Vol. XIX 
January-April, 1919 
Nos. 1, 2 
University Studies 
Published by the University of Nebraska 
COMMITTEE OF PUBLICATION 
F. M. FLING 
P. H. FRYE 
C. A. SKINNER 
P. H. GRUMMANN 
L. A. SHERMAN 
M. G. WYER 
CONTENTS 
Congenital Anomalies of the Heart. C. W. 
M. Poynter... i 
LINCOLN, NEBRASKA University Studies 
Vol. XIX 
JANUARY-APRIL, 1919 
No. 1-2 
CONGENITAL ANOMALIES OF THE HEART 
BY C. W. M. POYNTER 
«•* 
Page 
Section* I. Introductory remarks 1 
Section II. Symptoms 6 
Section III. Classification 8 
Section IV. Anomalies of the pericardium 10 
Section V. Misplacements of the heart 11 
Section VI. Anomalies of the heart as a whole 15 
Section VII. Anomalies of the interventricular septum 16 
Section VIII. Anomalies of the interatrial septum 19 
Section IX. Abnormalities within the cavities of the heart 23 
Section X. Abnormalities of the truncus communis arteriosus ... 27 
Section XI. Abnormalities of the pulmonary trunk ■... 34 
Section XII. Abnormalities of the aorta 37 
Section XIII. Abnormalities of the semilunar valves 38 
Section XIV. Abnormalities of the atrio-ventricular openings 40 
Section XV. Persistent patency of the ductus arteriosus 41 
Section XVI. Anomalies of the veins entering the heart 43 
Section XVII. Clinical classification of cases 44 
Section XVIII. General summary 53 
Section XIX. A list of literature relating to congenital cardiac disease 55 
Synopsis 
§1. INTRODUCTION 
For a number of years I have been studying the abnormalities 
of the circulatory system resulting from developmental disturb- 
*Note.-The section arrangement above is for the benefit of the study 
as a whole and is not meant for the body of the text, which is arranged 
under an anatomico-embryological classification, see page 8, or a clinical 
classification, see page 44. 
1 2 
ances. One paper relating to the aortic arches has already ap- 
peared, Poynter (1916), and in this one I shall confine myself 
to the anomalies of the heart. There are few subjects which 
have attracted more attention among the medical profession than 
the irregularities in the development of the heart and great ves- 
sels, but in the case of the heart the interest is not so much from 
the teratological side as in the case of the arteries; its develop- 
mental defects are frequently of such serious consequence to the 
life of the individual as to command the attention of the clinician 
and pathologist, with the result, that these cases have been studied 
as a pathological problem rather than an embryological one. 
I had first intended to report the cases I have had the oppor- 
tunity of studying, but as my bibliography has grown there has 
seemed to be no profit in adding more examples to those already 
reported, since I have observed no new conditions or complexes. 
'In the earlier study it was frequently difficult to find the literature 
relating to any specific lesion, consequently I have included a full 
literature list so that the cases which appear as a basis for this 
study may be readily available to any one desiring to consult 
them. 
Etiology.-The etiology of malformations of the heart cannot 
be any more definitely stated than that of any other develop- 
mental anomaly. Experimental research has taught us that if 
the normal developmental conditions are interfered with anoma- 
lies will result. Such anomalies are not confined to any anatom- 
ical system and vary in degree or extent depending on the time 
and intensity of the action and, no doubt, on other factors as well. 
Dareste has been able to produce a wide variety of anomalies by 
varying the temperature of the incubator during the development 
of the chick, and other investigators have been equally successful 
with fishes by growing them in various chemical solutions. 
Many hybrids develop irregularly and the proper application of 
the X-ray will produce growth disturbances. I have produced a 
wide variety of the recorded anomalies by incubating chick eggs 
then subjecting them to a temperature near freezing for a time 
before continuing the incubation. It would seem that the only, 
or principal, action of the cold is to inhibit oxidation and so dis- Congenital Anomalies of the Heart 
3 
turb the growth balance between different parts; this conclusion 
is supported by the fact that I have been able to produce the same 
results by growing the eggs in an atmosphere low in oxygen. 
All of these experiments seem to support the theory presented by 
Mall, namely, that faulty implantation or uncongenial environ- 
ment of the ovum is responsible for a large part, at least, of the 
anomalies, in man, with which we are acquainted. 
In the case of the heart anomalies we must consider the inter- 
ference with the growth process as a minor one, notwithstanding 
the later physiological importance of the resulting irregularity, 
for the majority of cases of cardiac defects reported show no 
extensive general growth disturbances. It is impossible to say 
that the factors which produce cardiac anomalies do or do not 
produce other lesions, but we at least know that no other lesion 
is always found in conjunction with them. I have shown in a 
previous paper (1916) that we must consider variations in devel- 
opment of the aortic arches independently of cardiac disturbances 
although they are frequently found associated in the same case; 
and likewise we are forced to conclude that each lesion of the 
heart must be studied separately, although it is the rule to find 
two or more lesions associated in the same heart. Stated in an- 
other way, defective ventricular septum and stenosis of the pul- 
monary artery must be considered as separate defects, notwith- 
standing that they are frequently in association; it would seem 
that even if the same factor produces both lesions its time of 
action or intensity must be different for each since each may 
appear alone. 
From time to time the suggestion has been made that heredity 
plays a part in etiology but I see no evidence that these cases be- 
long in the group with polydactylism and hemophilia. In the 
cases where two or more children in the same family have defect- 
ive hearts it seems to me more reasonable, from the experimental 
evidence at hand, to look on these cases as due to a diseased 
uterine mucosa in the mother rather than a defective germ plasm. 4 
C. IV. M. Poynter 
Investigators, as well as clinicians, have been interested in car- 
diac malformations ever since they were first reported. Their 
relationship to other anomalies was early recognized and in 1671 
Stenson reported a defect of the inter-ventricular septum asso- 
ciated with cleft-palate. Since that time a great many different 
types of anomaly have been found in association. Rokitansky 
collected twenty-four defective hearts, a third of which cases had 
other developmental irregularities. It is impossible to regard the 
presence of the other anomalies as a mere coincidence, yet there 
is no constant specific type association. 
Senac (1749) saw in congenital cardiac disease only a weak- 
ening of the formative influence, while Meckel (1812) pointed 
out the resemblance of certain of these hearts to those of lower 
animals, explaining them as reversions; he classified them as am- 
phibian, reptilian, etc., and, although his theory has never been 
generally accepted, his insistence that arrest of development was 
the primary cause of these anomalies pointed the way to embryo- 
logical study which has formed the basis of all modern attempts 
at scientific classification and explanation. Lee (1880) saw in 
single and associated anomalies the result of baneful influences 
acting during the early weeks of pregnancy sometimes selecting 
one part and sometimes another. 
Kreysig (1817) offered the suggestion that foetal endocarditis 
was responsible for congenital cardiac disease. This theory has 
been very widely accepted, particularly by pathologists. It has 
been considered as affecting not only the early developing heart 
but the fully formed heart as well. With a better understanding 
of heart development, the modern tendency is to explain the ma- 
jority of cardiac irregularities as due to arrest of development 
caused perhaps by a variety of factors. There still remains a 
certain proportion of cases in which it is impossible to say that 
foetal endocarditis has not been present and has not disturbed the 
normal course of development; however, the presence of thick- 
ened tissues does not necessarily prove that a defect is due to an 
inflammatory process. The final discussion of these cases must 
HISTORICAL Congenital Anomalies of the Heart 
5 
wait till we have a better understanding of the reaction of em- 
bryonal tissues to inflammatory processes. 
Rheumatism, tuberculosis and syphilis have all been studied as 
possible etiological factors but there is no positive evidence that 
they act even in an indirect way. 
Frequency.-As early as 1814 Gintrac suggested that cardiac 
defects were more frequently to be found in Great Britain than 
in France and Germany and that they were quite rare in Italy 
and Holland. This observation seems to be true at the present 
time with the United States occupying a place of slightly greater 
frequency than Italy and Holland. 
It is very difficult to secure statistics which will throw light on 
the relative frequency, for without postmortem examination very 
few cases can be positively identified as congenital defects and 
many cases present no symptoms calling attention to the heart 
for perhaps years after birth. Pott (1895) found of 30,000 chil- 
dren from clinics 95 had heart disease and of these 27 were 
under two years old, so might be considered as congenital; this 
is but a rude approximation and, as suggested, takes no account 
of the cases presenting no symptoms at the time of examination, 
so the number may be greater than this study suggests. Ellis 
(1905) found that there were 51 cases of all cardiac defects in 
3,875 autopsies at the Pennsylvania hospital, or 1.16 per cent.; of 
this number 42 were patent foramen ovale or persistent patency 
of the ductus arteriosis. 
The question of sex frequency does not seem to be of much 
significance; there is, however, a slightly greater preponderance 
of males affected, as the following table shows: 
Cases 
Males 
Gintrac, 1814 
44 
63.64% 
Friedeberg, 1844 
43 
67.44% 
Stolker, 1864 
79 
54-00% 
Peacock, 1866 
IIO 
55-54% 
Theremin, 1895 
57 
56.14% 
Abbot, 1915 
5i3 
55-34% 
The present study agrees with the above tables, the percentage 
of males being 55.69 per cent. 6 
C. W. M. Poynter 
§11. SYMPTOMS 
Cyanosis.-One of the subjects inseparably linked with con- 
genital cardiac disease is cyanosis congenita or morbus cocruleus. 
Its cause has been the subject of debate over a long period. 
Paracelsus (1500) mentioned Icteritia Coelestena and later Cham- 
seau (1789) speaks of Ictere violet, but I believe Senac (1749) 
was the first to definitely connect cyanosis with anomalies of the 
heart. 
Morgagni (1761) declared that cyanosis was caused by stasis 
of the blood in the venous system. This theory has been ac- 
cepted by a large number of investigators, notably, Louis, Bouil- 
laud, Farre, Haase, Peacock and Rokitansky. The idea that 
cyanosis is due to admixture of arterial and venous blood is 
probably older than the theory just mentioned and has been very 
generally accepted; even now it seems to be quite firmly estab- 
lished, notwithstanding the fact that Stille (1841) showed that 
admixture of blood may occur without cyanosis and that cyanosis 
may occur without any admixture. Other theories relating to 
changes in the blood and tissues extend beyond the scope of this 
paper and may be consulted elsewhere. The question is not as 
yet entirely settled; certainly more than half of the cases of con- 
genital cardiac disease do not exhibit cyanosis except for a very 
short period pro exitu. It is most frequently associated with 
obstruction of the pulmonary circulation but may be absent in 
these cases, Mazaroff (1895), and, since it is observed under 
other conditions than'congenital cardiac disease, it would seem 
that the simple circulatory disturbance due to the lack of a normal 
functioning heart should not be considered as anything more than 
a contributing factor in any case. 
Clubbed fingers have been observed in many cases of congenital 
cardiac disease, but are by no means a constant finding even in 
the cases which have lived past the first decade. The condition 
is probably due to congestion and toxaemia, Carpenter (1909). 
§ III. CLASSIFICATION 
Classification of congenital cardiac abnormalities presents many 
difficulties. A review of the various essays on the subject shows Congenital Anomalies of the Heart 
7 
that many different arrangements have been employed and none 
seem to be entirely free from objections. It would seem that the 
ideal arrangement would be one based on the embryological stage 
at which the developmental disturbance occurred. I believe the 
first attempt at such a classification was made by Friedeberg 
(1844), who grouped the anomalies as those belonging to the 
first stage of development, the second stage, etc. Peacock fol- 
lowed this idea, but added a class of misplacements after the 
plan of Breschet (1826). Rokitansky (1875) classified his cases 
on the basis of developmental stages as far as they were then 
known and Vierordt (1898) followed the same plan. Keith 
(1909) carried the same idea somewhat further as the result of 
recent research in cardiac development, particularly of the infun- 
dibulum. There are still questions of development which must 
be cleared up before this plan can be freely applied. There is 
also the possibility that, with development fully understood and 
etiological factors less obscure than at present, developmental 
stages may not seem so important. 
Hershfelder (1913) recognized the difficulty of classifying 
these cases, but seemed to think that an anatomical basis was most 
satisfactory. Such a purely anatomical arrangement, though 
quite complete, does not meet all requirements because among 
other things it does not take into consideration the relation of 
individual lesions to each other in the same case. It seems evident 
that the factors which produce developmental disturbances result- 
ing in arrest or delayed development of the different parts of the 
heart may bring about very different conditions not only of the 
anatomical structure but of function as well, depending on the 
embryonal stage in which they are active. A classification based 
on the various complexes which are found in the postmortem 
room would certainly be most satisfactory from a clinical stand- 
point but presents great difficulty in examining and explaining 
developmentally. Abbott (1915) suggests, what seems to me the 
best solution of the question, a grouping " on mixed principles," 
that is, an embryological anatomical basis. I will follow this 
classification with some unimportant modifications and at the 
end will give an additional resume of the cases as they are en- 8 
C. IV. M. Poynter 
countered clinically, that is, of the different pathological com- 
plexes for, as Hershfelder has pointed out, " Since the lesions are 
usually produced in groups rather than singly, it is quite as im- 
portant from a clinical standpoint to recognize these groups and 
understand their effect upon the circulation as to recognize the 
individual lesions." 
The group of cases here presented total 886 and are taken as 
largely as possible from the individual cases reported in the litera- 
ture rather than the studies of museum specimens. After a dis- 
cussion of each lesion a list of the cases upon which the conclu- 
sions are based is appended. The references are given by using 
the reporter's name and date so, by referring to the literature list 
at the end, title and publication may be known. 
I. Malformations about the Heart. 
A. Anomalies of the Pericardium. 
i. Deficiency. 
2. Diverticulum. 
B. Misplacements of the Heart'. 
I. Internal. 
a. Within the Chest (Dextrocardia). 
b. Within the Abdomen. 
c. Diverticulum. 
2. External (Ectopia Cordis). 
a. Cervical. 
b. Pectoral. 
c. Abdominal. 
II. Anomalies of the Heart as a Whole. 
A. Acardia. 
B. Bifid Apex. 
C. Congenital Hypertrophy. 
III. Anomalies of the Cardiac Septa. 
A. Interventricular Septum. 
I. Absence of Septum. 
2. Defective at Base. 
a. Below Aorta. 
b. Pars Membranacea. 
c. Elsewhere than Base. 
B. Interatrial Septum. 
I. Absence of Septum. 
2. Anomalies of Septum Primum. 
3. Anomalies of Septum Secundum. 
Classification Congenital Anomalies of the Heart 
9 
a. Persistent Foramen Ovale. 
b. Other Anomalies. 
IV. Abnormalities Within the Cavities of the Heart'. 
A. Right Atrium 
i. Contracture or Dilatation. 
2. Accessory Septa. 
B. Left Atrium. 
i. Contracture and Dilatation. 
2. Accessory Septa. 
C. Right Ventricle. 
I. Absence or Contracture. 
2. Accessory Septa. 
D. Left Ventricle. 
i. Absence or Contracture. 
2. Accessory Septa. 
V. Abnormalities of the Truncus Communis Arteriosus. 
A. Persistence of the Truncus. 
B. Defective Aortic Septum. 
C. Deviation of the Aortic Septum (Transposition). 
i. Simple Transposition. 
2. Transposition in Situs Transversus. 
3. Transposition of Ventricular Loop. 
D. Aorta Opening from Both Ventricles. 
E. Aorta from Right Ventricle Without Transposition. 
VI. Abnormalities of the Pulmonary Trunk. 
A. Pulmonary Stenosis. 
i. Of Orifice. 
2. Of Trunk. 
B. Pulmonary Atresia. 
i. Of the Orifice. 
2. Of the Trunk. 
3. Absence of Trunk. 
VIL Abnormalities of the Aorta. 
A. Aortic Stenosis. 
1. Of Orifice. 
2. Of Trunk. 
B. Aortic Atresia. 
VIII. Anomalies of the Semilunar Valves. 
A. Pulmonary Valves. 
B. Aortic Valves. 
IX. Anomalies of the Atrio-ventricular Openings. 
X. Anomalies of the Ductus Arteriosus (Persistent Patency) 
XL Anomalies of the Veins Entering the Heart. 
A. Pulmonary Veins. 
B. Systemic Veins. 10 
C. W. M. Poynter 
§IV. 
I. MALFORMATIONS ABOUT THE HEART 
A. ANOMALIES OF THE PERICARDIUM 
i. Deficiency.-Entire absence of the pericardium seems to 
be unknown except in cases of extensive developmental disturb- 
ances in which the heart is found outside of the thoracic cavity. 
More or less complete absence of the parietal pericardium is a 
rare anomaly, a slight ridge or fold on the right of the great ves- 
sels represents the remains of this layer. In other cases of less 
pronounced defect the pericardium covers the right half of the 
heart, while in others the pericardial case is complete except for 
a small or large foramen on the left causing a communication 
between the pleural cavity of the left side and the pericardial 
cavity. The opening is always on the left and, when large, some 
of these cases have been referred to as cases in which the heart 
is found in the left pleural cavity. The left phrenic nerve is dis- 
placed, running down on the inner chest wall parallel to the in- 
ternal mammary artery. 
The first to suggest an explanation of the anomaly was Keith 
(1907), who reported a case of small defect and said: "This is 
clearly a case of patent pleuro-pericardial foramen. Evidently 
the condition has been produced by the lung bud growing within 
and expanding the communication between the pleura and the 
pericardium, for the communication lies immediately ventral to 
the point at which the lung bud appears." McGarry (1914) 
points out a difficulty with the above explanation in that the lung 
bud does not develop until after the separation of the two cavities 
is complete. He calls attention to the other developmental errors 
of the coelom in his case and thinks that the whole is due to some 
early disturbance interfering with the development of the pleuro- 
pericardial membrane or its anlage. 
Haller (1757) did not believe that such abnormality could 
occur and Peacock (1856) thought that some, at least, of the 
reported cases were not true lack of membrane but universal Congenital Anomalies of the Heart 
11 
adherence of the two layers and that true congenital absence was 
of rare occurrence. 
Two cases in this group deserve special mention, and, as far 
as I am aware, are unique; in one, by Tait (1868) the pleural 
cavity was intact while the heart, naked of parietal layer, was 
in the normal position between the two pleural sacs; the other 
case, by Turner (1870), showed the parietal pericardium normally 
developed except that it was not attached to the diaphragm. The 
latter condition has been observed as normal for the walrus. 
The condition of defective pericardial development is not read- 
ily diagnosed and seems to be without clinical interest; the causes 
of death are entirely independent of the condition and the aver- 
age age is over forty years. Twice as many males as females are 
affected. Cases studied are by: 
de Mortel (1700), Baillie (1791), Walter (1805), Otto (1824), Breschet 
(1826), Meniere (1826), Wolf (1827), Curling (1839), Baly (1852), Bris- 
towe (1855), Peacock (1866), Powell (1869), Tait (1868), Weisbach 
(1868), Turner (1870), Bjorsstrom (1871), Lebec (1874), Faber (1878), 
Chiari (1880), Hughes (1883), Boxall (1887), Hewson (1895), Bernard 
(1898), Gay (1899), Schendewolf (1900), Primrose (1901), Saxer (1902), 
Keith (1906) 2 cases, Perna (1909), Verse (1909), Ebstein (1910), Plaut 
(1913) 2 cases, Cameron (1914), McGarry (1914). Total 36 cases. 
2. Diverticula of the Pericardium.-This condition is of little 
clinical importance but should be remembered in considering 
mediastinal tumors. Out pocketings of the parietal pericardium 
occur, sometimes as cysts, and may reach' considerable size. The 
etiology has not been fully worked out but is probably an arrest 
of development of some of the layers of the pericardial wall. 
The condition is rarely encountered and is well illustrated by the 
following: 
Speir (1865), Cuffer (1875), Bandy (1879), Coen (1885), Atyas-Maraty 
(1895). Five cases. 
§ V. 
The heart may be found in the neck or as low as the abdomen; 
it may be simply misplaced in the thorax (dextrocardia) or it 
may protrude through a fissure in the ventral body wall (ectopia). 
B. MISPLACEMENTS OF THE HEART 12 
C. IV. M. Poynter 
For the convenience of presentation we will divide the cases, 
after Breschet (1826), into internal and external misplacements. 
1. Internal Misplacements 
(a) Those displacements of the heart in the chest are gener- 
ally known as dextrocardia. They are most frequent of all mis- 
placements of the heart and consist of a transfer of the heart to 
the right side of the chest in a mirror position to that it nor- 
mally occupies. When all of the other viscera are also trans- 
posed the condition is known as viscerum transversus; this 
condition was first reported by Ricolanus in 1649 and is of suffi- 
ciently frequent occurrence to need no discussion here. The 
transposition of the heart alone is of much rarer occurrence. 
When unassociated with other anomalies the condition is without 
clinical interest and is only discovered when general examina- 
tions are made or at postmortem. 
Paltauf (1901) has pointed out that all cases are not alike. 
In one group the heart has simply rotated to the right, so that 
the dorsal and ventral relations are reversed, the tricuspid ven- 
tricle still receiving the venous blood. The other group repre- 
sent true transposition and are very rare, Graanboom's (1891) 
case being an example. 
The cases of congenital dextrocardia must be distinguished 
from those cases of misplacement due to some pathological 
process as contracture of adhesions or pressure of pleuritic 
effusions. A large number of clinical cases have appeared in the 
literature in the last two decades since the X-ray has come into 
such general use in study of chest conditions, some of these cases 
are no doubt congenital, but none of them are included in this list. 
Foggie (1910) has an extensive bibloigraphy of clinical cases. 
1. (a) Dextrocardia: Otto (1814), Otto (1816), Breschet (1826), Thore 
(1845), Mosier (1866), Falck (1877), Smith (1878), Robinson (1881), 
Ghose (1882), Pope (1882), Jacoby (1884), Bamberger (1888), Chabrely 
(1888), Grus (1888), Northrup (1888), Grunmach (1890), Sandhop (1890), 
Becker (1891), Graanboom (1890), Birmingham (1892), Williams (1892), 
Lochte (1894), Auche & Bouyer (1897), Reifschlager (1897), Petit et 
Ravant (1898), Dalton (1899), Lowenthal (1900), Paltauf (1901), Baum- 
garth (1902), Lucchi (1902), Wendling (1903), Carletti (1906), Garrod & Congenital Anomalies of the Heart 
13 
Langmead (1906), Potter (1906), Horaud (1907), Pal (1907), Scandola 
(1909), Foggie (1910), Benjamin (1911), Bello-Morales (1912). Forty 
cases. 
(&) Heart in the Abdomen.-These cases are frequently classed 
with the group of ectopia cordis but I have placed them in this 
class because the ventral body is normally closed, and until we 
have a clear idea of the etiology it seems proper to assume that 
other factors than those causing the cleft in the body wall are 
responsible for the cardiac misplacement. The diaphragm is 
defective and the heart is situated in the peritoneal cavity. The 
condition is very rare but should not be difficult to recognize and 
is apparently not incompatible with long life. The cases re- 
ported by Deschamps (1778) and Ramel (1778) had both passed 
the thirty-fifth year; Holt's (1897) case was 'n a child. 
(c) Diverticulum of the Heart.-In these cases the heart is 
prolonged as a muscular diverticulum from the left ventricle and 
extending into the abdomen through a defect in the diaphragm. 
I know of no suggested explanation of the anomaly except that 
of Gibert which is to the effect that the condition is a type of 
early aneurysm of the tip of the ventricle which prevents the 
complete development of the diaphragm. A diverticulum of the 
right ventricle, Fennell (1901), but which is well above the dia- 
phragm, may possibly belong in this group. Following the work 
of Peacock I have placed these cases among misplacements, 
although they are probably in no way related etiologically to the 
cases of malposition of the whole organ. Cases are from 
O'Bryan (1837), Thaden (1868), Gibert (1883), Arnold (1894), 
and Kotter-Aeby (1907), Fennell (1901). 
2. External Misplacements 
These cases are generally described under the title ectopia 
cordis. The heart protrudes through a median fissure in the 
ventral body wall and comes, in many cases, to lie on the surface 
of the body. In a few cases the pericardial sac is complete but 
in the majority the parietal layer is lacking ventrally, its borders 
being attached to the borders of the body fissure. 
The cause of the misplacement is not known; the first theory 14 
C. W. M. Poynter 
was that the heart developed in an abnormal position and so pre- 
vented the closure of the body wall; this is not consistent with 
what we know of development. It has been suggested that an 
over-distended heart from increased blood pressure prevented 
early closing of the sternal bars. Adhesions have been blamed 
for this as for many other anomalies. The condition has been 
repeatedly produced in experimental teratology in chicks and 
seems to have to do with disturbance of the body wall as well as 
the heart; probably separate factors affect each part, for cases 
are encountered in which the heart is in position and the sternum 
is defective. 
Breschet recognized three forms: (a) cervical, in which the 
heart is beneath the chin; (b) pectoral, in which the heart pro- 
trudes through a defect in the sternum; and (c) abdominal, in 
which the cleft extends to the abdominal wall and in which ab- 
dominal viscera as well as the heart are protruded. The heart 
in these cases of ectopia may show maldevelopment intrinsically 
or, more rarely, may be normal; the condition is incompatible 
with life, the average age for all cases being but a few hours. 
Cases of Ectopia Cordis. 
(a) Cervical: Vaubonnis (1712), de Torres (1741), Breschet (1826). 
(b) Pectoral: Walter (1745), Biittner (1768), Wiedemann (1794), 
Chaussier (1814), Weesg (1818) Walter's case, Haan (1825), Breschet 
(1826), Pecchioli (1839), Wittstock (1839), Cruveilhier (1841), Jones 
(1854), Brown (1855), Jones (1855), Frickhoffer (1856), Dotzauer (1857), 
Gross u. Heim (1859), March (1859), Marchal (1850), Daniel (i860), 
Forster (1861), Rezek (1868), Obermeier (1869), Schlesenger (1870), 
Jahn (1875), Deserte (1876), Hodgen (1878), Fischer (1879), Hofmeier 
(1880), Charpentier (1883), Grant (1896), Barnado (1897) Grant's case, 
Goode (1904), Ellis (1905), Fox (1909). 
(c( Abdominal: Martinez (1723), Prochaska (1734), Schultz (1763), 
Wahlbom (1764), Sandifort (1772), Herold (1787), Fleischmann (1810), 
Barret (1835), Becker (1839), Mitchel (1844), Follin (1850), Francois- 
Franck (1877). Total 46 cases. Congenital Anomalies of the Heart 
15 
§ VI. 
II. ANOMALIES OF THE HEART AS A WHOLE 
A. Acardia 
Acardia or hemicardia indicates a pronounced disturbance of 
the heart anlage. Stockard (1915) has greatly added to the in- 
terest of this subject by his work on Fundulus. He has shown 
that the growth of the heart may be entirely arrested by the use 
of the proper percentages of alcohols in the water in which they 
are hatched. 
Of course these cases are not of clinical interest but valuable 
in indicating the extreme degree in which factors affecting the 
development of the heart may operate. The condition is gener- 
ally found in monsters and is naturally incompatible with any 
extended period of development. Early cases were reported by 
Mery (1720) and Winslow (1740) and others studied by Nacke 
& Benda (1907) and Kehrer (1908). 
Multiple hearts are probably due to an early division of the 
heart anlage, then cessation of the malignant influences. An in- 
teresting case of double heart has been reported by Collomb 
(1798) in a human cyclops. 
B. Bifid Apex of the Heart 
In these cases the apices of both ventricles project below the 
interventricular groove. The condition is usually present in a 
heart which is otherwise normal. The first case which I have 
found recorded was by Bartholinus (1654), who described it as 
" Mucrone non acuto ut fieri solet, sed bifido." In explaining the 
condition Mall (1912) showed that there is a tendency for the 
divided apex to remain for some time, as in embryos of 11-25 
mm. stage, after the adult form should be assumed; this agrees 
with a like observation made by Paget (1831), p. 282. Mall 
considered that the bifid apex is due to arrest of development. 
The condition is normal for the dugong. The condition is rare, 
constituting 2.3 per cent, in Abbott's series. 
Bartholin (1654), Meckel (1805), Parise (1837), Schattuck (1891), 
Rolleston (1891), Hare (1902), Carpenter (1908), Mall (1912) 16 
C. W. M. Poynter 
C. Congenital Hypertrophy 
The condition was first suggested by Paget (1831), who said 
that the condition is represented by an increase of all of the parts 
naturally belonging to the heart. Columnae carnae are sometimes 
hypertrophied; in a case reported by Louis (1823) these had so 
much enlarged as to touch and seem a continuous plane. Peacock 
does not speak of a congenital hypertrophy although he discusses 
the early hypertrophy due to destruction in balance of the cir- 
culation as in congenital stenosis of the pulmonary artery. Vir- 
chow (1896) said that he had seen several cases that he consid- 
ered due to congenital hypertrophy. Simmonds (1899) reported 
a case in which the heart at term weighed 44 grams; he sug- 
gested that the cause was a growth disturbance in early life. 
Other cases have been reported by Effron (1903) and Kalb 
(1906). 
§ VII. 
III. ANOMALIES OF THE CARDIAC SEPTA 
A. INTERVENTRICULAR SEPTUM 
Among the anomalies of the internal structure of the heart, 
defective development of the ventricular septum is most fre- 
quently met with. The septum may be completely absent, par- 
tially developed or defective at the base. In the last the defect 
may be of the fleshy or membranous portion. 
Schliemann (1831) considered the thin portion of the inter- 
ventricular septum near the base as a pathological condition; 
Thurnman (1838) described this portion of the septum as "The 
highest part of the septum which occupies the angle between the 
posterior and right aortic valves, is in the human subject formed, 
not of muscular fibers, but simply of endocardium of the left and 
right ventricles and strengthened only by the interposition of a 
little fibrous tissue continuous with that of the aorta." He states 
that the structure was well known to anatomists, also that it was 
sometimes defective from malformation. I have been unable to 
find in the anatomies of the time or those of the previous century 
1. Absence of Septum Congenital Anomalies of the Heart 
17 
any description of the heart which revealed an understanding or 
recognition of this portion of the septum. 
Huschka (1855) described the thin area on the basis of a study 
of 300 hearts; he pointed out that it was always present and was 
a normal structure. He corrected Schliemann's error and claimed 
that he was the first to discover and describe the structure as 
a normal part of the heart. Peacock (1855) described its pres- 
ence normally, designated it as "the undefended space" and so 
liable to developmental error. He seemed to think at this time 
that this point was the most frequent seat of septal defect, an 
error corrected somewhat later. Reinhard (1857) suggested the 
name " pars membranacea," which has been quite generally ac- 
cepted. 
Rokitansky (1875) studied the development of the septum and 
on this basis divided the base into a posterior muscular portion, a 
pars membranacea, and an anterior fleshy portion, the latter being 
subdivided into an anterior and posterior portion. Defects occur 
most frequently in the posterior part of the anterior septum 
(Rokitansky) and less frequently in the pars membranacea 
When the defect is in the anterior part of the anterior septum 
Keith has shown that it is an anomaly of the bulbar septum. De- 
fects of the septum near the apex are extremely rare and may 
be multiple. 
Septum defect is frequently encountered in conjunction with 
stenosis of the pulmonary artery and the question as to which 
is the primary lesion has been much discussed. Hunter (1786) 
was the first, I believe, to suggest that the obstruction of the 
pulmonary circulation prevented the closure of the septum. 
Other theories have been so frequently discussed that they do 
not need review here. It must be noted in examining any theory 
that many examples have been found of each lesion occurring 
without the other. As I interpret the later experimental work 
in teratology it reveals a much less interdependence of parts in 
development than was formerly supposed and suggests a much 
more obscure disturbing factor than simple mechanics. 
The total number of septal anomalies is 594; of these 99 or 
16.6 per cent, are total absence of septum, listed as follows: 18 
C. W. M. Poynter 
Schenck (1600), Chemeneau (1699), Wilson (1798), Standert (1805), 
Farre (1814), Otto (1814), Fleischmann (1815), Meckel (1815), Hein 
(1816), Kreysig (1817), Marx (1820), Tiedemann (1824), Breschet (1826) 
two cases, Martin (1826), Mauran (1827), Mayer (1827), Stoltz (1841), 
Thore (1842, 1843, 1845), Chevers (1846), Crisp (1846), Ramsbotham 
(1846), Foster (1847), Clark (1848), Bednar (1852), Hale (1853), Buhl 
(1857), Vernon (1856), Carson (1857), Clar (1858), Bernard (i860), 
Devilliers (i860), Gulbert (i860), Almagro (1862), Rauchfuss (1864), 
Playfair (1870), Bradley (1873), Elliot (1877), Martin (1877), Chiari 
(1879), Pott (1879), Kleinschmidt (1881), Robinson (1881), Bianchi 
(1882), Turner (1882), Shattock (1883), Clarke (1884), Jacoby (1884), 
Brewer (1885), Bull (1885), Fussell (1888), Northrup (1888), Ziegen- 
speck (1888), Revilliod (1889), Sanger (1889), Holt (1890), Preisz (1890), 
Ruge (1891), Williams (1892), Jellett (1897), Reifschlager (1897), Huns- 
burger (1898), Keith (1898) 2 cases, Potter (1900), Rudlof (1900), Cautley 
(i90i),Baumgarth (i9O2),Champeter (1903), Grosse (1903), Wright (1903), 
Bouchacourt (1904), Lefas (1904), Letulle (1904), Emanuel (1906) 2 
cases, Konstantinowitsch (1906), Young (1906), Young & Robinson (1907), 
Cautley (1908), Paterson (1908), Stokes (1908), Paterson (1909), Wenner 
(1909), Girauld (1910), Sokolow (1910), Robertson (1911), Penner 
(1911), Fortman (1912), Knope (1912), Pappenheimer (1913), Rive et' 
Girard (1913), Gladstone & Russmann (1915). 
2. Defective at Base 
(a) Ventricular Septum Defective Below the Aorta.-The 
large majority of interventricular septum defects are of the base 
and of these the most frequent site of arrested development is 
the posterior part of the anterior septum (Rokitansky). It has 
been impossible to determine the percentage of defects in either 
group because observers so frequently make no report as to the 
portion of the base involved. This list and the one immediately 
following represent only a small part of the cases of defective 
septum reported; for other cases see the clinical classification of 
ventricular defects. 
(a) Ventricular septum defective below aorta: Howship (1813), Cheever 
(1821), Cerutti (1827), Lexis (1835), Quain (1856), Loschner & Lambl 
(i860) 2 cases, Peacock (i860), (1869), Johnson (1872), Rex (1874), 
Buhl (1878), Pott (1878) 2 cases, Babesiu (1879), Pott (1879) 2 cases, 
Peacock (1879), O'Sullivan (1880), Cronk (1881), Petit (1881), Revilliod 
(1882), Grant (1883), Moutart (1883), Hayward (1884), Menetrier 
(1884), Dumontpallier (1885), Habershon (1888), Mann (1889), Muhr Congenital Anomalies of the Heart 
19 
(1889), Preisz (1890) 4 cases, Variot et Gampert (1890), Rolleston (1891), 
Steven (1892), Geipel (1892), Meslay (1895), Eisenmenger (1897), 
(1898), Griffith (1899), Spalverini et Barbieri (1902), Amenville (1905), 
Rogers & Fortiscue (1905), Carpenter (1909), Erdmenger (1912), Griffith 
(1915). 
(b) Ventricular septum defective in pars membranacea: Loschner & 
Lambl (i860) 2 cases, Crocker (1878) (1879), Stone (1881), Toennies 
(1884), Willcocks (1886), Pryor (1889), Stadler (1891), Passow (1894), 
Rheiner (1896), Freyberger (1898), Spalverini & Barbieri (1902), Cowan 
(1903), Carpenter (1908), Bissell (1913), Heller & Gruber (1914), Morse 
(1915), Parrura (1916). 
(c) Other Defects of the Interventricular Septum.-Defects 
in other portions of the septum than the base are very unusual. 
The cases are generally of multiple openings and may be at any 
point in the body of the septum. The condition no doubt repre- 
sents a growth disturbance which was of short duration or suffi- 
ciently slight to permit the final normal developmental stages. 
Interesting cases have been reported by: 
Chiari (1881), Toennies (1884), Griffith (1897), Chessman (1905), and 
Robertson (1911). 
§ VIII. ANOMALIES OF THE INTERATRIAL SEPTUM 
The atrial septum presents, through its complexities of devel- 
opment, several problems which must be considered in inter- 
preting and classifying anomalies. The cavity of the primitive 
atrium is divided to form two chambers by a septum which is 
known as the septum primum. This septum grows downward 
into the cavity until it unites with the endocardial cushions. Be- 
fore this union is complete the lower border of the septum is free 
and the atria communicate below it by an opening which is known 
as the ostium primum. About the time that the division of the 
chambers is complete an opening appears in the septum primum 
which is the foramen ovale. A second septum, the septum secun- 
dum, grows downward to the right of the septum primum and 
some time after birth closes the foramen ovale. 
This study indicates that developmental disturbances of the 
interatrial septum are slightly more than half as frequent as 
those of the interventricular septum. Some defect of the atrial 20 
C. W. M. Poynter 
septum is present in about 36 per cent, of all cases of heart 
anomalies. As shown by the number of cases living to an ad- 
vanced age the disturbance to the circulation, even from a com- 
plete absence of the septum, is readily compensated. 
B. INTERATRIAL SEPTUM 
In these cases the growth disturbance has inhibited the devel- 
opment of both the septum primum and secundum. I have not 
found the condition as an isolated anomaly, but it is frequently 
found in conjunction with absence of the interventricular septum. 
The condition constitutes 16 per cent, of atrial septum dis- 
turbances. 
1. Atrial septum absent: Mery (1700), Wilson (1798), Ring (1805), 
Standert (1805), Farre (1814), Otto (1814), Meckel (1815), Marx (1820), 
Cheever (1821), Martin (1826) 2 cases, Cerutti (1827), Mauran (1827), 
Mayer (1827), Thore (1842) (1845), Crisp (1846), Foster (1846), Rams- 
botham (1846), Foster (1847), Darrach (1857), Clar (1858), Bernard 
(i860), Guibert (i860), Ahnagro (i860), Cameron (1871), Maier (1876), 
Marchand (1881), Robinson (1881), Shattock (1883), Jacoby (1884), Bull 
(1885), Northrup (1888), Chapatot' (1889), Birmingham (1892), Probyn- 
Williams (1894), Cade (1897), Ewald (1898), Hunsberger (1898), Rudlof 
(1900), Blondel (1901), Griffith (1902), Champeter (1903), Lefas (1904), 
Chartier (1905), Bernstein (1906), Konstantinowitsch (1906), McCrae 
(1906), Carpenter (1908), Girauld et Tissier (1910), Metzger (1911), 
Knope (1912). 
i. Atrial Septum Absent 
2. Anomalies of the Septum Primum 
In these cases two different conditions must be recognized. 
When the defect is along the dorsal (venous) wall-Ingalls (1907) 
has pointed out that it seems to be due to development of the 
septum primum too far to the right, so that instead of passing 
to the left of the opening of the superior vena cava it passes di- 
rectly through it and so creates an opening. When the opening 
is in the lower part of the septum, above the ventricles, it may 
be explained as a persistence of the ostium primum either through 
arrest of development of the septum primum or of the endocar- 
dial cushions. The latter cases are characterized by a semi- 
lunar opening low down in the septum. Congenital Anomalies of the Heart 
21 
It is sometimes impossible to tell in a given case whether the 
defect is of the septum primum or secundum; in general, how- 
ever, it may be said that lesions of the septum primum are located 
on the lower or posterior part of the atrial septum, while those 
of the fossa ovalis and upper part of the septum are defects of 
the septum secundum. 
Lacroix (1844), Bednar (1852), Smith (1880), Hopkins (1889), Preisz 
(1890) 3 cases, Hawkins (1891), Ruge (1891) 2 cases, Burke (1902), 
Dhotel (1902), Wright & Drake (1903), Ebbinghaus (1904), Soldner 
(1904), Ingalls (1907), Abbott (1910), Morrison (1912), Lusenbacher 
(1916). Nineteen cases. 
3. Anomalies of the Septum Secundum 
(a) Open Foramen Ovale.-A patent foramen ovale is so fre- 
quently encountered that it should not be considered as an anom- 
aly. In our dissecting rooms the foramen has been found patent 
in 25 per cent, of the subjects if we consider any condition in 
which a probe will pass as patency. Bizot (1837) found the 
foramen patent in 13 per cent, of cases in adults and Adami in 
14.5 per cent of 1,374 autopsies. Peacock (1852) explained the 
closure of the foramen showing that the shifting of the cornua 
and the drawing up of the valve about the margin of the opening 
produces a physiological closure even when the finger can be 
thrust through and the valve so displaced. The fact that an ad- 
hesion had not formed between the septum and the valve he did 
not consider as an anomaly. On the other hand, those cases, so 
frequently described, in which the foramen is sufficiently open 
to admit a finger, must be considered as anomalous. The condi- 
tion of fully open foramen ovale was recognized as an anomaly 
by Peneau in 1598. 
All degrees of failure of closure of the foramen may be seen, 
but this group consists largely of cases in which there is an ab- 
sence of the septum ovale. Cases in which the septum contains 
so many openings as to be spoken of as "cribiform" are included 
in this list. Twenty per cent, of all cases present no other devel- 
opmental defect. The condition represents 70 per cent, of all 
atrial septum defects and is encountered in 23 per cent, of all 
hearts studied. 22 
C. IV. M. Poynter 
(a) Open ovale: Littre (1700), Widmann (1717), Amyand (1736), du 
Hamel (1740), Hunter (1783) 2 cases, Moreau (1790), Baillie (1808) 2 
cases, Schuler (1810), Langstaff (1811), Dorsay (1812), Jurine (1815) 2 
cases, Fleischmann (1815), Gamage (1815), Knox (1815), Meckel (1815), 
Hein (1816), Howship (1816), Kreysig (1817), Nasse (1811), Pasqualine 
(1827), Basedow (1828), Graves & Houston (1830), Braune (1833), Monet 
(1833), Bloxam (1834), Fearn (1834), Lexis (1835), Spittai (1835), 
Chassenat (1836), Napper (1840), Stolz (1841), Smith (1841), Douglas 
(1842), Mansfeld (1843), Thore (1843), King (1844), Harrison (1845), 
Iliff (1845), Shearman (1845), Taylor (1845), Chevers (1846), Hare 
(1846) 2 cases, Peacock (1846) 2 cases, Dittrich (1849), Toynbee (1849), 
Johnson (1850), Hale (1853), Blin (1854), Keil (1854), Graily-Hewitt 
(1856), Quain (1856), Carson (1857), Meyer (1857), Schilling (1857). 
Baly (1858), Devilliers (i860), Mallwo (i860), Gubler (1861), Heine 
(1861), Hervieux (1861), Ollivier (1861), Gueniot (1862), Mannkopf 
(1862), Code (1863), Foster (1863), Lebert (1863), Buchanan (1864), 
Peacock (1864), Rauchfuss (1864), Kussmaul (1866), Vulpian (1868), 
Hunter (1869), Peacock (1869), da Costa (1870), Hunter (1870), Gelan 
(1873), Peacock (1873), Landouzy (1874), Lucas (1874), Longhurst 
(1874), Rex (1874), Bogler (1875), Barlow (1876), Katz (1877), Saundby 
(1877), Caton (1878), Finlay (1878), Heinman (1878), Johnson (1878), 
Crocker (1879) 3 cases, Makuna (1879) 2 cases, Pott (1879), Bucquay 
(1880), Ballet (1880), Chiari (1880), Crocker (1880), Desnos et Callias 
(1880), Gibier (1880), Lees (1880), Luneau (1880), O'Sullivan (1880) 
3 cases, Smith (1880), Tirard (1880), Stif el (1880), Peacock & Ashby 
(1881), Eskridge (1881), v. Etlinger (1881), Fowler (1882) 2 cases, Liv- 
ingston (1883), Toupet (1883), Barand, Barry (1884), Bury (188L4), 
Chaffey (1884), Holt (1884), Kruger (1884), Moore (1884), Brewer 
(1885^ Epstein (1886), Vilon et Leveque (1884), Leo (1886), Harris 
(1887), Hendly (1887), Toupet (1887), Gampert' (1889), Klipstein (1890) 
2 cases, Mackenzie (1889) 2 cases, Miura (1889), Oliver (1889) 2 cases, 
Revilliod (1889), Doming (1890), Hadden (1890), Haw (1890), Monisset 
(1890), Holt (1890), Griffith (1891), Howard (1891), Lewis (1892), 
Moore (1891), Turner (1891), Laffitte (1892), Moore (1892), Burgess 
(1893), Lepine (1894), Nazaroff (1895), Caille (1896), Frenkel (1896), 
Monod (1896), Packard (1896), Rheiner (1896), Roth (1896), Siredey 
(1896), Coyon (1897), Griffith (1896), Jacobson (1897), Hun (1897), 
Grothe (1898), Lamouroux (1899), Rolly (1899), Armand (1900), Starck 
(1900), Cautley (1901), Andrews (1902), Ardissonne (1902), Bourlot 
(1902), Burke (1902) 3 cases, Cautley (1902) 2 cases, Cowan (1903) 3 
cases, Delherm et Laignel (1903), Griffith (1903), Gutkind (1903), 
Schreiber (1903), Tylecote (1903), Cohn (1904), Minkowski (1904), 
Pritchard (1904), Ellis (1905) 2 cases, Krausse (1905) 2 cases, Rogers 
(1905), Emanuel (1906) 2 cases, Lucien & Harter (1907), Ohm (1907), Congenital Anomalies of the Heart 
23 
Young & Robinson (1907), Carpenter (1908), Paterson (1908), Carpenter 
(1909), Gandy et Brule (1909), Planchu et Gardere (1909), Weiss-Eder 
(1909), Wenner (1909) 4 cases, Serverog (1910), Boulach (1910), Bokay 
(1911), Robertson (1911), Boxwell (1912), Erdmenger (1912), Keith 
(1912). Black (1914), Gasquet (1913), Hebb (1913), Hingar (1913), 
Pappenheimer (1913), Morse (1915), Monteiro (1917). Two hundred and 
twenty-five cases. 
(&) Other Anomalies of the Septum Secundum.-The septum 
ovalis may be cribiform as in the case of Finlay (1878), Smith 
(1880), Oliver (1889) and others. This is a different anomaly 
than simple arrest of growth leading to an open foramen ovale, 
but I have included it in the group above. The septum secundum 
may fail to develop as in the case of Hebb (1889), or may be 
defective at other points than in the fossa ovalis. An opening 
above and anterior to the fossa ovalis may be considered as a 
defect in the development of the septum secundum. The condi- 
tion seems to occur with about the same frequency as defect of 
the septum primum. They represent 7.5 per cent, of all defects 
of the atrial septum. 
Kelly (1869), Peacock (1877), Pott (1878) 3 cases, Chiari (1880), Liv- 
ingston (1883), Greenfield (1889), Hebb (1889), Sanger (1889), Probyn- 
Williams (1894), Prezewoski (1896), Keith (1898), Griffith (1899), Moore 
(I9°3), Thompson (1903), Carpenter (1908), Wassenbach (1910), Reed 
(1911). Twenty cases. 
§ IX. 
IV. ABNORMALITIES WITHIN THE CAVITIES OF 
THE HEART 
A. RIGHT ATRIUM 
i. Contracture or Dilatation 
It seems to me that there may be some question of the propriety 
of including cases of contracture and dilation among congenital 
malformations. Many of these cases are of sufficient age and 
the circulation is so disturbed that it is entirely possible that the 
cases are simple pathological reactions of the same type with 
which we are familiar in other cardiac diseases; this applies espe- 24 
C. W. M. Poynter 
cially to the cases of dilation. Cases of congenital dilation 
and contracture have been reported and it is possible that a cham- 
ber may over or under develop, due to factors interfering with 
growth; however, it seems hardly worth while to burden this 
study with a group of borderline cases. 
2. Accessory Septa in the Right Atrium 
This consists of a network or delicate membrane originating 
from the region of the Eustachian or Thebesian valve and ex- 
tending across the atrium to attach to some point on the septum. 
Chiari (1897) explained the condition as the mal-development 
of the valvula venosa sinistra or septum spurium. He was de- 
scribing particularly the network; a number of observers have 
since called a similar structure the "Chiari Net or Netz." Other 
cases characterized by a definite band, Ruge (1891) thought may 
be a redundant septum primum. 
Monet (1833), Thompson (1843), Eskridge (1881), Geffrier (1881), 
Moore (1882), Cayla (1884), Leo (1886), Ruge (1891), Lepine (1894), 
Chiari (1897), Swan (1898), Le Count (1901), Ebbinghaus (1904), Lesieur 
et Froment (1911). 
B. ABNORMALITIES OF THE LEFT ATRIUM 
1. Contraction and Dilation 
The left atrium has been the seat of a congenital contraction 
or arrest of development in cases observed by Peacock (1866), 
Roach (1880), Packard (1896), and Lamouroux (1899). 
I have found no cases in which a dilation suggesting congenital 
origin has been described. 
2. Accessory Septa in the Left Atrium 
This condition does not seem to have been recognized by the 
earlier observers. The accessory septum stretches across the 
atrium dividing off a right posterior superior chamber into which 
the pulmonary veins open. Borst (1906) considers this septum 
to be a misplaced septum primum; Griffith (1903a) concludes 
that the band is a redundancy of the tissue of the valve of the Congenital Anomalies of the Heart 
25 
fossa ovalis, "An exaggeration of a state of affairs not usually 
recorded as abnormal, viz., the presence of a reticula proceeding 
from the margins of the valve of the foramen ovale." Williams 
& Abrekossoff (1911) conclude, "That the muscular portion of 
the anomalous septum in its posterior right part is a continuous 
portion of the muscular structure of the right posterior portion 
of the atrial wall . . . and that the abnormal septum arose from 
a separation of the atrial wall and that the splitting had its origin 
in the right angle of the wall." 
The following cases have been studied: 
Andral (Ref. Paget, 1831), Church (1868), Fowler (1882), Moore 
(1882), Rolleston (1896), Papillon (1897), Martin (1899), Griffith (1903) 
3 cases, Potter & Ransom (1904), Hosch (1907), Stoeber (1908), William 
& Abrekossoff (1911), Sternberg (1913). 
C. RIGHT VENTRICLE 
1. Contracture of the Right Ventricle 
The right heart seems to be especially sensitive to develop- 
mental disturbances. The right ventricle is made up of two ele- 
ments developmentally; Keith has shown that the proximal por- 
tion of the bulb becomes incorporated in the wall of the right 
ventricle to form the conus arteriosus or infundibulum. In many 
of the cases of contracture the conus portion of the ventricle has 
suffered from arrest of development and in some cases the re- 
mainder of the ventricle is also only slightly developed or absent. 
The condition is usually accompanied by stenosis or atresia of 
the pulmonary artery, particularly the orifice. 
Meckel (1815), Jacobson (1849), Loschner & Lambl (i860), Mallwo 
(i860), Gubler (1861), Kussmaul (1866), Demange (1874), Jackson 
(1875), Crocker (1879), O'Sullivan (1880), Etlinger (1882), Moutart- 
Marten (1883), Menetrier (1884), Kronig (1887), Preisz (1890), Variot 
et Gampert' (1890), Barbillon (1886), Howard (1891), Laffitte (1892), 
Boquet (1893), Haury (1894), Northrup (1894), Passow (1894), Rheiner 
(1896), Siredey (1896), Young (1896), Jacobson (1897), Armand (1900), 
Fennell (1901), Spalverine (1902), Cohn (1904), Ellis (1905), Young & 
Robinson (1907), Gandy et Brule (1909), Wassenbach (1910)- These 
cases relate particularly to arrest of development of the conus while in 
the following the entire ventricle is contracted. 
Hare (1852), Heinman (1878), Moore (1891), Leo (1886), Potter 
(1900), Bernstein (1906), Carpenter (1909). 26 
C. W. M. Poynter 
2. Accessory Septum in Right Ventricle 
These cases are characterized by a septum in the upper part of 
the ventricle. They are related to the preceding group in that 
the developmental disturbance is of the conus, they differ in that 
the conus may develop proportionately with the rest of the ven- 
tricular wall and a portion of the bulb about the bulbar orifice 
fails to drop out. When the conus is large and the bulbar orifice 
is small the condition has been referred to as " three ventricles." 
Chassinat (1836), Husson (1836), Pegne (1847), Peacock (1869) 2 
cases, Peacock (1876), Crocker (1878) (1879), Mackenzie (1879) 2 cases, 
Nixon (1879), Lees (1880), Kleinschmidt (1881), Stone (1881), Toupet 
(1883), Mackenzie (1889), Cassell (1891), Ruge (1891), Wendle (1898), 
Young & Robinson (1907) 2 cases, Cautley (1908), Black (1914). 
D. LEFT VENTRICLE 
i. Contracture of the Left Ventricle 
There is difficulty in accounting for the stenosis of the left 
conus as a simple developmental defect. As already stated the 
literature shows that congenital disturbances have a marked predi- 
lection for the right half of the heart; Rauchfuss stated that the 
relation of lesions between the right and left sides was as io: I. 
Keith thinks that only a small portion of the bulb is incorporated 
in the left ventricle, so left contractures are not quite comparable 
to those of the right side. If we consider these cases as a simple 
arrest of development of the ventricular chamber, as has been 
suggested, and as has been accepted for the last of the preceding 
group (contracture of right ventricle), then the left chamber 
seems to be more prone to mal-development than the right. It 
seems to me probable that the following list contains more cases 
in which the bulbar element is responsible for the stenosis than 
those of arrest of development of the primary ventricular cham- 
ber; it seems, however, that this question cannot be settled by 
examination of the specimens. Even in the cases of an anular 
thickening of the ventricular wall just below the orifice of the 
aorta it is difficult to distinguish the congenital cases from those 
of stenosis due to endocarditis. Congenital Anomalies of the Heart 
27 
Peacock (1846), Parker (1847), Dittrich (1852), Banks (1857), Hare 
(1853), Peacock (i860), Heine (1861), Virchow (1861), Rauchfuss (1864), 
Smith (1866), Hallopeau (1869), Allis (1872), Klumpke (1887), Ziegen- 
speck (1888), Miura (1889), Preisz (1890), Lamouroux (1899), Lowen- 
thal (1900), Schmencka (1907), Cautley (1908), Wienner (1909), Girauld 
et Tissier (1910), Gladstone & Russmann (1915). 
2. Accessory Septum in the Left Ventricle 
Turner (1895) described a "moderator" band which arose 
from the anterior septal wall, passed directly across the chamber 
and was attached to the posterior wall. It does not seem that 
this condition is analogous to the diaphragm encountered in the 
right ventricle, more probably it is related to the anomalous cordae 
tendinae which have been occasionally encountered. These run 
across the ventricle in an irregular way and may be attached to 
the semilunar valves. In some cases they form a reticular net- 
work, suggesting a division of the ventricle into two chambers. 
They may represent an over stimulus of the process which leads 
to the development of the normal papilli and cordae tendinae; 
they may be the result of a foetal endocarditis as suggested by 
Tawara (1906). They are not incompatible with life but may 
cause musical murmurs. 
Bouillaud (1862), Archer (1878), Bailey (1894), Rohrle (1896), Lewis 
(1897), Marckewald (1898), Hamilton (1899), Rossie (1902), Winkler 
(J9O3), Poscharessky (1904), Gallis (1904), Tawara (1906), Monckeberg 
(1908). 
§ x. 
V. IRREGULARITIES IN THE DEVELOPMENT OF 
THE TRUNCUS COMMUNIS ARTERIOSUS 
Anomalies in this section are frequently classed with arterial 
irregularities, but belong properly with the heart. Early in the 
development of the heart there is a slight contracture of the tube 
at intervals dividing it into five parts, of which the last two are 
the bulbus cordis and the truncus arteriosus. When the heart 
assumes an " S " shape the bulbus cordis comes to lie in front of 
the ventricle the adjacent walls of the bulb and the ventricle fuse, 
then disappear and the proximal part of the bulbus becomes in- 28 
C. W. M. Poynter 
corporated in the ventricular wall. This adjustment brings the 
truncus arteriosus against the atrial wall ventrally and its open- 
ing over the two ventricles. Later the canal of the bulbus cordis 
and truncus arteriosus is divided by a septum, the aortic septum, 
which in the truncus arteriosus produces the aorta and pulmonary 
artery and in the bulbus grows down to meet the ventricular 
septum and helps to complete the separation of the ventricles. 
The close association of the development of these structures 
with the general development of the heart is indicated by the 
frequency with which anomalies of their development are asso- 
ciated with other cardiac irregularities, particularly defective 
interventricular septum. In this group of cases 20 per cent, of 
the hearts which showed complete lack of ventricular septum 
also lacked an aortic septum. Approximately 27 per cent, of all 
defects of the ventricular septum were associated with irregu- 
larities of the aortic septum. 
A. Persistent Truncus Communis 
As seen above, the aorta and pulmonary artery are developed 
by the growth of the aortic septum which begins as two distal 
ridge-like thickenings in the lumen of the truncus communis; 
these grow out, fuse and so form a septum which normally takes 
a spiral course. When the septum fails to develop the embryonal 
truncus communis persists; this common trunk is generally con- 
sidered as the homologue of the aorta and the case is spoken of 
as lacking the pulmonary artery, but this interpretation is incor- 
rect. There is a condition of arrest of development of the pul- 
monary artery to be spoken of later but it may be distinguished 
from persistent truncus by the fact that the two pulmonary 
arteries do not spring from the back of the common artery. The 
persistent truncus may open from the right ventricle as in the 
early embryo or from both ventricles over the defect in the inter- 
ventricular septum. 
Various degrees of arrest of development less than complete 
absence of the aortic septum have been reported, the septum may 
begin its normal development then be arrested; in such cases a 
truncus communis arises from the heart and in a short distance Congenital Anomalies of the Heart 
29 
divides into aorta and pulmonary artery as in Clark's (1885) 
case. Rokitansky reported a somewhat more interesting case in 
which, in addition to the above condition, a remnant of aortic 
septum was present in the common trunk. Defects of the septum 
spoken of as communication between the aorta and pulmonary 
artery no doubt represent minor disturbances in the develop- 
mental process. 
Persistent truncus communis is always associated with defect- 
ive development of the ventricular septum and in 70 per cent, 
there is also defective atrial septum. There are no characteristic 
clinical symptoms belonging to the condition. While the anomaly 
adds to the embarrassment of the circulation, it is difficult to say 
how much since there are so many other factors to consider. In 
cases occurring in single ventricled hearts the average age was 
slightly more than two months, while in the cases associated with 
simply defective ventricular septum the average was slightly 
more than three years; in the first group the maximum age was 
ten months, in the latter nineteen years. Cyanosis was present 
to a greater or less degree in over one third of the cases. The 
following list shows the condition present in 4.8 per cent, of all 
hearts studied. 
Wilson (1798), Standert (1805), Farre (1814), Meckel (1815), Laurence 
(1837), Stoltz (1841), Foster (1846-8), Ramsbotham (1846), Clark (1848), 
Toynbee (1849), Hyernaux (1851), Vernon (1856), Clar (1858), Bernard 
(i860), Hervieux (1861, Buchanan (1864), Bradley (1873), Pott (1879) 
2 cases, Ribinson (1881), Barand, Barry et Rachet (1884), Barbillon 
(1886), Clark (1884), Muhr (1889), Preisz (1890), Charrin et LeNoir 
(1891), Bellot (1895), Gallois (1896), Cade (1897), Martin (1897), Pet- 
schel (1897), Civatte (1900), Cautley (1902), Spalverini et Barbieri 
(1902), Wright & Drake (1903), Rispal & Bay (1904), Elsbergen (1905), 
Krausse (1905), Hand (1908), Wenner (1909) 2 cases, Knope (1912), 
Dickson (1913). 
B. Defect of the Aortic Septum 
These cases are characterized by a communication between the 
aorta and pulmonary artery above the semilunar valves. In 
almost half of the cases there are other defects of the heart. 
The average age is 3 years 1 month, the maximum age 25 years. 
The lesion produces no symptoms (Livingston 1883), and is with- 30 
C. W. M. Poynter 
out clinical interest. The lesion is present in 1.7 per cent, of the 
hearts studied in this group. 
Lediberder (1836), Wilks (i860), Fraentzel (1868), da Costa (1870), 
Baginsky (1879), Caesar (1880), Chiari (1880), Rickards (1881), Charteris 
(1883), Livingston (1883), Cayla (1885), Girarde (1895), Cazin (1897), 
Hektoen (1899), case in Guys Hospital Museum. 
C. Transposition of Aorta and Pulmonary Artery 
Abnormal positions of the great vessels coming from the heart 
has generally been discussed under the title of transposition. 
This condition results from anomalous rotation of the aortic 
septum. The whole subject was clarified by the wonderful work 
of Rokitansky (1875), but more recent investigations have sim- 
plified his classification and corrected errors which at the time 
of his work could not be recognized. 
Greil (1903) has shown that the bulbus cordis of more primi- 
tive forms is represented in the mammalian heart, first forming 
part of the anterior limb and later becoming incorporated in the 
wall of the right ventricle and truncus arteriosus. The truncus 
arteriosus, as shown above, becomes differentiated into the aorta 
and pulmonary artery by the development of the septum which 
divides its lumen. Robertson (1913) has shown that, in Lepido- 
siren, the septum described a spiral in a clockwise direction from 
its distal beginning of 270 degrees. In man this spiral is some- 
what less, or about 135 degrees. Distally the septum develops 
laterally so that the pulmonary artery is dorsal and the aorta 
ventral in position and as they approach the heart the positions 
are reversed. 
In situs viscerum transversus normal rotation is reversed and 
this septum together with other structures of the thorax and 
abdomen present a mirror picture of the normal. When the 
condition of reversal is limited to the heart it is known as dextro- 
cardia. Lochte (1898) suggested that the ventricular loop could 
rotate normally or the reverse independently of the remainder of 
the heart. Lewis (1915) accepted this theory and by recon- 
structing the different developmental stages in reverse rotation 
showed that such development is possible. Much experimental Congenital Anomalies of the Heart 
31 
work has been done with the problem of reverse rotation and 
while the subject still is obscure in many particulars, there seems 
to be no reason why disturbing factors should not produce a 
reversal of the ventricular loop without other heart structures 
being influenced by them. 
The various types of transposition seem to be the result of dis- 
turbances of normal rotation of the various parts of the heart. 
Rokitansky (1875) believed that if the concavity of the aortic 
septum be reversed the relation of the aorta and pulmonary 
artery would be reversed. His extensive classification failed to 
take into account fhe possible movement of the ventricular loop, 
also he considered a ventricle, even when guarded by a bicuspid 
valve, as right when it occupied a position on the right side of 
the viscus. It has since been shown by Lochte and others how 
important it is to identify the ventricle as tricusped or bicusped. 
Keith (1909) suggested that the atrophy of the bulbus cordis 
around the pulmonary artery is responsible for the transposition; 
Robertson (1913) has shown that his theory is contrary to fact, 
for while he places the aortic orifice on the right and the pul- 
monary on the left of the bulbus cordis, exactly the reverse is 
true in the dipnoan heart. Robertson concludes from a study of 
lower forms that " If the bulbus cordis develops as a short, 
straight tube without any disparity in the length of the walls of 
its middle segment, no torsion of the vessels, that is, the aortico- 
pulmonary septum, will take place, the middle part of the bulbus 
cordis where it should occur being so to speak wiped out." 
A study of the cases seems to reveal three distinct conditions 
which may be classified as follows (Poynter 1916) : 
1. A failure of rotation of the aortic septum in a heart in 
which the ventricular loop has developed normally. The aorta 
is in front of the pulmonary artery and opens from a tricusped 
ventricle. This is the most frequent form of transposition. 
2. A failure of rotation of the aortic septum in a heart which 
has developed by rotation in the reverse direction. The aorta is 
in front of the pulmonary artery and opens from a tricusped 
ventricle. The condition is the mirror picture of the previous 
group and may be found in situs viscerum transversus. 32 
C. IV. M. Poynter 
3. The aorta is in front of the pulmonary artery and opens 
from a bicusped ventricle. This condition is very difficult to 
explain; the most acceptable theory is that there has been a left- 
to-right twist of the left around the right ventricle with a corre- 
sponding right-to-left deviation of the septum (Lochte). 
Clinically the condition presents no special symptoms. It is 
usually associated with other congenital lesions of the heart, par- 
ticularly defective interventricular septum; however, nine cases 
were encountered in this study which presented no other lesion 
of importance. The condition was found in 12 per cent, of all 
hearts studied and the cases showed an average age of 3 years. 
The maximum age was 39 and 75 per cent, of the cases died 
under one year. 
Class 1: Ring (1805), Baillie (1808), Langstaff (1811), Kreysig (1817), 
Nasse (1811), Muller (1822), d'Alton (1824), Tiedemann (1825), Martin 
(1826) 2 cases, Martin (1839), Ducrest (1840), Thore (1843), King 
(1844), Thore (1845), Beck (1846), Parker (1846), Johnson (1850), Ward 
(1851), Keil (1854), Darrach (1857), Meyer (1857), Reynolds (1857), 
Code (1863), Lebert (1863), de Bary (1864a), Meigs (1867), Arnold 
(1868), Frankel (1870), Kelly (1871), Barlow (1876), Maier (1876), Elliot 
(1877), Janeway (1877), Martin (1877), Babesiu (1879), Crocker (1879), 
Lees (1879), Mackenzie (1879), Mazatti (1879), Peacock & Ashby (1881), 
Rickards (1881), Bianchi (1882), v. Etlinger (1882), Holl (1882), Pope 
(1882), Scott (1882), Turner (1882), Shat'tock (1883), Durozier (1885), 
Epstein (1886), Harris (1887), Klumpke (1887), Fussell (1888), Gampert 
(1889), Mackenzie (1889), Ramm (1889), de Renzie (1889), Revilliod 
(1889), Doming (1890), Preisz (1890), Geipel (1892), Hochsinger (1891), 
Lewis (1891), Saunders (1892), Mirinescu (1893), Bonne (1895), Lochte 
(1894), Freyberger (1895), Theremin (1895), Caille (1896), Litten 
(1896), Monod (1896), Rotch (1896), Coyon (1897) 2 cases, Freyberger 
(1898), Rolly (1899), Rudlof (1900), Starck (1900), Meinertz (1901), 
Peters (1901), Thiele (1902), Champeter (1903), Cowan (1903), Brain 
(1905), Ellis (1905), Apert et Brezaud (1906), Emanuel (1906), Young 
(1906), Lucien & Harter (1907), Young & Robinson (1907) 3 cases, 
Planchu & Gardere (1909), Wenner (1909) 3 cases, v. Bokay (1911), Lubs 
(1911), Robertson (1911), Variot et Moranci (1911), Erdmenger (1912), 
Fortmann (1912), Keith (1912), Bissell (1913), Pozdyum (1912), Rivet et 
Gerard (1913), Heller & Gruber (1914). 
Class 2: Gamage (1815), Hickman (1869), Schrotter (1870), Ogston 
(1874), Graanboom (1891), Griffith (1891), Birmingham (1892), McCrae 
(1906), Stokes (1909), Wenner (1909). 
Class 3: Walsh (1842), Stoltz (1851), Gutwasser (1870), Pye-Smith Congenital Anomalies of the Heart 
33 
(1872), Rokitansky (1875), Toennies (1884), Klumpke (1887), Mann 
(1889), Grunmach (1890), Lochte (1898), Thiele (1902), Wenner (1909), 
Lubs (1911). 
D. Aorta Opening from Both Ventricles (Rechtslage) 
There is still some question as to how this group of cases should 
be placed, but, since the theory advanced by Rokitansky basing 
their etiology on an irregular development of the aortic septum 
is still generally accepted, they are placed in this group. The 
aorta is not carried as far to the left as normal and opens over a 
defect in the interventricular septum. The condition is gener- 
ally associated with pulmonary stenosis or atresia, but there is 
no transposition. 
Sandifort (1777), Cailliot (1807), Obet (1808), Meckel (1809), Palois 
(1809), Howship (1816), Reeland (1818), Cheever (1821), Basedow 
(1828), Smith (1841), Peacock (1847), Greig (1852), Sturock (1859), 
Mallwo (i860), Peacock (i860), Hervieux (1861), Peacock (1871), Wyss 
(1871), Pott (1878), Peacock (1880), Abercrombie (1881), Rickards 
(1881), Grant (1883), Toupet (1883), Hayward (1884), Moore (1885), 
Vilon (1884), McKee (1887), Murray (1887), Bingham (1889), Hebb 
(1889), Pryor (1889), Voelcker (1892), Thomson (1903), Gutkind (1905), 
Young & Robinson (1907), Carpenter (1908), Hebb (1913), Morse (1915). 
E. Aorta Opening from the Right Ventricle 
This group may be considered as due to the same factors which 
produced the last condition, carried to a slightly greater degree. 
The pulmonary artery is normally placed in relation to the aorta, 
but there are some irregularities of the vessels in relation to the 
right ventricle which deserve special mention. In Peacock's 
(1856) case the aorta arose from the sinus and the pulmonary 
artery from the infundibulum, in Tooth's (1883) case conditions 
were just reversed, van Hall (1825) reported a case in which 
the aorta communicated with the right ventricle through a long 
canal placed in the muscular wall of the cavity. Hickman (1869) 
found the condition in a case of situs viscerum transversus. 
The pulmonary is generally contracted. 
Mery (1700), Abernethy (1794), van Hall (1825), Babington (1846), 
Chevers (1846), Peacock (1846), Peacock (1856), Quain (1856), Meyer 34 
C. W. M. Poynter 
(1857), Mallwo (i860), Heine (1861), Hickman (1869), Hunter (1869), 
Peacock (1873), Barlow (1876), Pott (1878), Smith (1880), Tooth (1883), 
Gevaert (1885), Bury (1887), Habershon (1888), Cadet de Gassecourt 
(1890), White (1891), Saunders (1892), Boquet (1893), Bornier (1907), 
Hebb (1913). 
§ XL 
VI. ABNORMALITIES OF THE PULMONARY TRUNK 
A and B. Pulmonary Stenosis and Atresia 
Anomalous development, leading to partial or complete closure 
of the pulmonary artery, is of frequent occurrence among con- 
genital heart irregularities. In this study it is present in almost 
34 per cent, of all cases. A variety of conditions is found; the 
artery may simply be smaller than normal or the stenosis may be 
confined to the orifice, the semilunar valves may be grown to- 
gether so that only a minute opening remains or closed forming 
an obstructive diaphragm, the artery may be shrunken to form 
a fibrous cord or be entirely wanting. 
The presence of this anomaly in conjunction with others of the 
heart has long been recognized. Morgagni (1728) considered 
the condition congenital and believed that it was responsible for 
the persistence of the foramen ovale by the stagnation of blood 
in the right ventricle. As already pointed out, Hunter saw a 
connection between the stenosed artery and defective ventricular 
septum. 
Many observers have considered that the condition resulted 
from foetal endocarditis and, although this cause is not now gen- 
erally accepted, it is impossible to prove that certain cases are not 
produced by an early inflammatory reaction. Peacock and Ro- 
kitansky looked on the condition as the result of error in devel- 
opment of the aortic septum. It seems to me that Keith (1909) 
has offered the most satisfactory explanation in his classification 
of the cases as partial or complete arrest of developmental expan- 
sion of the infundibulum. 
Cases of complete obstruction of the pulmonary artery may be 
compensated for by defective ventricular septum, open ductus 
arteriosus or, more rarely, enlarged bronchial arteries. Cyanosis Congenital Anomalies of the Heart 
35 
is more frequently found in these cases than any other type of 
irregularity, but is by no means constant. There seems to be 
no foundation for the statement, which has been frequently made, 
that they are particularly subject to pulmonary tuberculosis. 
This anomaly has been of more interest clinically than any 
other congenital cardiac condition. Various symptoms and phys- 
ical signs have been suggested as characteristic for the lesion; it 
is, I think, generally admitted that the exact diagnosis of the 
other anomalies which so frequently accompany it is impossible. 
Its association with other lesions may be seen by reference to the 
clinical classification in Section XVII. Many of the statistical 
studies of age at death, etc., are of slight value because they do 
not take into account the part played by the associated anomalies. 
The frequency relationship of stenosis to atresia has been re- 
ported as follows: 
Peacock 90:29 
Rauchfuss 81: 33 
Deguise 30:4 
Kussmaul 64:26 
Abbott 116:34 
This Study 158:94 
A. Pulmonary Stenosis 
The narrowing of the pulmonary trunk may involve the orifice 
or a part or all of the canal or both. Keith thinks that in 90 per 
cent, of the cases the right ventricle in its infundibular portion 
is also involved. I am sure that such an estimate is too high if 
we are to rely on the published reports in this series. Hyper- 
trophy and dilatation of the right ventricle occur in many cases, 
but these conditions are by no means constant. 
As already pointed out, the position of the aortic opening is 
changed in many cases so that it may open from the right ventricle. 
The same general statements apply equally to atresia of the 
pulmonary artery, consequently a separate discussion for such 
cases is not called for. Lists of cases for both stenosis and 
atresia follow, grouping the cases according to the anatomical 
position of the lesion. 1 36 
C. W. M. Poynter 
i. Stenosis of the pulmonary orifice: Baillie (1808), Marshall (1830), 
Lexis (1835), Escalier (1845), Itiff (1845), Shearman (1845), Peacock 
(1846), Denuce (1849), Quain (1856), Hare (i860), Heine (1861), Mann- 
koff (1862), Vulpian (1868), Peacock (1869) 2 cases (1871), Deguise 
(1872), Johnson (1872), Rex (1874), Peacock (1876), Saundby (1877), 
Crocker (1878), Bussey (1880), Fereol (1881), Petit' (1881), Rickards 
(1881), Revilliod (1882), Livingston (1883), Bury (1884), Kruger (1884), 
Bull (1885), Dumontpallier (1885), Gevaert (1885), Schrotter (1887), 
Toupet (1887), Bingham (1888), Luzet (1890), Liegeois (1891), Ruge 
(1891), Moore (1892), Steven (1892), Freyberger (1895), Nazaroff 
(1.895), Rheiner (1896), Coyon (1897), Hun (1897), Keith (1898), Thom- 
son (1898), Rudlof (1900), Burke (1902), Krausse (1905), Bissell (1913), 
Milland (1914). Total 54 cases. 
2. Stenosis of the pulmonary trunk: Chemeneau (1699), Sandifort 
(1777), Hunter (1783), Abernathy (1794), Palois (1809), Schuler (1810), 
Dorsay (1812), Knox (1815), Hein (1816), Marx (1820), Muller (1822), 
Graves & Houston (1830), Bloxam (1834), Napper (1840), Ward & 
Parker (1846), Peacock (1846) (1849), Maurice (1853), Quain (1856), 
Peacock (1856), Voss (1856), Carson (1857), Meyer (1857), Peacock 
(i860), Virchow (1861), Peacock (1870), Wyss (1871), Allis (1872), 
Assmus (1877), Buhl (1878), Cossy (1878), Crocker (1879) 2 cases, 
Mackenzie (1879), Peacock (1879), Lees (1880), Peacock (1880), Schantz 
(1880), Abercrombie (1881), Eskridge (1881), Cadet de Gassecourt 
(1882), Graves & Houston (1883), Toupet (1883), Hayward (1884), 
Moore (1884), Durozier (1885), Moore (1885), Sewastianoff (1885), 
Vilon et Leveque (1885), Barbillon (1886), Murray (1887), Schule (1888), 
Hebb (1889), Mann (1889), Moore (1889), Cadet de Gassecourt (1890), 
Holt (1890), Preisz (1890) 3 cases, Stadler (1890), Variot (1890), Moore 
(1891), Renvers (1891), Rolleston (1891), Ruge (1891), Brauner (1892), 
Moore (1892), Voelcker (1892), Pic (1893), Boquet (1893), Lepine 
(1894), Frenkel (1896), Jacobson (1897), Trepp (1898), Wendle (1898), 
Starck (1900), Burke (1902) 2 cases, Cautley (1902), Spalverini et Bar- 
bieri (1902) 2 cases, Cowan (1903), Griffith (1903), Peiper (1903), 
Schreiber (1903), Letulle (1904), Minkowski (1904), Ellis (1905), Eman- 
uel (1906), Kiihne (1906), Carpenter* (1908) (1909), Paterson (1909), 
Serverog (1910), Wassenbach (1910), Boxwell (1912), Keith (1912), 
Black (1914), Hebb (1913) 2 cases, Hinger (1913), Pozdyunm (1912), 
Heller & Gruber (1914). Total 104 cases. 
B, 1. Atresia of the pulmonary orifice: This list also includes all cases 
in which the position of the obliteration is not stated. Fleischmann (1815), 
Meckel (1815), Howship (1816), Cheever (1821), van Hall & Vrolik 
(1825), Mauran (1827), Fearn (1834), Spittai (1835), Douglas (1842), 
Mansfeld (1843), Friedeberg (1844), Shearman (1843), Chambers (1846), 
Chevers (1846), Peacock (1846), Bednar (1852), Wallach (1852), Hare Congenital Anomalies of the Heart 
37 
(1853), Darrach (1857), Graily-Hewitt (1856), Morey (1857), Baly 
(1858), Gueniot (1862), Peacock (1864), Rauchfuss (1864), Arnold 
(1868), Peacock (1869) 2 cases, Deguise (1872), Peacock (1873), Lucas 
(1874), Heinman (1878), Pott (1878) 2 cases, Raub (1878), Nixon (1879), 
Pott (1879), Luneau (1880), Stifel (1880), Cronk (1881), Vilon et 
Leveque (1884), Ashby (1884), Leo (1886), Vincenzi (1886), Bury (1887), 
Bingham (1888), Howard (1891) (1892), Burgessl (1893), Probyn- 
Williams (1894), Hunsberger (1898), Civatte (1900), Potter (1900), 
Symington (1900), Thomson (1900), Andrews (1902), Audry (1902), 
Bourlot (1902), Bouchacourt et Coudert (1904), Nau (1904), Kiihne 
(1906), Bornier (1907), Hand (1908), Wenner (1909) 2 cases, Hebb 
(1913), Rivet et Gerard (1913). Total 66 cases. 
2. Pulmonary artery a solid cord: Hunter (1783), Basedow (1828), 
Chassinat' (1836), Smith (1841), Babington (1846), Crisp (1846), Sturock 
0859), Olliver (1861), Hickman (1869), Hunter (1869), Peacock (1871), 
Turner (1882), Brewer (1885), McKee (1887), Habershon (1888), Griffith 
(1891), Grothe (1898), McCrae (1906), Young & Robinson (1907), Pap- 
penheimer (1913), Morse (1915). Total 21 cases. 
3. Entire absence of the pulmonary trunk: Crisp (1846), Almagro 
(1862), Hunter (1870), Peacock (1879), Grant (1883), Pryor (1889), 
Gutkind (1903), Hebb (1913) 2 cases. Total 9 cases. 
§ XII. 
VII. ABNORMALITIES OF THE AORTA 
A. Aortic Stenosis and Atresia 
These cases are not common and are difficult to distinguish 
from the results of post-natal endocarditis. It seems reasonable 
to suppose that the congenital cases are the result of the same 
type of developmental disturbance which produces similar condi- 
tions of the pulmonary trunk. Theremin collected 17 cases, but 
it seems probable that a number of these are not of congenital 
origin. The condition is associated with defective ventricular 
septum and patent ductus arteriosus. The average duration of 
life is 2 days. Devillier's (i860) case was an obliteration of the 
orifice, but those reported by Ziegenspeck (1888), Klipstein 
(1890), Konstantinowitsch (1906) and Gladstone & Russmann 
(1915) showed obliteration of the ascending portion as well. 
1. Stenosis of aortic orifice: Dittrich (1852), Blin (1854), Hare (i860), 
Allis (1872), Pott (1879), Etlinger (1882) 2 cases. Eppinger (1889). 38 
C. W. M. Poynter 
2. Stenosis of the ascending trunk: Parker (1847), Dittrich (1849), de 
Bary (1846), Maier (1876), Peacock (1877), Geffrier (1881), Holt (1883), 
Ziegenspeck (1888), Eppinger (1889), Klipstein (1889), Preisz (1890) 3 
cases, Lamouroux (1899), Cautley (1908), Wenner (1909) 3 cases. 
B. Atresia of the Aortic Arch 
These cases do not belong with a study of the heart, but are 
presented here because they are frequently encountered with con- 
genital heart disease and act physiologically just as the preceding 
group. The condition consists of the complete or partial oblit- 
eration of the aorta just above the opening of the ductus arte- 
riosus, so that the descending aorta receives its blood from the 
pulmonary artery through the persistent ductus. 
Two groups of cases must be recognized. In the first the left 
subclavian artery arises normally and the anomaly consists of 
the obliteration of the dorsal root of the left fourth arch and the 
persistence of the left pulmonary arch. In the second group the 
left subclavian artery springs from the juncture of the ductus 
and the descending aorta, and the anomaly is an obliteration of 
the fourth left arch and dorsal root and the persistence of the 
left pulmonary arch. 
Cases showing a constriction in the region of the fourth arch 
and dorsal root have been reported by Valenti & Pisenti (1896), 
Lewis (1903) and Pansch (1905). The condition of atresia 
may occur without cardiac anomalies, but even so, no case lived 
longer than 9 months and dyspnoea and cyanosis were frequently 
observed; cases studied as follows : 
Gibert (1832), Greig (1852), Schilling (1857), Smith (i860), Cameron 
(1871), Barlow (1876)^ Osler (1880), Potocki (1886), de Renzi (1889). 
§ XIII. 
VIII. ABNORMALITIES OF THE SEMILUNAR 
VALVES 
These conditions were recognized by the earlier observers, but 
attracted very little interest; later, when the development of the 
valve became better understood, more attention was given to the 
subject. Congenital Anomalies of the Heart 
39 
The causative factors are still in debate; Peacock discussed the 
possibilities and came to the conclusion that in the cases where 
the number of cusps was reduced a large majority were of con- 
genital origin but that in certain cases a fusion of the leaflets from 
endocarditis might occur after birth and be difficult to recognize. 
Abbott quotes Osler as saying that the cases are due to fusion 
during foetal life because: (i) The presence of a low, sometimes 
half-obliterated raphe behind one of the cusps; (2) compensa- 
tory changes in the cusps so that their free edge becomes equal 
to or even shorter than the single segment, and (3) the fusion 
of the coronary or right and left segments. Launois et Villaret 
(T9°5) concluded that the cases they studied were congenital 
because there was no histological evidence of inflammation or 
adhesion. In the cases of supernumerary leaflets there is gen- 
erally no question of the congenital origin of the case. A few 
cases have been found in which a band stretches across the lumen 
of the artery above the valves; Archer (1878) thinks these are 
anomalous supernumerary cusps. 
The classification is simple, as indicated by the arrangement of 
the following cases: 
A. Pulmonary Semilunar Valves. 
1. No valves: Whittle (1889). 
2. One valve: Moore (1892). 
3. Two valves: Graves (1841), Ward & Parker (1846), Jackson (1849), 
Peacock (1849), Buhl (1857), Peacock (1856), Loschner & Lambl (i860), 
Peacock (1866) 4 cases (1871), Deguise (1872), Buhl (1878), Pott (1878) 
2 cases, Mackenzie (1879), Peacock (1879), Borresi (1880), Lees (1880), 
O'Sullivan (1880), Revilliod (1882), Tooth (1883), Durozier (1885), Vite 
(1886), Foot (1888), Hebb (1889), Oliver (1889), Preisz (1890) 2 cases, 
Fennell (1891), Delitzin (1892), Saunders (1892), Rheiner (1896), Hebb 
(1897), Minkowski (1904), Carpenter (1906), Kiihne (1906), Carpenter 
(1908), Girauld et Tissier (1910), Wassenbach (1910), Hebb (1913) 2 
cases, Monteiro (1917). 
4. Four valves: Tuineau-de Mussy 1836), Loschner & Lambl (i860), 
Carter (1873), Wilson (1876), Bernard (1880), Briininghausen (1880), 
Tirard (1880), Martenotti (1886), Vite (1886), Delitzen (1892) 3 cases, 
Virchow (1896), Crowder (1897), Griffith (1897), Launois et Villaret 
(1905), Reid (1911). 
B. Aortic Semilunar Valves. 
1. One valve: Martenotti (1886). 40 
C. W. M. Poynter 
2. Two Valves: Spittai (1830), Andral (1838), Blin (1854), Quain & 
Sibbald (1856), Hare (i860), Greenfeld (1876), Alezias (1880), Tirard 
(1880), Rickards (1881), Sailer (1885), Vite (1886) 2 cases, Foot (1888), 
Berger (1890), Preisz (1890) 2 cases, Ucke (1895), Hebb (1897), Rainer 
(1897), Barbo (1900), Macaigne et Lucien (1912). 
3. Four valves: Lindenberger (1893) 2 cases. 
Summary: 
Pulmonary Artery 
Aorta 
Type Variation 
I 
No valve 
I 
I 
One valve 
44 
21 
Two valves 
17 
2 
Four valves 
§ XIV. 
IX. ANOMALIES OF THE ATRIO-VENTRICU- 
LAR ORIFICES AND VALVES 
In the cases on single atrio-ventricular opening the right is 
most frequently wanting and the condition generally occurs in 
bilocular hearts. No very satisfactory explanation has been 
offered for the irregularity. Mauran (1827a) found a single 
auricle and ventricle connected by a tricuspid valve, also Keith 
(1912) reported an arrest of development of the left heart with 
no atrio-ventricular opening on that side. Potter (1906), Rogers 
(1905) and Cohn (1904) found the right atrio-ventricular open- 
ing lacking in four chambered hearts ; other anomalies were pres- 
ent in each case. In cases by Ballet (1880) and Andrews (1902) 
there was no connection between the right atrium and ventricle, 
but the right atrio-ventricular opening was into the left ven- 
tricle. Martin (1877) reported a long canal from the right 
atrium opening into the posterior wall of the ventricle and taking 
the place of the normal orifice. 
It was not thought necessary to collect the cases of stenosis 
because all of the cases examined seemed to be of undoubted 
inflammatory origin. 
Anomalies of the valves are of rare occurrence; Cordell (1884) 
reported a single mitral valve and Geipel (1903) three cases. 
Stuhlweissenburg (1912) found a case of double left atrio- 
ventricular opening, each guarded by valves. Pisenti (1888) 
reported a congenital anomaly of the tricuspid valve. Congenital Anomalies of the Heart 
41 
Following are cases of single atrio-ventricular opening: 
Martin (1826), Mauran (1827), Thore (1842) (1843), Vernon (1856), 
Martin (1877), Jacoby (1884), Chapatot (1889), Reifschlager (1897), 
Turner (1891), Grothe (1898), Grosse (1903), Schreiber (1903), Wright 
& Drake (1903), Cohn (1904), Lefas (1904), Rogers (1905), Kiihne 
(1906), Paterson (1908), Keith. (1912). 
§ XV. 
X. IRREGULARITIES IN DEVELOPMENT OF THE 
DUCTUS ARTERIOSUS 
This structure is a part of the arterial system and is only con- 
sidered with cardiac anomalies on physiological grounds. Our 
interest is principally in persistent patency which is the only 
condition which will be presented here. 
The first case of persistent duct was probably not described by 
Botallenus, after whom it has been called, but by Galenus, who 
seemed to know of the changes which occur after birth. Fallo- 
pius and Cardanus both knew of the duct and that it could 
remain open after birth. The function seems to have been well 
described by Harvey in his Motu Cordis en Sanguinis (1648). 
The factors which prevent the normal obliteration are no better 
understood than those which cause the right aortic arch to per- 
sist in certain cases, or, indeed, bring about any other develop- 
mental irregularity; a number of theories have been advanced 
which it is not profitable to discuss here. 
Persistent patency may occur as an isolated lesion or, more 
frequently, in conjunction with other congenital cardiac anoma- 
lies. In the isolated lesions Goodman (1910) found that females 
are affected more frequently than males in the ratio of 20:11. 
The oldest case was 53; death could not be attributed to the open 
duct, although 7 were persistently cyanotic and 16 suffered from 
dyspnoea. There seems to be no pathognomonic sign or symp- 
tom, yet from the symptom complex a clinical diagnosis may be 
made. A full review of the clinical diagnosis has been made by 
Wells (1908). Vierordt thought that the condition of isolated 
frequency constituted about 4 per cent, of all congenital cardiac 
disease but Wells thinks the frequency is much greater. The 42 
C. W. M. Poynter 
condition is not incompatible with a fair duration of life, but few 
cases lived beyond 50 years. As one element in maldevelopment 
complexes the condition is not of unusual occurrence. In this 
study open ductus arteriosus is present in slightly more than 25 
per cent, of the hearts studied, making it the third lesion in order 
of frequency; as an isolated lesion it is present in 3.7 per cent, 
of cases. 
Hunter (1783), Standert (1805), Baillie (1808) 2 cases, Obet (1808), 
Meckel (1809), Langstaff (1811), Howship (1813), Jurine (1815), Krey- 
sig (1817), Reeland (1818), Cheever (1821), Tiedemann (1825), van Hall 
et Vrolik (1825), Martin (1826), Cerutti (1827), Houzelot' (1827), Mauran 
(1827), Basedow (1828), Graves & Houston (1830). Gibert (1832), Spittai 
(1835), Chassinat (1836), Smith (1841), Douglas (1842), Babington 
(1846), Peacock (1846), Rees (1848), Bernutz (1849), Denuce (1849), 
Peacock (1849), Johnson (1850), Stoltz (1851), Greig (1852), Hare 
(1853), Keil (1854), Luys (1855), Graily-Hewett (1856), Peacock (1856), 
Willigk (1854), Darrach (1857), Meyer (1857), Morey (1857), Schilling 
(i857), Baly (1858), Sturock (1859), Devilliers (i860), Hare (i860), 
Saunders (i860), Smith (i860), Heine (1861), Metcalf (1861), Ollivier 
(1861), Almagro (1862), Duroziez (1862), Gueniot (1862), de Bary 
(1864), Peacock (1864), Arnold (1868), Hickman (1869), Hunter (1869), 
Cameron (1871), Peacock (1871), Johston (1872), Fogge (1873), Pea- 
cock (1873), Lucas (1874), Barlow (1876), Katz (1877), Walsham (1877), 
Francais (1878), Heniman (1878), Pott (1879), Hildrith (1880), Lees 
(1880), Malherbe (1880)', Osler (1880), Stifel (1880), Tirard (1880), v. 
Etlinger (1881) 2 cases, Holl (1882), Scott (1882), Turner (1882), Holt 
(1883), Livingston (1883) 2 cases, Ashby (1884), Coupland (1884), Foulis 
(1884), Holt (1884), Darier (1885), Epstein (1886), Gilbert (1886), Leo 
(1886), Potocki (1886), Vincenzi (1886), Harris (1887), Klumpke (1887), 
McKee (1887), Murray (1887), Hopkins (1888), Ziegenspeck (1888), de 
Renzi (1889), Klipst'ein (1889) 2 cases, Miura (1889), Preisz (1890), 
Howard (1891), Lewis (1891), Moore (1891), Ruge (1891) 2 cases, 
Hochhaus (1892), Moore (1892), Saunders (1892), Laine (1893), Haury 
(1894), Probyn-Williams (1894), Stembo (1894), Freyberger (1895), 
Monod (1896), Rheiner (1896), Coyon (1897), Drasche (1898), Gerard 
(1898), Grothe (1898), Hunsberger (1898), Lamouroux (1899), Lowen- 
thal (1900), Potter (1900), Starck (1900), Audry (1902), Bourlot (1902), 
Spalverini et Barbieri (1902), Cowan (1903) 3 cases, Gutkind (1903), 
Lewis (1903), Moore (1903), Schreiber (1903), Brittauer (1905), Chartier 
(1905), Chessman (1905), Ellis (1905) 2 cases, Pansch (1905), Apert et 
Brezaud (1906), Konstantinowitsch (1906), Bornier (1907), Lucien et 
Harter (1907), Young & Robinson (1907), Carpenter (1908) 2 cases, Caut- 
ley (1908), Wells (1908), Carpenter (1909), Wenner (1909) 4 cases, Congenital Anomalies of the Heart 
43 
Weiss-Eder (1909), Bellubekranz (1910) 2 cases, Mead (1910), Kingsley 
(1911), Robertson (1911), Keith (1912) 2 cases, Pappenheimer (1913), 
Heller & Gruber (1914), Milland (1914), Morse (1915)- Total 183 cases. 
§ XVI. 
XI. IRREGULARITIES OF THE VEINS ENTERING 
THE HEART 
An exact study of the venous variations will appear later, but 
since these anomalies are frequently encountered in connection 
with congenital cardiac disease, I have included the following 
references for those who may be interested in such irregularities. 
A. Pulmonary Veins.-Of the pulmonary veins those on the 
left more frequently unite to form a common trunk before en- 
tering the atrium. This condition is probably brought about by 
the absorption of the original single common trunk into the atrial 
wall, so that each comes to open separately; this is hardly 
anomalous. 
The upper vein on the right may open into the superior vena 
cava as in cases by Wilson (1798), Breschet (1826), Otto (1830), 
Meckel (1820), Gruber (1876), and Ingalls (1907). 
According to Federow (1910) the pulmonary veins develop as 
buds of the sinus venosus after the heart and other vessels have 
been established; hence these may form irregular connections by 
union with aberrant branches of vessels- already developed. Brown 
(1913) found an early vascular plexus, splanchnic plexus, in the 
cat, which is carried down as the lung bud develops and early 
connects with the sinus venosus and the post cava. By persist- 
ence of the post caval tap he explains the case of Park (1912) 
in which the right pulmonary vein pierces the diaphragm and 
connects with the post cava. Harrison (1844) reports a case of 
the pulmonary veins opening into the vena azygos major and 
Schattock (1883) a case in which they opened into the systemic 
veins. 
The following reports are of the pulmonary veins entering the 
right atrium: Lacroix (1844), Taylor (1845), Chiari (1880), v. 
Etlinger (1881), Epstein (1886), Hepburn (1887), and Hick- 44 
C. W. M. Poynter 
man (1869); and Crocker (1879) the homologous condition in 
situs viscerum transversus. 
Duchek (1862) reported a very interesting condition in which 
the right pulmonary veins opened into the right ventricle. 
B. Systemic Veins.-Occasionally two superior venae cavae are 
encountered. In these cases the right opens into the right atrium 
in the normal way, while the left enters the right atrium through 
the coronary sinus. This is a case of persistence of the left duct 
of Cuvier and part of the anterior cardinal vein; cases are not 
infrequent. 
Longhurst (1874) reported the inferior vena cava entering the 
left atrium and Crocker (1879) and Miura (1889) observed the 
superior vena cava entering the same chamber. Cases in which 
both superior and inferior venae cavae entered the left atrium 
were reported by Jacoby (1884) and Lucien & Harter (1907). 
Barbo (1900) saw the superior and inferior venae cavae open into 
the right atrium in a case of situs viscerum transversus. 
§ XVII. 
In discussing the difficulties of classification I have already- 
pointed out that to properly understand the congenital heart 
anomalies it is necessary to study each lesion independently of all 
others which may be present. The first section of this study has 
been taken up with the examination of each anomaly which this 
collection of hearts has furnished, and considering each without 
regard to any other irregularity which may be, occasionally or 
frequently, found in association with it. 
In this section the cases are regrouped according to the differ- 
ent lesion complexes which they present. I have used the defects 
of the cardiac septa as the leading lesions simply because they 
are of frequent occurrence, any other scheme would lead to the 
same results. Many simple conditions which have been fully 
treated in the first part are omitted here to avoid repetition. The 
more exact distinctions in lesions, as the position of a defect of 
the interventricular septum or of pulmonary stenosis are not at- 
CLINICAL CLASSIFICATION Congenital Anomalies of the Heart 
45 
tempted, but by a critical comparison of any of the following lists 
with those in the various previous sections such information can 
be readily gained. 
I. Cases of Single Ventricle 
(No Other Lesion) 
No symptoms seem to be characteristic; one case had cyanosis 
and one was dyspnoeic. The average age was slightly more than 
io months if we exclude Kleinschmidt's case which lived to be 64. 
Schenck (1600), Playfair (1870), Chiari (1879), Kleinschmidt (1881), 
Jellett (1897), Baumgarth (1902), Cautley (1908), Sokolow (1910), Pen- 
ner (1911), Gladstone & Russmann (1915). 
(a) With Defective Atrial Septum. 
Average age 2^2 months, excluding one case which lived to be 
24 years, persistent cyanosis slightly more frequent than in the 
preceding. 
Otto (1814), Mackel (1815), Tiedemann (1825), Mayer (1827), Thore 
(1842), Hale (1853), Guibert (i860), Jacoby (1884), Sanger (1889), Preisz 
(1890), Keith (1898), Rudlof (1900), Cautley (1901), Grosse (1903), 
Paterson (1908), Girauld et Tissier (1910). 
(&) With Patent Ductus Arteriosus. 
Only two cases by Ziegenspeck (1888) and Letulle (1904); 
the first was complicated by an atresia of the aorta which is not 
receiving separate recognition in this group, lived 15 days; the 
second may perhaps have had a congenital stenosis of the pul- 
monary artery, although I have not so interpreted it; case lived 
16 years and died of tuberculosis. 
(c) With Atrial Septum Defective and Ductus Arteriosus Per- 
sistent. 
Case by Kreysig (1817) lived 22 years; that of Devilliers 
(i860) and Konstantinowitsch (1906) less than one week, each 
of the latter had atresia of the aorta. 
(d) With Pulmonary Stenosis. 
Chemeneau (1699), Buhl (1857), Emanuel (1906) ; latter was 
cyanotic and lived for 7 years, others were foetuses. 46 
C. W. M. Poynter 
(?) With Pulmonary Stenosis and Open Ovale. 
Meckel (1815), Hein (1816), Marx (1820), Carson (1857), Bull (1885), 
Holt (1890), Paterson (1909). 
(/) With Pulmonary Stenosis, Open Ovale and Ductus Arte- 
riosus Persistent. 
Fleischmann (1815), Chevers (1846), Crisp (1846), Bednar (1852), 
Almagro (1862), Rauchfuss (1864), Brewer (1885), Northrup (1888), 
Ruge (1891), Williams (1892), Hunsburger (1898), Potter (1900), 
Bouchacourt et Coudert (1904). 
Average age 1 year 8 months, maximum 12 years. 
(g) With Transposition of Aorta and Pulmonary Artery. 
Elliot (1877), Martin (1877), Bianchi (1882), Fussell (1888), Boucha- 
court et Coudert (1904), Emanuel (1906), Young (1906), Young & Robin- 
son (1907), Stokes (1908), Fortman (1912), Rivet' et Gerard (1913). 
Average age about 10 years 3 months. 
(h) With Transposition and Open Ovale. 
Breschet (1826) 2 cases, Martin (1826), Mauran (1827), Thore (1843) 
(1845), Arnold (1868), Turner (1882), Shattock (1883), Revilliod (1889), 
Reifschlager (1897), Champeter de Ribes (1903), Robertson (1911), Pap- 
penheimer (1913). 
The following cases of the two preceding groups had in addi- 
tion an atresia of the pulmonary artery: Mauran, Arnold, Turner, 
Pappenheimer, and Rivet; it is to be noted in Arnold's case that 
the ovale was closed but the ductus arteriosus was patent. 
(/) With Truncus Communis Arteriosus. 
Wilson (1798), Standert (1805), Farre (1814), Stoltz (1841), Rams- 
botham (1846), Foster (1847), Clark (1848), Vernon (1856), Clar (1858), 
Bernard (i860), Bradley (1873), Pott (1879), Robinson (1881), Clarke 
(1884), Keith (1898), Wright & Drake (1903), Lefas (1904), Wenner 
(1909), Knope (1912). 
The average for this group is 2 months 10 days; all of the 
cases show a defective atrial septum and in the majority the 
septum is entirely wanting, see group immediately following 
which is abstracted from all the preceding cases to cover the 
title bilocular heart. Congenital Anomalies of the Heart 
47 
II. Single Ventricle and Single Atrium (Cor biloculare) 
This group contains, in addition to the common irregularities 
of septum, pulmonary stenosis and atresia, transposition and per- 
sistent truncus. 
Wilson (1798), Standert (1805), Otto (1814), Meckel (1815), Breschet 
(1826), Martin (1826), Mauran (1827), Mayer (1827), Thore (1842) 
(1845), Crisp (1846), Foster (1846), Ramsbotham (1846), Clar (1858), 
Bernard (i860), Guibert (i860), Almagro (1862), Elliot (1877), Robinson 
(1881), Schattock (1884), Jacoby (1884), Bull (1885), Turner (1882), 
Northrup (1888), Hunsburger (1898), Rudlof (1900), Champeter (1903), 
Grosse (1903), Lefas (1904), Girauld (1910), Knope (1912). 
By removing Hunsberger's case aged 12 years and Bull's aged 
5 years the average age of the remainder of the group is only 
50 days. 
III. Ventricular Septum Present but Defective 
(No Other Lesion) 
The average for this group is io years 9% months, the maxi- 
mum age 65, of a case reported by Meyer. 
Cailliot (1807), Meckel (1809), Howship (1816), Pulteney (1818), Louis 
(1823), Wittcke (1828), Husson (1836), Kiirschner (1837), Parker (1847), 
Peacock (1847), Hare (1846), Greig (1852), Pellizzari (1858), Loschner 
& Lambl (i860), Hillier (1861), Bouillaud (1862), Vulpian (1868), Kelly 
(1869), Guillon (1873), Boissel (1875), Palaillon (1876), Descaisne (1877), 
Coupland (1878), Crocker (1878), Huart (1879), Pott (1879), Bernobie 
(1881), Chiari ■ (1881), Duret (1881), Grandi (1881), Hadden (1881), 
Rickards (1881), Orth (1881), Stone (1881), Tooth (1883), Haywood 
(1884), Chaffey (1885), Barbillon (1886), Willcocks (1886), Foot (1887), 
Hebb (1889), Audry et Lecroix (1890), Macaigne (1890), Preisz (1890), 
Dupre (1891), Rolleston (1891), Renvers (1891), White (1891), Tate 
(1891), Wilbouschewitch (1891), Geipel (1892), Guttmann (1892), Bir- 
mingham (1893), Bennetz (1895), Meslay (1895), Railton (1895), Eisen- 
menger (1897), Gordon (1897), Hebb (1897), Keim (1897), Broesmer 
(1898), Eisenmenger (1898), Lowenthal (1900), Vinay (1900), Andrews 
(1902), Audry (1902), Durante (1902), Cowan (1903), Apert (1904), 
Delepine & Borse (1904), Ferraro (1904), Aneille (1905), Carpenter 
(1906), Petit (1906), Valz (1907), Carpenter (1909), Norris (1911), 
Bartels (1913), Black (1914), Hebb (1913), Meyer (1913), Griffith (1915), 
Gladstone & Russmann (1915), Parrura (1916). 48 
C. W. M. Poynter 
(a) With Defective Atrial Septum. 
Mery (1700), Cerutti (1827), Hare (1846), Mallwo (i860), Mackenzie 
(1889), Gelan (1873), Laine (1893), da Costa (1870), Bullet' (1880), 
O'Sullivan (1880), Smith (1880), Geffrier (1881), Marchand (1881), 
Barand & Barry (1884), Chaffey (1884), Epstein (1886), Chapatot (1889), 
Preisz (1890), Ruge (1891), Turner (1891), Packard (1896), Griffith 
(1897) (1902), Blondel (1904), Pritchard (1904), Rogers & Fortiscue 
(1905), Boulach (1910), Foggie (1910), Erdmenger (1912). 
(b) With Patent Ductus Arteriosus. 
Obet (1808), Meckel (1809), Greig (1852), Hildrith (1880), Osler 
(1880), Coupland (1884), Potocki (1886), de Renzi (1889), Haury (1894), 
Bellubekranz (1900), Chessman (1905), Cautley (1908), Carpenter (1909), 
Keith (1912). 
(c) With Open Ovale and, Patent Ductus Arteriosus. 
Reeland & Freiderich (1818), Cameron (1871), Barlow (1876), Lees 
(1880), Tirard (1880), Klipstein (1889), Lamouroux (1899), Moore 
(1903), Chartier (1905), Carpenter (1908), Wenner (1909). 
(d) With Pulmonary Artery Stenosed. 
The average age for this group is 9^4 years, maximum 36 
years, or roughly there died in the first decade 66 per cent., in 
•the second 15 per cent., in the third 17 per cent, and in the fourth 
1 per cent. 
Sandifort (1777), Abernethy (1794), Palois (1809), Marshall (1830), 
Escalier (1845), Peacock (1846), Ward & Parker (1846), Jackson (1849), 
Maurice (1853), Peacock (1856), Voss (1856), Meyer (1857), Quain & 
Sibbold (1856), Hare (i860), Loschner & Lambl (i860), Mallwo (i860), 
Peacock (i860) (1869) (1870) (1871), Wyss (1871), Deguise (1872), 
Demange (1874), Jackson (1875), Peacock (1876), Assmus (1877), Buhl 
(1878), Cossy (1878), Crocker (1878) (1879), Mackenzie (1879), Pea- 
cock (1879), Borresi (1880), Bussey (1880), Lees (1880), Peacock (1880), 
Schantz (1880), Abercrombie (1881), Orth (1881), Fereol (1881), Petit 
(1881), Rickards (1881), Stone (1881), Cadet de Gassecourt (1882), Re- 
villiod (1882), Moutart-Marten (1883), Hayward (1884), Menetrier 
(1884), Dumontpallier (1885), Gevaert (1885), Moore (1885), Sewastia- 
noff (1885), Barbillon (1886), Murray (1887), Schrotter (1887), Schule 
(1888), Bingham (1888), Hebb (1889), Moore (1889), Oliver (1889), 
Cadet de Gassecourt' (1890), Preisz (1890), Stadler (1890), Variot et 
Gampert (1890), Liegeois (1891), Renvers (1891), Rolleston (1891), 
Braunner (1892), Steven (1892), Voelcker (1892), Boquet (1893), Haury 
(1894), Northrup (1894), Passow (1894), Rheiner (1896), Young (1896), Congenital Anomalies of the Heart 
49 
Keith (1898), Wendle (1898), Trepp (1898), Fennell (1901), Cautley 
(1902), Spalverini (1902), Peiper (1903), Ellis (1905), Young (1907), 
Thomson (1908), Norris (1911), Keith (1912), Bissell (1913), Hebb 
(1913), Henger (1913). 
(^) With Pulmonary Stenosis and Open Ovale. 
Average age at death 9% years, maximum 23 years; 32 per 
cent, of this group showed marked cyanosis as against 25 per 
cent, in the preceding group. 
Hunter (1783), Dorsay (1812), Knox (1815), Bloxam (1834), Lexis 
(1835), Napper (1840), Itiff (1845), Denuce (1849), Quain (1856), Gubler 
(1861), Kussmaul (1866), Rex (1874), Crocker (1878) (1879), O'Sullivan 
(1880), Toupet (1883), Moore (1884), Vilon et Leveque (1885), Toupet 
(1887), Lepine (1894), Nazaroff (1895), $iredey (1896), Jacobson (1897), 
Armand-Delille (1900), Andrews (1902), Burke (1902), Cohn (1904), 
Krausse (1905), Gandy (1909), Serverog (1910), Black (1914), Hinger 
(1913), Minkowski (1914). 
(/) With Pulmonary Stenosis and Patent Ductus Arteriosus. 
Graves & Houston (1830), Peacock (1849) (1856), Johnson (1872), 
Spalverini et Barbieri (1902), Carpenter (1908), Milland (1914). 
(g) With Pulmonary Stenosis, Open Ovale and Patent Ductus 
Arteriosus. 
Graily-Hewitt (1856), Baly (1858), Heine (1861), Rheiner (1896), 
Starck (1900), Cowan (1903), Schreiber (1903), Ellis (1905). 
(A) With Pulmonary Atresia. 
Nevin (1789), Lediberder (1836), Chambers (1846), Crisp (1846), Wal- 
lach (1852), Peacock (1869), Pott (1878), Nixon (1879), Cronk (1881), 
Grant (1883), Bury (1887), Habershon (1888), Bingham (1889), Pryor 
(1889), Howard (1892), Civatte (1900), Symington (1900), Thomson 
(1900), Kiihne (1906), Hand (1908), Hebb (1913). 
(/) With Pulmonary Atresia and Open Ovale. 
Mansfeld (1843), Shearman (1845), Chevers (1846), Hervieux (1861), 
Makuma (1879), Luneau (1880), Vilon et Leveque (1884), Probyn- 
Williams (1894), Gutkind (1903), Wassenbach (1910), Hebb (1913). 
(&) With Pulmonary Atresia and Patent Ductus Arteriosus. 
Howship (1813), van Hall (1825), Chaissinat (1836), Friedeberg (1844), 
Babington (1847), Peacock (1846), Morey (1857), Sturock (1859), Pea- 
cock (1869) (1871), Hickman (1869), Peacock (1879), Pott (1879), 
Vincenzi (1886), McKee (1887), Moore (1892), Lowenthal (1900), Audry 
(1902). 50 
C. W. M. Poynter 
(Z) With Pulmonary Atresia, Open Ovale and Patent Ductus 
Arteriosus. 
Cheever (1821), Basedow (1828), Graves and Houston (1830), Spittai 
(1835), Chassinat (1836), Smith (1841), Douglas (1842), Hunter (1869) 
(1870), Lucas (1874), Stifel (1880), Burgess (1893), Grothe (1898), 
Bourlot (1902), Bornier (1907), Morse (1915). 
The average age at death for this group is 1 year and 9 months. 
It is interesting to compare the groups of defective ventricular 
septum, open ovale, patent ductus and stenosis of the pulmonary 
with the same first three defects and atresia of the pulmonary; 
in the first, that is, with stenosis, the average age is 7 years 7 
months, in the atresia the age is 5 years 4 months. 
(m) With Transposition of Aorta and Pulmonary Artery. 
Martin (1839), Parker (1846), de Bary (1864), Babesiu (1879), Toen- 
nies (1884), de Renzie (1889), Preisz (1890), Geipel (1892), Saunders 
(1892), Coyon (1897), Freyberger (1898), Wenner (1909), Bissell (1913). 
(n) With Transposition and Atrial Septum Defective. 
Gammage (1815), Nasse (1811), King (1844), Lebert (1863), Maier 
(1876), Crocker (1880), Peacock & Ashby (1881), Gampert (1889), Mac- 
kenzie (1889), Birmingham (1892), Preisz (1890), Rotch (1896), Starck 
(1900), Thiel (1902), Carpenter (1909), Planchu et' Gardere (1909), Keith 
(1912). 
(0) With Transposition and Patent Ductus Arteriosus. 
Walshe (1842), Lees (1879), Scott (1882), Saunders (1892), Monod 
(1896), Apert et Brezaud (1906), Keith (1912). 
With Transposition, Defective Atrial Septum and Patent Ductus. 
Martin (1826), Monod (1896), Wenner (1909), Robertson (1911). 
(p) With Transposition and Pulmonary Stenosis. 
Durozier (1885), Mann (1889), Grunmach (1890), Meinertz (1901), 
Pozdyunm (1913). 
(q) With Transposition, Pulmonary Stenosis and Open Ovale. 
Ring (1805), Mueller (1822), Kussmaul (1866), Stadler (1890), Bir- 
mingham (1892), Griffith (1899), Rolly (1899), Rudlof (1900). 
(r) With Transposition, Pulmonary Stenosis, Patent Ductus Art. 
Etlinger (1882), Freyberger (1904), Heller & Gruber (1914). Congenital Anomalies of the Heart 
51 
(s') With Transposition and Pulmonary Atresia. 
Griffith (1891). 
(t) With Transposition, Pulmonary Atresia and Defective Atrial 
Sept. 
Fearn (1834), McCrae (1905). 
(w) With Transposition, Atresia, Defective Atrial Sept, and 
Patent Ductus. 
Darrach (1857), Young & Robinson (1907). 
(v} With Persistent Truncus Communis Arteriosus. 
Tonybee (1849), Hyernaux (1851), Pott (1879), Barbillon (1886), 
Preisz (1890), Charrin et LeNoir (1891), Bellot (1895), Gallois (1896), 
Petschel (1897), Spalverini et Barbieri (1902), Rispal & Bay (1904), 
Elsbergen (1905), Dickson & Fraser (1913). 
(w) With Persistent Truncus and Defective Atrial Septtim. 
Laurence (1837), Buchanan (1864), Barand, Bary (1884), Cade (1897), 
Martin (1897), Cautley (1902), Krausse (1906), Wenner (1909). 
IV. Foramen Ovale Open 
(With No Other Lesion) 
Littre (1700), Widmann (1717), Amyaud (1736), du Hamel (1740), 
Moreau (1790), Jurine (1815), Pasqualini (1827), Braune (1833), Moret 
(1833), Ecker (1839), Harrison (1844), Dittrich (1849), Blin (1854), 
Foster (1863), Landouzy (1874), Longhurst (1874), Bogler (1875), Fin- 
lay (1878), Caton (1878), Johnson (1878), Makune (1879), Bucquay 
(1880), Chiari (1880), Desnos et Callias (1880), Gibier (1880), Smith 
(1880), Fowler (1882), Hendly (1887), Oliver (1889), Hadden (1890), 
Haw (1890), Monisset (1890), Ruge (1891), Ardissone (1902), Cautley 
(1902), Cowan (1903), Delhern (1903), Tylecote (1903), Ohm (1907), 
Gasquet (1913). 
The average age for this group is 28 years, with a maximum 
age of 70 years. 
(a) With Patent Ductus Arteriosus. 
Jurine (1815), Katz (1877), v. Etlinger (1881), Livingston (1883), Holt 
(1884), Klipstein (1889), Miura (1889), Hektoen (1899), Carpenter 
(1908), Weiss-Eder (1909). 52 
C. W. M. Poynter 
(b) With Transposition of Aorta and Pulmonary Artery. 
d'Alton (1824), Schilling (1857), Code (1863), Doming (1890), 
Caille (1896), Emanuel (1906), Bokay (1911). 
(c) With Transposition and Patent Ductus Arteriosus. 
Baillie (1808), Langstaff (1811), Tiedemann (1825), Johnson (1850), 
Keil (1854), Meyer (1857), Holl (1882), Epstein (1886), Harris (1887), 
Lewis (1891), Coyon (1897), Cowan (1903), Ellis (1905), Lucien et Har- 
ter (1907), Wenner (1909). 
(d) With Pulmonary Stenosis. 
Tacconi (1783), Schuler (1810), Craigie (1843), Peacock (1846), Mann- 
kopf (1862), Vulpian (1868), Peacock (1869), Saundby (1877), Bury 
(1884), Kruger (1884), Laffitte (1892), Moore (1892), Frenkel (1896), 
Hun (1897), Burke (1902), Griffith (1903), Boxwell (1912). 
(e) With Pulmonary Stenosis and Patent Ductus Arteriosus. 
Moore (1891). 
(f) With Atresia of Pulmonary Artery and Patent Ductus 
Arteriosus. 
Hunter (1783), Howship (1816), Ollivier (1861), Gueniot (1862), Pea- 
cock (1864) (1873), Heinman (1878), Livingston (1883), Leo (1886), 
Howard (1891). 
V. Atrial Septum Defective (not Ovale) 
(No Other Lesion) 
Lacroix (1844), Taylor (1845), Kelly (1869), Peacock (1877), Hep- 
burn (1887), Hopkins (1889), Greenfield (1889), Hebb (1889), Hawkins 
(1891), Ruge (1891), Ewald (1898), Henry (1898), Griffith (1899), 
Dhotel (1902), Thomson (1903), Ebbinghaus (1904), Soldner (1904), 
Ingalls (1907), Carpenter (1908) (1909), Abbott (1910), Metzger (1911), 
Reed (1911), Morrison (1912), Lusenbacher (1916). 
(a) With Pulmonary Stenosis or Atresia. 
Probyn-Williams (1894), Burke (1902), Bernstein (1906). 
VI. Transposition of Aorta and Pulmonary Artery 
(No Other Lesion) 
Beck (1846), Ward (1851), Hickman (1869), Kelly (1871), Ogston 
(1874), Pye-Smith (1872), Lees (1880), Ramm (1889), Bonne (1895), Congenital Anomalies of the Heart 
53 
Peters (1904), Lubs (1911). The average age is 2 months 4 days if 
Hickman's case which lived for 28 years is excluded. 
VIL Patent Ductus Arteriosus 
(No Other Lesion) 
Houzelot (1827), Gibert (1832), Rees (1848), Bernutz (1849), Luys 
(1855), Willigk (1854), Hare (i860), Saunders (1860), Smith (i860), 
Metcalf (1861), Duroziez (1862), de Bary (1864b), Fogge (1873), Wal- 
sham (1877), Francais-Franck (1878), Malherbe (1880), Holt (1883), 
Livingston (1883), Foulis (1884), Darier (1885), Gilbert (1886), Murray 
(1887), Hochhaus (1892), Stembo (1894), Drasche (1898), Gerard (1898), 
Wagner (1903), Britt'auer (1905), Pansch (1905), Wells (1908), Good- 
man (1910), Mead (1910), Kingsley (1911). 
(a) With Pulmonary Stenosis. 
Hare (1853), v. Etlinger (1882), Ashby (1884). 
(b) With Transposition of Aorta and Pulmonary Artery. 
Stoltz (1851), Klumpke (1887). 
VIII. Trilocular Heart, Two Ventricles and One Atrium 
This group is an abstract from the preceding cases in sections 
of defective ventricular and atrial septa for the benefit of the 
clinical reports on "Trilocular Heart." 
Mery (1700), Ring (1805), Cheever (1821), Martin (1826), Cerutti 
(1827), Darrach (1857), Almagro (1862), Cameron (1871), Maier (1876), 
Marchand (1881), Chapatot (1889), Birmingham (1892), Probyn-Williams 
(1894), Cade (1897), Ewald (1898), Rudlof (1900), Blondel (1901), 
Griffith (1902), Chartier (1905), Bernstein (1906), McCrae (1906), Car- 
penter (1908) (1909), Metzger (1911). 
The preceding study was undertaken as a part of the work of 
examining the developmental anomalies of the circulatory sys- 
tem ; in this relation it does not appear that the heart is any more 
susceptible to growth disturbances than other parts of the system. 
The importance which heart anomalies have gained is due to 
their effect on longevity and individual well being. 
Factors disturbing the orderly development of different parts 
§ XVIII. GENERAL SUMMARY 54 
C. W. M. Poynter 
of the heart may act independently of, and without disturbing 
the normal processes of, the remainder of the body. When the 
physiological function of the circulatory system is seriously inter- 
fered with by this anomalous development of some portion or 
portions of the heart it appears that a compensation through 
arrest or over development of normal parts is attempted in some 
instances, but with our present knowledge it is not possible to 
distinguish between primary lesions and secondary effects. 
As has been found in the arteries, factors disturbing develop- 
ment of the heart apparently act at a very early age and on very 
restricted areas. A sufficient number of isolated lesions have 
been encountered to make it a comparatively easy problem to 
break up any complex into its individual elements for the pur- 
poses of analysis. 
We are able to interpret many anomalies in their relation to the 
orderly course of development, but the actual factors producing 
them are not revealed or even suggested by this method of study. 
Prenatal inflammations and endocarditis can be apparently disre- 
garded as primary disturbing factors. 
Near 40 per cent, of the hearts presented but a single lesion, 
while the total number of separate lesions encountered in the 
886 hearts was 1,978, or 3^2 lesions for each heart showing more 
than one. Certain complexes were more frequent than others, 
but no associated lesions were so constant as to be in any way 
instructive. Other bodily anomalies were occasionally found in 
association with those of the heart, but none constantly or in any 
way suggestive of a relation to any specific cardiac lesion. 
The statement has frequently been made that the right side 
of the heart is more susceptible to developmental disturbances 
than the left; this would certainly seem to be true if we consider 
only the aortic and pulmonary trunks, but if we consider all 
anomalies as revealed by this study such a claim-cannot be sub- 
stantiated. 
There are no particular diseases to which cases suffering with 
congenital cardiac lesions are especially susceptible. There are 
no pathognomic symptoms surely indicating the condition of 
anomaly. Congenital cyanosis is not a common symptom, in- 
deed it is not present in one third of the cases. Congenital Anomalies of the Heart 
55 
It is impossible to arrive at the frequency of congenital cardiac 
disease, but it appears certain that the cases are of more fre- 
quent occurrence in England and France than in this country. 
It is evident that many congenital cardiac lesions and com- 
plexes very much interfere with the normal physiological func- 
tions, but it is apparent from the examination of longevity in 
any group of cases that such lesions are only one of several fac- 
tors in early curtailment of life. 
The following list of figures shows the relative frequency of 
the lesions encountered in this study. These can have no value 
as general statistics except as this particular group of cases may 
be representative of the total distribution of such lesions. 
Per Cent. 
Anomalies of the pericardium 4.65 
Misplacements of the heart 10.0 
Anomalies of the heart as a whole 1.3 
Anomalies of the ventricular septum 61.0 
Anomalies of the atrial septum 35.6 
Irregularities in development of the truncus 28.5 
Abnormalities of the pulmonary artery 28.5 
Abnormalities of the aorta 2.9 
Irregularities of the pulmonary valves 7.0 
Irregularities of the aortic valves 2.6 
Persistent patency of the ductus arteriosus 20.6 
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