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Fetal cardiac failure resulting from congenital anomalies of the heart
7"he J o u r n a l of P E D I A T R I C S
699
Fetal cardiac failure resultingfrom congenital anomalies of the beart Cardiac failure during fetal life is uncommon, even among subjects with cardiovascular malformations. The occurrence of fetal cardiac failure appears to depend upon the presence of some condition which places a burden upon the right ventricle. Classically, premature closure of the foramen ovaIe is such a condition. In the three cases of fetal cardiac failure reported the malformations represented were (1) right ventricular endocardial fibroelastosis, (2) Ebstein's malformation of the tricuspid valve, and (3) le# ventricular endoeardial fibroelastosis and mitral insufficiency.
J a m e s H. Moiler, M.D., "x" R i c h a r d P. L y n c h , M.D., a n d Jesse E. E d w a r d s , M . D . M I N N E A P O L I S AND ST. PAUL~ M I N N .
@ E N E R A L I Z E D e d e m a associated with ascites in the fetus or the n e w b o r n infant is u n c o m m o n . A m o n g the causes of this state are erythroblastosis, congenital malformations of the h e a r t or other organs, m a t e r n a l diseases such as nephritis or toxemia, a n d u n k n o w n factors? This r e p o r t is concerned with certain congenital c a r d i a c m a l f o r m a t i o n s of the in, fant which resulted in congestive cardiac failure at the time of birth. T h e r e have been few reports of fetal c a r d i a c failure, a n d of the r e p o r t e d cases p r e m a t u r e closure of the f o r a m e n ovale is given as the most comm o n cause. Less frequently, arteriovenous fistulas a n d congenital p u l m o n a r y v a l v u l a r From the Depa;tments of Pediatrics and Pathology, University of Minnesota, Minneapolis, and the Department of Pathology, The Charles T. Miller Hospital, St. Paul. T h b study was supported by Research Grant HE-5694 and Training Grant 5 T1 H E 5570 of the National Institutes of Health, United States Public Health Service. "~'Postdoetoral Fellow No. HE I9, 867, National Heart Institute, United States Public Health Service.
insufficiency have been associated with congestive c a r d i a c failure at birth. I n this report, the clinical a n d pathologic findings in three cases of fetal c a r d i a c failure are presented. T h e congenital c a r d i a c m a l formations were: (1) right ventricular endocardial fibroelastosis with a n a r r o w pulm o n a r y v a l v u l a r orifice, (2) left v e n t r i c u l a r e n d o c a r d i a l fibroelastosis a n d m i t r a l insufficiency, a n d (3) Ebstein's m a l f o r m a t i o n of the tricuspid valve. REPORT
OF CASES
Case 1. This male stillborn infant of 35 weeks' gestational age and weighing 2,880 grams was delivered by cesarean section to a 22-year-old, Rh-positive mother with abruptio placentae. The mother had had two previous pregnancies, each yielding male infants, the first of whom died at 8 days of age of unknown causes. T h e second died 15 minutes after birth with fetal hydrops of a cause unknown to us. Subsequent to the birth of the subject of this report, the mother delivered a normal, full term male infant. We have reviewed the histologic sections of the heart and the lungs of the second infant
7 O0
Moller, Lynch, and Edwards
and did not observe any abnormalities in these tissues. T h e heart was reported to have been grossly normal. In our patient (Case 1) the necropsy revealed marked edema of the entire body including the scalp, eyelids, subcutaneous tissue, and scrotum. The abdomen was protuberant and contained 200 ml. of ascitic fluid. The subcutaneous tis;ue was markedly increased in thickness; a small amount of pleural fluid was present bilaterally, and the liver showed chronic passive congestion. Endocardial fibroelastosis was present in the hypertrophied right ventricle (Fig. l a ) . The pulmonary valve was normal, although its annulus appeared small in relation to the size of the right ventricle. The only valvular abnormality demonstrated was that of the mitral valve, which resembled anatomically those seen in endocardial fibroelastosis of the left ventricle; this was characterized by high insertion of the papillary muscles and shortened chordae tendineae to the anterior leaflet (Fig. lb). The endocardium of the right side of the heart was toughened by collagenous and elastic tissue, while the endocardium of the left ventricle was normal (Fig. 2). The foramen ovale exhibited patency of the valvular competent type. Case 2. This male infant was born to a 35year-old, Rh-positive mother who had had six previous pregnancies, each resulting in a normal
May 1966
child. During this pregnancy, the mother had developed acute hydramnios and a murmurlike sound was evident over her abdomen. The infant was delivered at term, but did not breathe spontaneously and was cyanotic. There was diffuse edema. The edge of the liver was at the level of the umbilicus. A loud, blowing, systolic murmur was present over the precordium. Tracheal intubation was performed, but the infant did not establish effective respiration and died 3 hours following birth. At necropsy, the body weighed 3,250 grams; generalized edema was present. Pericardial as well as bilateral pleural effusions were present. Approximately 400 c.c. of clear, y e l l o w fluid were present in the peritoneal cavity. The left ventricle of the heart showed marked hypertrophy of its wall, measuring 1 cm. in thickness, while the right ventricular wall was 4 mm. thick. There was a deformity of the mitral valve. The anterior leaflet was short and was adherent to the left ventricular wall. This finding was related to short chordae tendineae, which appeared to insert directly into the left ventricular wall since the papillary muscles were so small as to be indistinct. The endocardium of both the left ventricle and left atrium was thickened and white. Histologic examination revealed features characteristic of endocardial fibroelastosis.
Fig. 1. Case 1. Endocardial fibroelastosis of right ventricle and hypoplasia of pulmonary valvular orifice, a, Interior of hypertrophied right ventricle. Endocardium thick, gray, and opaque. The pulmonary valvular annulus is small but the pulmonary valve is normal in basic structure, b, Left ventricle and left atrium. Normal endocardium. Papillary muscles arise high from left ventricular wall and attach to the mitral valve leaflets by short chordae tendineae.
Volume 68
Number 5
Case 3. This was a stillborn female infant, born to a 39-year-old mother who was Rh-negatire and in whom the Coombs test was negative. Twenty-four hours prior to delivery the mother felt no fetal movements. The infant's weight was, 3,290 grams. Neither
Fetal cardiac failure
70 1
peripheral edema nor ascites was present but the liver was enlarged and congested and weighed 250 grams (normal = 150 grams), while the spleen weighed 15 grams (normal = 10 grams). The heart exhibited a stenotic bicuspid pulmonary valve (Fig. 3a) and features of Eb-
Fig. 2. Case 1. Photomicrographs of ventricular walls stained for elastic tissue. Endocardium at upper part of each illustration. Each x 40. a (left), Right ventricular endocardium shows proliferation of elastic tissue characteristic of endocardial fibroelastosis, b (right), Left ventricular endocardium is normal.
Fig. 3. Case 3. Pulmonary valvular stenosis and Ebstein's malformation of tricuspid valve. a, Unopened stenotic bicuspid pulmonary valve viewed from above, b, Right atrium and right ventricle. Septal and posterior leaflets of tricuspid valve attach to right ventricular wall below annulus (dotted line). Chordae tendineae to these leaflets were short and poorly defined. (From Edwards, Carey, Neufeld, and Lester: Congenital Heart Disease. Correlations of Pathologic Anatomy and Angiocardiography, Philadelphia, 1965, W. B. Saunders Company.)
70 2
Moiler, Lynch, and Edwards
stein's malformation of the tricuspid valve (Fig. 3b). The basal aspects of the septal and posterior leaflets of the tricuspid valve were abnormally inserted, the leaflets originating from the right ventricle. As a result of this valvular malformation, the receiving chamber was greatly enlarged, while the portion of the right ventricle distal to the tricuspid valve was small. The valve of the foramen ovale was herniated into the left atrium, suggesting that during fetal life there was elevation of right atrial pressure. COMMENT A m o n g the causes of p a r a n a t a l generalized edema, congenital cardiac .disease resulting in congestive cardiac failure is rare. T h e most frequent cardiac m a l f o r m a t i o n resulting in fetal cardiac failure is p r e m a t u r e closure of the f o r a m e n ovale. Several authors 2-~ have i n d i c a t e d this association, a n d the recent r e p o r t by Naeye a n d Blanc ~ suggests t h a t c a r d i a c failure in this circumstance m a y result from two factors. T h e first is the increased volume-load imposed on the right-sided c a r d i a c chambers. T h e second is related to an increased muscle mass in the small p u l m o n a r y arterioles, indicating increased p u l m o n a r y arteriolar resistance. Arteriovenous fistulae t h a t have caused c a r d i a c failure in fetal life have been identified. A case of p u l m o n a r y arteriovenous fistula with fetal cardiac failure was the subject of separate reports by S h i n o h a r a a n d SekP a n d by Ehrlich a n d associates. 6 T w o cases of cerebral arteriovenous fistula causing fetal c a r d i a c failure were r e p o r t e d by G o m e z a n d co-workers. 7 C o n g e n i t a l p u l m o n a r y v a l v u l a r insufficiency occurring as an isolated c a r d i a c malf o r m a t i o n resulting in c a r d i a c failure in infancy has been the subject of two reports s' 9 a n d in one case congestive failure was present at birth. 19 I n a discussion of the latter case the fetal h e m o d y n a m i c s were considered i,a relation to d e v e l o p m e n t of fetal c a r d i a c failure. T w o of the m a j o r differences between the fetal a n d the a d u l t circulations are: (1) the elevation of the p u l m o n a r y arterial pressure, a n d (2) the p a t e n c y of the ductus arteriosus in the fetus. I n fetuses with p u l m o n a r y v a l v u l a r insufficiency the
May 1966
characteristically high p u l m o n a r y arterial pressure would favor a larger volume of p u l m o n a r y regurgitation t h a n in postnatal life w h e n the p u l m o n a r y arterial pressure is lower. If d u r i n g p o s t n a t a l life the ductus arteriosus remains patent, p u l m o n a r y valvular insufficiency would favor a greater shunt t h r o u g h the ductus. E n d o c a r d i a l fibroelastosis of the left ventricle, as n o t e d in Case 2, tends to be associated w i t h m i t r a l insufficiency. 1~ I n d e e d , in the present case a murm u r characteristic of m i t r a l insufficiency was present. I n the presence of m i t r a l regurgitation the left atrial pressure is elevated and m a y effectively close the f o r a m e n ovale. This m i g h t have led to a m e c h a n i s m of cardiac failure similar to that in p r e m a t u r e closure of the f o r a m e n ovale. T h e r e p o r t e d cases suggest t h a t the occurrence of fetal c a r d i a c failure depends u p o n a state in which there is excessive b u r d e n u p o n the right ventricle. SUMMARY
T h r e e cases of cardiac m a l f o r m a t i o n s with c a r d i a c failure d u r i n g the fetal life are presented. T h e m a l f o r m a t i o n s were: (1) right ventricular e n d o c a r d i a l fibroelastosis, (2) Ebstein's m a l f o r m a t i o n of the tricuspid valve, a n d (3) left v e n t r i c u l a r e n d o c a r d i a l fibroelastosis a n d m i t r a l insufficiency. Fetal cardiac failure is a rare occurrence a n d usually results from a h e m o d y n a m i c b u r d e n u p o n the right ventricle. REFERENCES
1. Potter, E. L.: Pathology of the fetus and the newborn, Chicago, 1952, Year Book Publishers, Inc., pp. 524-526. 2. Tait, L.: A case of general dropsy in a foetus, Tr. Obst. Soc. Lond. 17: 307, 1875. 3. Benner, M. C.: Premature closure of the foramen ovule. Report of two eases, Am. Heart J. 17: 437, 1939. 4. Naeye, R. L., and Blanc, W. A.: Prenatal narrowing or closure of the foramen ovale, Circulation 30: 736, 1964. 5. Shinohara, Y., and Seki, M.: Dystocia due to fetal ascites. Report of a case with congenital malformations of liver and lung, Bull. New York Acad. Med. 37: 136, 1961. 6. Ehrlich, J. C., Goodfriend, M. J~, Shinohara, Y., and Seki, M.: Fetal ascites and portal dysplasia of the liver (polycystic disease without cysts). With pulmonary arterlo-
Volume 68
Number 5
venous fistula and cystic lung, Pediatrics 33" 216, 1964. 7. Gomez, M. R., Whitten, C. F., Nolke, A., Bernstein, J., and Meyer, J. S." Aneurysmal malformation of the great vein of Galen causing heart failure in early infancy. Report of five cases, Pediatrics 31: 400, 1963. 8. Smith, R. D., DuShane, J. W., and Edwards, J. E.: Congenital insufficiency of the pulmonary valve including a case of fetal cardiac failure, Circulation 20: 554, 1959.
Fetal cardiac failure
70 3
9. Ito, T., Engle, M. A., and Holswade, G. R.: Congenital insufficiency of the pulmonic valve. A rare cause of neonatal heart failure, Pediatrics 28" 712, 1961. 10. Moller, J. H., Lucas, R. V., Jr., Adams, P., Jr., Anderson, R. C., Jorgens, J., and Edwards, J. E.: Endoeardial fibroelastosis. A clinical and anatomic study of 47 patients with emphasis on its relationship to mitral insufficiency, Circulation 30: 759, 1964.
699
Fetal cardiac failure resultingfrom congenital anomalies of the beart Cardiac failure during fetal life is uncommon, even among subjects with cardiovascular malformations. The occurrence of fetal cardiac failure appears to depend upon the presence of some condition which places a burden upon the right ventricle. Classically, premature closure of the foramen ovaIe is such a condition. In the three cases of fetal cardiac failure reported the malformations represented were (1) right ventricular endocardial fibroelastosis, (2) Ebstein's malformation of the tricuspid valve, and (3) le# ventricular endoeardial fibroelastosis and mitral insufficiency.
J a m e s H. Moiler, M.D., "x" R i c h a r d P. L y n c h , M.D., a n d Jesse E. E d w a r d s , M . D . M I N N E A P O L I S AND ST. PAUL~ M I N N .
@ E N E R A L I Z E D e d e m a associated with ascites in the fetus or the n e w b o r n infant is u n c o m m o n . A m o n g the causes of this state are erythroblastosis, congenital malformations of the h e a r t or other organs, m a t e r n a l diseases such as nephritis or toxemia, a n d u n k n o w n factors? This r e p o r t is concerned with certain congenital c a r d i a c m a l f o r m a t i o n s of the in, fant which resulted in congestive cardiac failure at the time of birth. T h e r e have been few reports of fetal c a r d i a c failure, a n d of the r e p o r t e d cases p r e m a t u r e closure of the f o r a m e n ovale is given as the most comm o n cause. Less frequently, arteriovenous fistulas a n d congenital p u l m o n a r y v a l v u l a r From the Depa;tments of Pediatrics and Pathology, University of Minnesota, Minneapolis, and the Department of Pathology, The Charles T. Miller Hospital, St. Paul. T h b study was supported by Research Grant HE-5694 and Training Grant 5 T1 H E 5570 of the National Institutes of Health, United States Public Health Service. "~'Postdoetoral Fellow No. HE I9, 867, National Heart Institute, United States Public Health Service.
insufficiency have been associated with congestive c a r d i a c failure at birth. I n this report, the clinical a n d pathologic findings in three cases of fetal c a r d i a c failure are presented. T h e congenital c a r d i a c m a l formations were: (1) right ventricular endocardial fibroelastosis with a n a r r o w pulm o n a r y v a l v u l a r orifice, (2) left v e n t r i c u l a r e n d o c a r d i a l fibroelastosis a n d m i t r a l insufficiency, a n d (3) Ebstein's m a l f o r m a t i o n of the tricuspid valve. REPORT
OF CASES
Case 1. This male stillborn infant of 35 weeks' gestational age and weighing 2,880 grams was delivered by cesarean section to a 22-year-old, Rh-positive mother with abruptio placentae. The mother had had two previous pregnancies, each yielding male infants, the first of whom died at 8 days of age of unknown causes. T h e second died 15 minutes after birth with fetal hydrops of a cause unknown to us. Subsequent to the birth of the subject of this report, the mother delivered a normal, full term male infant. We have reviewed the histologic sections of the heart and the lungs of the second infant
7 O0
Moller, Lynch, and Edwards
and did not observe any abnormalities in these tissues. T h e heart was reported to have been grossly normal. In our patient (Case 1) the necropsy revealed marked edema of the entire body including the scalp, eyelids, subcutaneous tissue, and scrotum. The abdomen was protuberant and contained 200 ml. of ascitic fluid. The subcutaneous tis;ue was markedly increased in thickness; a small amount of pleural fluid was present bilaterally, and the liver showed chronic passive congestion. Endocardial fibroelastosis was present in the hypertrophied right ventricle (Fig. l a ) . The pulmonary valve was normal, although its annulus appeared small in relation to the size of the right ventricle. The only valvular abnormality demonstrated was that of the mitral valve, which resembled anatomically those seen in endocardial fibroelastosis of the left ventricle; this was characterized by high insertion of the papillary muscles and shortened chordae tendineae to the anterior leaflet (Fig. lb). The endocardium of the right side of the heart was toughened by collagenous and elastic tissue, while the endocardium of the left ventricle was normal (Fig. 2). The foramen ovale exhibited patency of the valvular competent type. Case 2. This male infant was born to a 35year-old, Rh-positive mother who had had six previous pregnancies, each resulting in a normal
May 1966
child. During this pregnancy, the mother had developed acute hydramnios and a murmurlike sound was evident over her abdomen. The infant was delivered at term, but did not breathe spontaneously and was cyanotic. There was diffuse edema. The edge of the liver was at the level of the umbilicus. A loud, blowing, systolic murmur was present over the precordium. Tracheal intubation was performed, but the infant did not establish effective respiration and died 3 hours following birth. At necropsy, the body weighed 3,250 grams; generalized edema was present. Pericardial as well as bilateral pleural effusions were present. Approximately 400 c.c. of clear, y e l l o w fluid were present in the peritoneal cavity. The left ventricle of the heart showed marked hypertrophy of its wall, measuring 1 cm. in thickness, while the right ventricular wall was 4 mm. thick. There was a deformity of the mitral valve. The anterior leaflet was short and was adherent to the left ventricular wall. This finding was related to short chordae tendineae, which appeared to insert directly into the left ventricular wall since the papillary muscles were so small as to be indistinct. The endocardium of both the left ventricle and left atrium was thickened and white. Histologic examination revealed features characteristic of endocardial fibroelastosis.
Fig. 1. Case 1. Endocardial fibroelastosis of right ventricle and hypoplasia of pulmonary valvular orifice, a, Interior of hypertrophied right ventricle. Endocardium thick, gray, and opaque. The pulmonary valvular annulus is small but the pulmonary valve is normal in basic structure, b, Left ventricle and left atrium. Normal endocardium. Papillary muscles arise high from left ventricular wall and attach to the mitral valve leaflets by short chordae tendineae.
Volume 68
Number 5
Case 3. This was a stillborn female infant, born to a 39-year-old mother who was Rh-negatire and in whom the Coombs test was negative. Twenty-four hours prior to delivery the mother felt no fetal movements. The infant's weight was, 3,290 grams. Neither
Fetal cardiac failure
70 1
peripheral edema nor ascites was present but the liver was enlarged and congested and weighed 250 grams (normal = 150 grams), while the spleen weighed 15 grams (normal = 10 grams). The heart exhibited a stenotic bicuspid pulmonary valve (Fig. 3a) and features of Eb-
Fig. 2. Case 1. Photomicrographs of ventricular walls stained for elastic tissue. Endocardium at upper part of each illustration. Each x 40. a (left), Right ventricular endocardium shows proliferation of elastic tissue characteristic of endocardial fibroelastosis, b (right), Left ventricular endocardium is normal.
Fig. 3. Case 3. Pulmonary valvular stenosis and Ebstein's malformation of tricuspid valve. a, Unopened stenotic bicuspid pulmonary valve viewed from above, b, Right atrium and right ventricle. Septal and posterior leaflets of tricuspid valve attach to right ventricular wall below annulus (dotted line). Chordae tendineae to these leaflets were short and poorly defined. (From Edwards, Carey, Neufeld, and Lester: Congenital Heart Disease. Correlations of Pathologic Anatomy and Angiocardiography, Philadelphia, 1965, W. B. Saunders Company.)
70 2
Moiler, Lynch, and Edwards
stein's malformation of the tricuspid valve (Fig. 3b). The basal aspects of the septal and posterior leaflets of the tricuspid valve were abnormally inserted, the leaflets originating from the right ventricle. As a result of this valvular malformation, the receiving chamber was greatly enlarged, while the portion of the right ventricle distal to the tricuspid valve was small. The valve of the foramen ovale was herniated into the left atrium, suggesting that during fetal life there was elevation of right atrial pressure. COMMENT A m o n g the causes of p a r a n a t a l generalized edema, congenital cardiac .disease resulting in congestive cardiac failure is rare. T h e most frequent cardiac m a l f o r m a t i o n resulting in fetal cardiac failure is p r e m a t u r e closure of the f o r a m e n ovale. Several authors 2-~ have i n d i c a t e d this association, a n d the recent r e p o r t by Naeye a n d Blanc ~ suggests t h a t c a r d i a c failure in this circumstance m a y result from two factors. T h e first is the increased volume-load imposed on the right-sided c a r d i a c chambers. T h e second is related to an increased muscle mass in the small p u l m o n a r y arterioles, indicating increased p u l m o n a r y arteriolar resistance. Arteriovenous fistulae t h a t have caused c a r d i a c failure in fetal life have been identified. A case of p u l m o n a r y arteriovenous fistula with fetal cardiac failure was the subject of separate reports by S h i n o h a r a a n d SekP a n d by Ehrlich a n d associates. 6 T w o cases of cerebral arteriovenous fistula causing fetal c a r d i a c failure were r e p o r t e d by G o m e z a n d co-workers. 7 C o n g e n i t a l p u l m o n a r y v a l v u l a r insufficiency occurring as an isolated c a r d i a c malf o r m a t i o n resulting in c a r d i a c failure in infancy has been the subject of two reports s' 9 a n d in one case congestive failure was present at birth. 19 I n a discussion of the latter case the fetal h e m o d y n a m i c s were considered i,a relation to d e v e l o p m e n t of fetal c a r d i a c failure. T w o of the m a j o r differences between the fetal a n d the a d u l t circulations are: (1) the elevation of the p u l m o n a r y arterial pressure, a n d (2) the p a t e n c y of the ductus arteriosus in the fetus. I n fetuses with p u l m o n a r y v a l v u l a r insufficiency the
May 1966
characteristically high p u l m o n a r y arterial pressure would favor a larger volume of p u l m o n a r y regurgitation t h a n in postnatal life w h e n the p u l m o n a r y arterial pressure is lower. If d u r i n g p o s t n a t a l life the ductus arteriosus remains patent, p u l m o n a r y valvular insufficiency would favor a greater shunt t h r o u g h the ductus. E n d o c a r d i a l fibroelastosis of the left ventricle, as n o t e d in Case 2, tends to be associated w i t h m i t r a l insufficiency. 1~ I n d e e d , in the present case a murm u r characteristic of m i t r a l insufficiency was present. I n the presence of m i t r a l regurgitation the left atrial pressure is elevated and m a y effectively close the f o r a m e n ovale. This m i g h t have led to a m e c h a n i s m of cardiac failure similar to that in p r e m a t u r e closure of the f o r a m e n ovale. T h e r e p o r t e d cases suggest t h a t the occurrence of fetal c a r d i a c failure depends u p o n a state in which there is excessive b u r d e n u p o n the right ventricle. SUMMARY
T h r e e cases of cardiac m a l f o r m a t i o n s with c a r d i a c failure d u r i n g the fetal life are presented. T h e m a l f o r m a t i o n s were: (1) right ventricular e n d o c a r d i a l fibroelastosis, (2) Ebstein's m a l f o r m a t i o n of the tricuspid valve, a n d (3) left v e n t r i c u l a r e n d o c a r d i a l fibroelastosis a n d m i t r a l insufficiency. Fetal cardiac failure is a rare occurrence a n d usually results from a h e m o d y n a m i c b u r d e n u p o n the right ventricle. REFERENCES
1. Potter, E. L.: Pathology of the fetus and the newborn, Chicago, 1952, Year Book Publishers, Inc., pp. 524-526. 2. Tait, L.: A case of general dropsy in a foetus, Tr. Obst. Soc. Lond. 17: 307, 1875. 3. Benner, M. C.: Premature closure of the foramen ovule. Report of two eases, Am. Heart J. 17: 437, 1939. 4. Naeye, R. L., and Blanc, W. A.: Prenatal narrowing or closure of the foramen ovale, Circulation 30: 736, 1964. 5. Shinohara, Y., and Seki, M.: Dystocia due to fetal ascites. Report of a case with congenital malformations of liver and lung, Bull. New York Acad. Med. 37: 136, 1961. 6. Ehrlich, J. C., Goodfriend, M. J~, Shinohara, Y., and Seki, M.: Fetal ascites and portal dysplasia of the liver (polycystic disease without cysts). With pulmonary arterlo-
Volume 68
Number 5
venous fistula and cystic lung, Pediatrics 33" 216, 1964. 7. Gomez, M. R., Whitten, C. F., Nolke, A., Bernstein, J., and Meyer, J. S." Aneurysmal malformation of the great vein of Galen causing heart failure in early infancy. Report of five cases, Pediatrics 31: 400, 1963. 8. Smith, R. D., DuShane, J. W., and Edwards, J. E.: Congenital insufficiency of the pulmonary valve including a case of fetal cardiac failure, Circulation 20: 554, 1959.
Fetal cardiac failure
70 3
9. Ito, T., Engle, M. A., and Holswade, G. R.: Congenital insufficiency of the pulmonic valve. A rare cause of neonatal heart failure, Pediatrics 28" 712, 1961. 10. Moller, J. H., Lucas, R. V., Jr., Adams, P., Jr., Anderson, R. C., Jorgens, J., and Edwards, J. E.: Endoeardial fibroelastosis. A clinical and anatomic study of 47 patients with emphasis on its relationship to mitral insufficiency, Circulation 30: 759, 1964.