f'T-v. „ 
Syphilis and the Rtiol of Atheroma 
F. PARKES WEBER, M.A., M.D., M.R.C.P. (Lond.), 
PHYSICIAN-¥CT¥hE GERMAN HOSPITAL, LONDON. 
THE AMERICAN JOURNAL OF THE MEDICAL SCIENCES, 
FROM 
May, 1896. Extracted from The American Journal of the Medical Sciences, May, 1896. 
SYPHILIS AND THE ETIOLOGY OF ATHEROMA. 
By F. Parkes Weber, M.A., M.D., M.R.C.P. (Lond), 
PHYSICIAN TO THE GERMAN HOSPITAL, LONDON. 
In this paper I purpose shortly to consider the nature of arterial athe- 
roma, more especially with regard to the part, if any, played by syphilis 
in its causation. Everyone is familiar with the appearance of atheroma 
in the aorta, the formation of thickened patches, the fibrous, pulpy, or 
calcareous formations in its inner coat. It is not my intention to describe 
these changes, which have already so often been described both macro- 
scopically and microscopically, but to discuss certain questions in their 
etiology. 
The importance of the part played by syphilis in the causation of 
aneurisms' must certainly be acknowledged, and hence some would argue 
that syphilis exerts a like influence in the production of arterial athe- 
roma, but the latter conclusion is not a fair one. In order to show that 
such a conclusion is not justified it becomes necessary to make a digres- 
sion and to discuss shortly the role of syphilis in the causation of aneur- 
isms. 
For this purpose it will be best to confine ourselves to aneurisms of 
the aorta, so as to exclude, as far as possible, aneurisms due to trauma- 
tism, bruising, and embolism, and especially to exclude those caused by 
septic inflammation of the arterial walls, set up by emboli in cases of 
infective endocarditis." Aortic aneurism occurs chiefly at the middle 
period of life ; out of ninety-two cases analyzed by Dr. Thomas Hayden, 
sixty occurred between the ages of thirty and fifty,3 whereas the same 
author found that atheroma was most common after the age of sixty. 
In spite of this, however, Dr. Hayden evidently considered aneurism to 
be due to atheroma, or at least to antecedent changes in the vessel-walls, 
of which atheroma may be looked on as the type ; this is what he said ; 
“ Thus, whilst deterioration of the arterial coats as typified in atheroma 
is most common after the age of sixty, one of its ordinary consequences, 
1 The statistics on this subject are, of course, as liable to error and as hard to ascertain cor- 
rectly as those of antecedent syphilis in cases of tabes dorsalis. Professor Clifford Allbutt tells 
me he would say that in 90, or even 95, per cent, of aneurisms there has been previous syphilis. 
See also P. H. Welch, “ On Aortic Aneurism in the Army.” Med.-Chir. Trans., 1876, vol. lix. 
2 See J. Langton and W. Bowlby, “Multiple Embolism of the Arteries of the Extremities.” 
Med.-Chir. Trans., 1887, vol Ixx. 
3 See “ Diseases of the Aorta,” in Quain’s Dictionary of Medicine, first and second editions. 
Other statistics agree in pointing to the period between the ages of forty and fifty as the com- 
monest for aortic aneurism. WEBER: SYPHILIS AND ETIOLOGY OF ATHEROMA. 
aneurism, belongs to an earlier period of life. The apparent discrep- 
ancy may be explained by the more frequent employment of men under 
fifty in severe labor, and their greater capacity for extreme muscular 
effort earlier in life, the condition of the arterial wall which favors aneur- 
ism having been already established.” 
That violent efforts and high blood-pressure are most important factors 
in the causation of aortic aneurisms there can be no doubt,1 but I be- 
lieve that the explanation given by Dr. Hayden is not sufficient to 
account for the discrepancy acknowledged by him between the favorite 
age for aortic aneurism and the period of greatest frequency of aortic 
atheroma. It appears to me more natural to conclude that ordinary 
atheroma is not, after all, the commonest cause of sacculated aneurism 
of the aorta, but that a localized inflammatory infiltration of the aortic 
wall2 usually precedes the anenrismal dilatation. 
There seems to be nothing against the view that such patches of sub- 
acute aortitis represent sometimes a true tertiary syphilitic process of the 
nature of a gummatous infiltration, and this view best explains the im- 
portance of syphilis as an etiological factor in aortic aneurisms. 
In 1868 Prof. Clifford Allbntt,3 when describing the histological char- 
acter of the diseased cerebral vessels in a syphilitic man, aged thirty-one 
years, drew attention to a condition of chronic arteritis with great nuclear 
and cellular proliferation, which affected all the coats to some extent, 
but especially the middle and inner coats. He said, “ The distinction 
between the coats was in many places lost; in other places the inner was 
detached from the middle coat by a nest of nuclei and granules. . . . 
1 Hence the much greater frequency, so often alluded to, of aortic aneurisms in men than in 
women, and in men who make great muscular efforts than in men who do not. This is con- 
firmed by the fact that the aortic arch, where naturally the strain is greatest, is the most com- 
mon site for aneurisms. Strain probably acts likewise as a predisposing cause of atheroma. 
The arteries of the lower extremities, which are more liable to strain than those of the upper 
extremities, are likewise more liable than the latter to atheroma ; the pulmonary artery, where 
the blood-pressure is much lower than in the aorta, is seldom affected by atheroma, except 
when the blood-pressure in the pulmonary artery is pathologically increased by pulmonary 
emphysema, disease of the mitral valve, etc. (See S. Wilks and W. Moxon, “Lectures on 
Pathological Anatomy,” 3d ed., 1889, pp. 155-57.) Precisely how strain can induce atheroma 
remains doubtful. A discussion as to whether a chronic inflammatory process plays an inter- 
mediate part in these cases would be unprofitable, but we may bear in mind that, though 
moderate functional activity and mechanical movements must he regarded as natural stimu- 
lants tending to the proper nutrition of the tissues, excessive functional activity and mechan- 
ical strain may probably cause malnutrition and irritation, giving rise to chronic degenerative 
and inflammatory changes. It is not then a matter for surprise that strain sometimes helps in 
the production of atheroma ; the part, however, which it plays in the production of atheroma 
is probably quite different to the part which it plays in inducing aneurism. In the latter case 
the usual action of strain is most likely the mechanical thrusting out of a part of the vessel- 
wall already softened by some true inflammatory process. 
2 The very first stages of a sacculated aneurism of the aorta are, however, not likely often to 
fall under the notice of the pathological anatomist. 
s “ Cerebral Disease in a Syphilitic Patient,” St. George’s Hospital Reports, 1868, vol. hi. p. 61. 
What appear to have been miliary gummata had already, in 1863, been noticed by Dr. S. 
Wilks in the bloodvessels of the brain in the case of a syphilitic woman, aged 38. See Guy’s 
Hospital Reports, 1863, 3d series, vol. ix. p. 45. webee: syphilis and etiology of atheroma. 
in other places, again, pear-shaped processes, thrust inward from the mid- 
dle and inner coats, projected into the lumen of the vessel, carrying the 
inner coat before them. . . . Their contents were chiefly of an opaque 
granular character. I found, however, no dark layers of fatty degenera- 
tion like those we see in common atheroma ; and on the whole the degen- 
eration was not of so low a kind as in atheroma, the products being gen- 
erally of higher physiological value.” Although this account and the 
subsequent paper by Heubner,1 of Leipzig, described syphilitic disease of 
the small arteries, it may be inferred that there is also likely to be a 
difference between a chronic or subacute syphilitic inflammation in the 
aorta and ordinary atheroma.2 
I now return to the original question: the nature of aortic atheroma 
and its relation to syphilis. The digression was undertaken to point 
out that syphilis may play a much greater part in the production of 
aortic aneurism than it does in the production of atheroma, not to urge 
that syphilis was of no account in the causation of atheroma. 
Any local inflammation seems to predispose to chronic atheromatous 
changes. It is an old observation that atheromatous changes are very 
likely to be found in valves which have been slightly affected by previous 
rheumatic endocarditis. Chronic atheromatous thickening is not rarely 
seen in congenitally malformed cardiac valves, such as when there are 
only two instead of three aortic or pulmonary valves. In these cases 
one of the valves is often divided into two parts by what John Hunter, 
in describing the condition, termed a “ crossbar.”'3 Probably such 
valves are sometimes the result of intrauterine endocarditis,4 the “ cross- 
bar of Hunter ” representing the part where two valves during foetal life 
have undergone inflammatory adhesion so as subsequently to form a 
single valve in the adult; it seems, therefore, fair to consider that when 
such valves undergo chronic thickening the intrauterine inflammation, 
like ordinary rheumatic endocarditis, or any other inflammation, has 
acted as a predisposing cause to the subsequent degenerative changes of 
atheromatous nature supervening in adult life. 
A patch of syphilitic aortitis, besides its chances of giving rise to an 
aneurism, would, like any other inflammation, predispose to a subsequent 
atheromatous process, and this is, I believe, the chief part played by 
syphilis in the causation of atheroma. 
Some would make of atheroma itself a chronic inflammatory process, 
but of this I think there is not sufficient evidence. As in the case of 
1 Professor O. Heubner: Die leutische Erkrankung der Hirnartefien, Leipzig, 1874. 
2’See S. Wilks and W. Moxon : Lectures on Pathological Anatomy, 8d ed., 1889, p. 152. 
8 Sir James Paget, in 1844, drew attention to the frequency of disease affecting the aortic and 
pulmonary valves, when there were congenitally only two instead of three of them. Med.- 
Chir. Trans., vol. xxvii. p. 188. See also Dr. J. B. Peacock : Monthly Journ. Med. Science, May, 
1853, vol. xvi. p. 387. 
4 See Dr. J. B. Peacock: Monthly Journ. Med. Science, May, 1853, vol. xvi. p. 385. 4 
webee: syphilis and etiology of atheeoma. 
arteriosclerosis, and as in some cases of granular contracted kidney,1 
and of chronic fibroid changes in the cardiac muscle,2 the question arises 
in this case, also, what definition of inflammation we are to accept as our 
criterion in judging whether inflammation is present or not. The “ rubor, 
tumor, calor et dolor ” of Celsus, though still of great service as ordinary 
clinical tests for inflammation when occurring in extensive areas accessi- 
ble to touch or view, is hardly satisfactory as a scientific definition. For 
the present purpose I would prefer such a modification of modern defi- 
nitions as that suggested in my recent paper on “ Arterio-sclerosis,” 3 
namely, that inflammation is ‘ ‘ the series of tissue-changes caused by an 
injury or by the presence of some harmful irritant, and usually leading 
to an accumulation of cells in the part affected.” 
This includes the cell-accumulation resulting from proliferation of the 
fixed cells as well as that resulting from the migration of leucocytes. 
It includes tuberculous affections and the other infective granulomata ; 
it will also include cancer and sarcoma, if ultimately the presence of 
coccidia-like organisms should be proved to be necessary to their devel- 
opment. The occurrence of necrobiosis, secondary to inflammation or 
due to the same original cause, will not confound the definition. 
If we accept such a definition, does atheroma fall under the head of 
inflammation ? The cell-accumulation is certainly present, but an injury 
or irritant cause is probably not essential to the production of atheroma, 
unless, indeed, deficient nutrition be regarded as an irritant cause. Mere 
malnutrition and deficient nutrition are causes of necrobiotic and degen- 
erative changes, acute and chronic; but, if they should be regarded as 
irritants, it would become hard, indeed, to separate chronic inflammatory 
from degenerative processes. 
It is doubtful whether in many conditions it is possible to draw a hard- 
and-fast line between chronic inflammation of tissue and chronic de- 
generation of tissue. One can understand that the blood by deficiency 
in quantity, or, at least, by deficiency in its chief nutrient com- 
ponents, may give rise to a process of simple malnutrition. Besides 
being merely deficient in quantity or nutrient quality the blood sup- 
plied to the tissues may contain injurious substances owing either to 
excessive formation in some tissue of the body of a natural toxic 
product of tissue-metabolism, or to its deficient excretion from the body,4 
1 Especially those cases chiefly seen in old people, in which the capsule of the kidney strips 
off quite readily, though the surface of the cortex appears somewhat pitted or granular, and 
the cortex of the whole kidney is slightly diminished in size. 
2 See H. Huchard: Maladies du Coeur et des Vaisseaux, 2d ed., Paris, 1893, pp. 170 et seq. 
s The American Journal of the Medical Sciences, September, 1894, p. 287. 
iOr to deficient washing out of products of catabolism from some particular organ. Thus, 
the increase of fibrous tissue taking place in the liver and spleen from passive congestion 
may be due not merely to the passive hypersemia, per se, nor to increased vcnosity of the blood, 
but rather to the accumulation of the products of tissue-catabolism occurring in the congested 
organs owing to the local stagnation of the blood. WEBER: SYPHILIS AND ETIOLOGY OF ATHEROMA. 
5 
or to the formation by diseased tissue-metabolism of toxic substances 
(true auto-intoxication) not formed at all in the healthy body, or, 
lastly, owing to the formation within the body of toxic products 
resulting from the metabolism of parasitic microbes. Such toxic sub- 
stances circulating in the blood may, of course, act as irritants and 
cause inflammatory changes in the tissues, the effects of inflammation 
then becoming added to those of simple degeneration. It is not surpris- 
ing, therefore, that just as the causes of simple degeneration may be 
associated with those of inflammation, so the pathological alterations in 
tissues due to mere degeneration are frequently associated with those due 
to inflammation. 
The difficulty of distinguishing between a simple degenerative process 
and the results of chronic inflammation is especially great in the case of 
atheroma, which is certainly often accompanied and preceded by un- 
doubted inflammatory changes. Dr. W. Moxon1 thought that atheroma 
was in continuity with arteritis, graduating from a condition in which no 
inflammatory results can be found into one in which inflammation is dis- 
tinctly present. According to Dr. Thomas Hayden,2 however, “Ather- 
omatous transformation of the coats of arteries is a result of malnutri- 
tion, and essentially degenerative,” though “ not infrequently the pro- 
ducts of a low form of inflammation of the internal and middle coats 
are combined with those of tissue-degeneration.” Dr. Douglass Powell3 
considers atheroma of the aorta to be a degeneration, the result most 
commonly of preceding inflammatory change, but sometimes occurring 
primarily as fatty transformation from senile decay. 
The difficulty is increased, since it is possible that in cases of tissue- 
degeneration the products of degeneration may themselves, if unremoved, 
even without the presence of microbes, act to some extent as irritants to 
the surrounding tissues. In this way a condition of secondary chronic 
inflammation would be induced, although the primary condition was one 
of simple degeneration. On the whole, although atheroma may be fre- 
quently preceded or even accompanied by inflammation4 the weight of 
evidence seems to be that it may likewise occur as a primarily degener- 
ative process. 
It is probably best to look on such primary atheroma as a process 
occurring in the larger arteries corresponding (etiologically, though not 
anatomically) with arterio-sclerosis5 in the arterioles. According to this 
view, the same condition of malnutrition (whatever the primary cause of 
1 Guy’s Hospital Reports, 1871, vol. xvi. 
4 Virchow and Niemeyer, however, considered inflammation a necessary antecedent to the 
changes found in atheroma. See R. Virchow’s Die Cellular Pathologic, 1858, p. 319; and 
Felix von Memeyer’s Lehrhuch, 9th ed., Berlin, 1874, pp. 443 et seq. 
2 Diseases of the Heart and of the Aorta, 1875, p. 1073. 
8 Reynolds’ System of Medicine, 1879, vol. v. p. 19. 
6 In the present paper the word “arterio-sclerosis” is used as synonymous with the arterio- 6 
WEBEE: SYPHILIS AND ETIOLOGY OF ATHEROMA. 
this malnutrition may be) which induces arterio-sclerosis in the walls of 
the smaller vessels may act on the coats of the aorta and larger vessels 
so as to induce atheromatous changes. 
With regard, however, to the anatomical difference between the pro- 
cess of arterio-sclerosis in the small vessels and that of atheroma in the 
large ones, it must be remembered that, since the walls of the larger 
arteries are thicker than those of the smaller ones, the former are espe- 
cially dependent for their nutrition upon the condition of their vasa 
vasorum.1 The peculiar feature of atheroma is the cell-accumulation 
which takes place in the deeper part of the tunica intima (i. e., that part 
of the intima nearer to the tunica media) of the affected artery. This 
is the portion of the arterial wall which is naturally worst nourished, for 
its blood-supply must be obtained from the vasa vasorum, whereas that 
of the immediate inner surface of the artery is derived from the blood 
which constantly bathes it. Consequently, when the vasa vasorum of a 
large artery are in any way stenosed the deeper (external) layer of the 
tunica intima is the first part to suffer in its nutrition. It has, indeed, 
been pointed out'2 that the position of the cell-accumulation in atheroma 
may be partly due to stenosis of the vasa vasorum by Bright’s disease 
or syphilis. 
Stenosis of the vasa vasorum, from whatever cause, is, then, likely to 
induce atheromatous change in the part of the arterial wall in which the 
vasa vasorum are affected. H. Huchard,3 of Paris, has gone so far as 
to make of atheroma a “ localization of arterio-sclerosis ; ” that is to say, 
he makes it due to a process of arterio-sclerosis affecting not to the same 
extent the arterioles over the whole body, but localized to the vasa vaso- 
rum of certain arteries, the stenosis of the vasa vasorum causing ather- 
omatous changes in the walls of the affected arteries. 
It is evident that alterations in the quality of the blood induced by 
gout, syphilis, and alcohol, and all the asserted causes of arterio-sclerosis 
may likewise be alleged as causes of atheroma. On these questions4 I 
shall not enter in the present paper, but shall content myself with having 
capillary fibrosis described by Gull and Sutton in 1872 (Med.-Chir. Trans., vol. lv.). This 
restricted use of the term is both usual and convenient. 
1 This difference in the conditions of nutrition between the main arteries and the small 
arteries has been aptly compared to the laws which the Romans made for the maintenance of 
their celebrated roads. The large arteries have their vasa vasorum, just as the Roman prlmx 
vise had their independent maintenance; whereas, just as the vise vicinales had to be kept in 
repair by the neighboring populations, so the nutrition of the walls of the smallest arteries 
largely depends on the state of the organ which they themselves supply. See S. Wilks and 
W. Moxon, op. cit. 3d ed., p. 159. 
2 See Dr. F. W. Mott’s paper on “ Cardio-vascular Nutrition,” Practitioner, 1888, vol. xli. pp. 
161-173. 
3 Maladies du Coeur et des Vaisseaux, 2d ed., Paris, 1893, pp. 96 et seq. 
* To some extent I have entered on these questions in The American Journal of the 
Medical Sciences, September, 1894. WEBER: SYPHILIS AND ETIOLOGY OF ATHEROMA. 
7 
summed up, I hope intelligibly, the evidence in favor of the views (cer- 
tainly not new ones) ; 
1. That atheroma of the aorta, though often preceded or accompanied 
by inflammation, is itself a merely degenerative process: that syphilitic 
or other inflammation may locally predispose to atheroma. 
2. That aneurism of the aorta is induced more often by the yielding 
of a portion of its wall affected by syphilitic or other inflammation than 
of a portion affected by simple atheroma. 
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