflt )<
NS OiOMIflt
••* DioMIM
■-• NO OioMMl
0 ^v-
30 40 SO 60 70 80 90
Median vessel scores for diabetic and nondiabetic
males and females. In the fifth and sixth decade* the
diabetic female has higher median vessel scores than
even the diabetic male.
Source:
Ila, G.C. Flora, A.B. Baker, R.B. Loewenson and A.C. Klassen:
A Comparative Study of Cerebral Atherosclerosis in Males and Females
Circulation, Volume XXXVIIT, November, 1968.
568
TABLE 78
Death Reft end Mortality Ratio* tor CHD and Stroke by History oi Diabetes
and High Blood Pressure by Sex and Age
CHD Stroke
Neither High Diabetes Both Neither High Diabetes Both
Diabetes Blood but not Diabetes Diabetes Blood but not Diabetes
nor High Pressure High and High nor High Pressure High and High
Age Blood but not Blood Blood Blood but not Blood Blood
Sex Group Pressure Diabetes Pressure Pressure Pressure Diabetes Pressure Pressure
Death Ra tes
40-49 152 423 400 1.078' 17 68 ... ...
M«?n 50-59 390 910 993 1.995 44 227 126 ...
60-69 803 1.735 1,950 1.891 163 507 258 729»
70-79 1.788 2.904 3.090 5.499 604 1.311 839 2.011*
40-49 15 81 182» 12 72 ...
women 50-59 57 196 411 550 28 91 83* ...
60-69 228 504 1,095 1.378 86 244 320 440
70-79 798 1.397 2.412 2,650 393 737 837 779
Mortality R ados
40-49 1.00 2.78 2.63 7.09* 1.00 4.00 ... ...
Men 50-59 1.00 2.33 2.55 5.12 1.00 5.16 2.86 ...
60-69 1.00 2.16 2.43 2.35 1.00 3.11 1.58 4.47*
70-79 1.00 1.62 1.73 3.08 1.00 2.17 1.39 3.33»
40-49 1.00 5.40 12.13* 1.00 6.00 ... ...
W-men 50-59 1.00 3.44 7.21 9.65 1.00 3.25 2.96* ...
60-69 1.00 2.21 4.80 6.04 1.00 2.84 3.72 5.12
70-79 1.00 1.75 3.02 3.32 1.00 1.88 2.13 1.98
* R_ites based upon only five to nine deaths.
Source: Illb, E.C. Hammond and L. Garfinkel: Coronary Heart Disease, Stroke, and
Aortic Aneurysm. Arch. Environ. Health, Vol. 19, August, 1969.
569
TABLE 79
Uj 130-
>
\ 120-
O
OQ 90-
<
o
UJ
u
a
u
80-
70-
60-
50-
40-
30-
20-
10-
0
210-
150
uoH
I I ASSENT
.RESENT
Z
Z
%
WOMEN
50-59 60-69 70-79 50-59 60-69 70-79
AGE AT EXAM
Average annual incidence of atherothrombotic brain infarction according to
diabetic status, age at biennial examination, and sex; 22-year follow-up. Diabetes is
significantly associated with ABI Incidence, p < 0.05 in men and p < 0.001 in women.
Source:
Illb, P.A. Wolf, T.R. Dawber, H.E. Thomas, T. Colton
and W.B. Kannel: Epidemiology of Stroke. Advances
in Neurology, Vol. 16.
570
TABLE 80
Number of deaths in which cerebrovascular disease was listed on the death certificate and percent that
also listed diabetes, arteriosclerotic heart disease or hypertensive disease in Baltimore City and
8 counties in Maryland based on multiple-cause tabulation of death certificates for I960*
Af e-edJiuUd to total cerebrovascular dlisaie <_4__U_« m« 50-7Bf
Race* M* No. CVD DiajnosU Perceataf a with diabetes Percentage with hyper-tensive disease j Percentage with ASHD
Balti-more Em Urn WaUrn Bald-store Eastern Western Balti-more Eaetem Western Balti-more Easier* Wssisra
WM WF NM NF 321 300 164 183 166 164 92 68 197 209 6.6 9.8 4.9 10.9 8.1 11.0 2.2 14.1 6.0 13.0 27.9 36.2 38.7 46.1 21.0 32.9 26.6 36.4 26.6 34.3 33.6 31.9 23.7 30.7 21.2 19.6 18.1 16.2 18.6 24.1
Toul 967 460 406
* 1960, 1961, 1962 death* in oouaties.
t Excludes deaths due to cerebral aneurysm.
Source:
tta t Kuller and R. Seltser:
Cer-b^vascular Disease Mortality In ^f^
^"?, «, Tournal »* F.nidemiology, Vol. 86, No.2.
571
TABLE 81
Distribution of Other Diseases Listed in Hospital Chart—Stroke Cases by Area (Ages 45-69)
Diseases
At
Hypertei nsion ASHD Diabetes least
Area Total stroke cases No. % No. % No. % No. %
Miami 531 159 29.9 206 38.8 91 17.1 .289 54.4
Denver 293 81 27.6 91 31.1 36 12.3 135 46.1
Kansas 130 42 32.3 32 24.6 15 11.5 62 47.7
Ssattle 365 90 24.7 82 22.5 44 12.1 142 38.9
Buffalo 532 224 42.1 237 44.5 143 26.9 348 65.4
North
Carolina 214 88 41.1 59 27.6 36 16.8 123 57.5
Georgia 93 30 32.3 31 33.3 15 16.1 54 58.1
South
Carolina 162 37 22.8 13 8.0 8 4.9 37 22.8
Total 2,320 751 32.4 751 32.4 388 16.7 1,190 51.3
Excludes deaths certified by medical examiner (five), cases discharged alive from hospital but subsequently
found dead in mortality study (40), and stroke on past history only.
Ib. L. Kuller « person .Peterson 1 -ssel.^.^lets^.^^.
. Paegel. M. Saslaw C. Sisk J. Wilbe , dlsease Morbidity s
Source: lib
A*. LUienfeld,R. Seltser, Nationwide c
Stroke 1:86-99, 1970.
Study.
572
TABLE 82
hrequency oi First Stroke in the Di.tlu-lic Cohort, Rochester, Minnesota, 1945-1969*
Patients
Person-years
nt risk
Relative
risk
Observed [vp.'Cted. (obs/exp)
Hypri tensive
22 10.7 2.1
36 2J.5 1.5
5ti 14 J Nonhvpi-nensive 1.7
3-4 M.J 1.1
21 17.7 1.2
5. III 0 11
P value
-IJ "u
conndence
intervals
oi obs^exp
Males
Females
Total
Males
Females
T.n.il
1,136
2,571)
J,712
4,29-1
3.172
7.-4I.D
<0.001
<0.05
<0.00l
NS
NS
NS
1.3-J.1
1.1-2.1
1.3-2.2
O.B-1.6
0.7-1 H
0.1M 5
*Ol)s = observed; exp = ex|>ectetl; NS = not sigmlicanl.
Source: Ilia, M.E. Roehmholdt, P.J. Palumbo, J.P. Whisnant and L.R. E^eback:
Transient Ischemic Attack and Stroke. Mayo Clin. Proc, Jan 1983, Vol. 58
573
TABLE 83
STROKE INCIDENCE
6r
CL
<
UJ
>-
o
o
o
UJ
o
UJ ^
Q
~^\ THROMBO-EMBOUC
■H HEMORRHAGIC
■ I
<£I22
122-149 150-188 189+
GLUCOSE (mg/dl)
Incidence of stroke by quartile of serum
glucose I hour after a SO gin oral had.
Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke
Incidence in Hawaii Japanese Men. The Honolulu Heart
Study. Stroke 1980;11:14-21.
574
TABLE 84
Age-adjusted Death Rates per 1000 (in 9 years)
by Level of Alcohol Consumption
Alcohol (oz/mo) CHD Thrombo-embolic stroke Hemorrhagic stroke
0 24.6 3.7 3.0
1-6 16.6 5.2 3.2
7-15 20.9 3.0 7.3
16-39 7.8 1.8 6.3
40-59 5.9 3.7 5.5
60+ 12.8 5.1 12.7
Abbreviation: CHD = coronary heart disease.
Kagan A, Yano K, Rhoads GG, et al.
Alcohol and Cardiovascular Disease:
The Hawaiian Experience. Circulation
1981;64(Suppl III):III-27-III-31.
575
TABLE 85
STROKE INCIDENCE
UJ
o
6r
cr
<
in
>- 4h
•*»
o
o
o
UJ
Q
O
2
| 1 THROMBOEMBOLIC
■ I HEMORRHAGIC
JJ
ill
1-16
17 +
ALCOHOL CONSUMPTION (ml/day)
Incidence of stroke by tertilc of alcohol con-
sumption.
Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke
Incidence in Hawaii Japanese Men. The Honolulu Heart
Study. Stroke 1980;11:14-21.
576
TABLE 86
-J
-J
0) UJ
Ui en
CO 3
a>
en *a
a < i
-_. 0)
a en
D <
O s__/
CO o
ivl o
> o o
_- »—
_D
0) LI
O 0)
*-•
(0 a) CO
>- _c
#^«
IO ca
a>
Q
• Black Men
o White Men
1-15
16-25
26-35
No. of Cigarettes Reported (per day)
No. Black Men: 11,748
No. White Men: 208.481
4.730
21.184
4.905
38.399
1.168
27.044
> 35
939
30.276
Neaton JD, Kuller LH, Wentworth D: Total and Cardiovascular Mortality in Relation
to Cigarette Smoking, Serum Cholesterol Concentration and Diastolic Blood Pressure
Among Black and White Men Followed Five Years.
TABLE 87
180
160
140
120
100
BO
I M
£ 20
C 180
s
E 160
140
120
Men
<. 40
_i35
41-49 ___j 36-47
2. SO B8 > 48
100-
8o|—
SO
40
20
Women
Stroke
____£
Risk of stroke or ischemic disease
according to level of hematocrit—age-ad-
justed.
Heyman A, Karp HR, Heyden S, et al: Cerebrovascular Disease in the
Biracial Population of Evans County, Georgia. Arch Intern Med 1971;128:949-955
578
TABLE 88
DEFINITE THROMBO-EMBOLIC STROKE*
■■ HYPERTENSIVE
| | NOT HYPERTENSIVE
0 12 3+ 0 12 +
NUMBER OF Rl$K FACTORS NUMBER OF OTHER RISK FACTORS
#• / CASE OMITTED BECAUSE OF MISSING DATA
Incidence of thromboembolic stroke according to number of risk factors:
hypertension (BP ^160/95); cigarette smoking: hyperglycemia (>170 mg/dl. I h after 50 gm
glucose, p.o.). increased hematocrit Ck48%); and/or left ventricular hypertrophy or strain on
the ECG. lumbers within bars denote the number of cases.
Kagan A, Popper JS, Rhoads GG: Factors Related to Stroke
Incidence in Hawaii Japanese Men. The Honolulu Heart
Study. Stroke 1980;11:14-21.
579
TABLE 89
%
30 r
25
20
10
Z2HDFP
■ IHI
255
WHITE BLACK BLACK
FEMALE MALE FEMALE
Change in prevalence of elevated diastolic
blood pressure: HDFP (1973-74) and IHI (1977-78) (DBP
_> 95 mm Hg).
Apostolides A, Cutter G Krauc ttt __«- „-v T
In_or._a._on o High Blo^L^ ££_ B^.Inl^^T
Hypertension 1980;2:708-713. en iy/J and 1978.
580
TABLE 90
Secular trends in hypertension control
Study
Minnesota Heart Survey (10)
Date
Anglos
1973-1974
Per cent under control*
Men
29%
Women
53%
Hypertension Detection and
Follow-up Program (23)
1973-1974
28%
52%
Impact of Hypertension
Information Study (8)
1977-1978
44%
69%
Minnesota Heart Survey (10)
1980-1981
72%
81%
San Antonio Heart Study
1979-1982
87%
97%
Laredo Study (12)
Mexican Americans
1979
37%
77%
San Antonio Heart Study
1979-1982
64%
87%
* Expressed as per cent of total hypertensives in the community, including both treated
and untreated.
+ These studies also present data on hypertension control in blacks which indicate that
black women are better controlled than black men and that the level of control in the
black community also improved from 1973-1974 to 1977-1978.
Franco LJ, Stern MP, et al: Prevalence, Detection and Control of
Hypertension in a Bi-Ethnic Community: The San Antonio Heart Study.
Am J Epidemiol (In Press).
581
TABLE 91
Baseline Body Mass Index (BMI) and 5-Year Mortality
Ln
00
to
Quintile of Stepped- care participants Refenred- care participants
Age-sex-race- Age -sex-race- [(SC-RO/RC)
body mass Sample Number Rate adj. rate Sample Number Rate adj. rate SC - x 100"
index size of deaths per 1,000 per 1,000 size of deaths per 1,000 per 1,000 RCfl (%)
All participants*
<23.89 1,139 105 92.2 90.2 1,040 141 135.6 127.5 -37.3 -29.3
23.89-26.42 1,112 71 63.8 65.5 1,066 76 71.3 72.0 -6.5 -9.0
26.43-28.78 1,043 50 47.9 44.6 1,135 81 71.4 70.6 -26.0 -36.8
28.79-32.25 1,090 59 54.1 55.4 1,099 59 53.7 54.5 0.9 1.7
2=32.26 1,090 62 56.9 59.9 1,094 59 53.9 62.5 -2.6 -4.2
DBPf 90- 104 mm Hg and not on antihypertensive drugs at basel ine^
<23.89 606 44 72.6 72.8 593 66 111.3 113.3 -40.5 -35.7
23.89-26.42 638 33 51.7 60.6 615 42 68.3 76.8 -16.2 -21.1
26.43-28.78 588 26 44.2 38.3 639 34 53.2 62.1 -23.8 -38.3
28.79-32.25 574 27 47.0 52.5 577 29 50.3 53.0 -0.5 -0.9
2*32.26 494 23 46.6 47.2 519 24 46.2 56.6 -9.4 -16.6
0 Based on age-sex-race-adjusted rates.
b \2 for homogeneity = 7.63 (P = 0.12); x2 for SC-RC difference in mortality adjusted for baseline BMI = 8.43 LP < 0.005).
r DBP = Diastolic blood pressure.
d x for homogeneity = 2.40 (P = 0.66); x2 for SC-RC difference in mortality = 5.10 LP = 0.025).
The Hypertension Detection and Follow-up Program Cooperative Group. Mortality
findings for stepped-care and referred-care participants in the Hypertension
Detection and Follow-up Program, stratified by other risk factors. Prev Med
1985;14:312-335.
TABLE 92
MtrfNIkWin. |cMTnf .imoi
3 £
M»*H«lfN«'ON (.Hill | SI I KOI
©
e
©
.mail vfssr_ scimosis
*T»€«OSCtt«'jSiS OF
CiMCl f *.(.n_
** irUt'ltn. moOr. ml- h~tst~r •** ^ fl'
Risk (blood pressure. tUolesteroh of cerebral in-
farction.
Takeva Y, Popper JS, et al: Epidemiologic Studies of Coronary
Heart Disease and Stroke in Japanese Men Living in Japan, Hawaii
and California: Incidence of Stroke in Japan and Hawaii.
Stroke 1984;15:15-23.
583
TABLE 93
Risk factor influence on distribution of stroke and coronary heart disease between geographic
areas and ethnic groups with associated topography of vascular involvement and
proposed model populations
Risk factor Disease
Class Blood lipid levels Blood pressure Stroke Coronary heart disease Model population
Incidence Site of vascular lesion Incidence
1 2 3 4 High High Low Low High Low High Low High Intermediate High Low Both intracranial and extracranial Mainly extracranial Mainly intracranial and intracerebral Few or none High High Low Low USA black USA white Japan Guatemala
Kuller L, Reisler DM: An explanation for variations in
distribution of stroke and arteriosclerotic heart disease
among populations and racial groups.' Am J Epidemiol
1971;93:1-9.
584
*U.S. GOVERNMENT PRINTING OFFICE:1986-620-638:^0716