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False aneurysm of left ventricle due to perforation of mitral-aortic intervalvular fibrosa with rupture and cardiac tamponade
False Aneurysm of Left Ventricle Due To Perforation of MitraI-Aortic Intervalvular Fibrosa with Rupture and Cardiac Tamponade Rare Complication of Infective Endocarditis ALl H. QIZILBASH, FRCP(C) COLIN J. SCHWARTZ, FRCPA Hamilton, Ontario, Canada
A case of subacute bacterial endocarditis occurring in a congenital bicuspid aortic valve in a 17 year old boy is presented. The infection secondarily involved the mitral-aortic intervalvular fibrosa, the junctional zone between the mitral and aortic valves. Perforation of this zone, with extension of infection and blood into the epicardial wedge overlying the fibrosa, resulted in the formation of a false aneurysm situated at the base of the left ventricle between the aorta and the left atrium. Rupture of the aneurysm with hemorrhage into the pericardial cavity resulted in death from cardiac tamponade.
R u p t u r e of the heart due to an erosive m y c o t i c a n e u r y s m into the pericardial cavity is rare. Available reports suggest t h a t the frequency of this cause of cardiac r u p t u r e is a little less t h a n 1 percent of t h a t of all other causes of rupture. 1 In this report we describe a case of s u b a c u t e bacterial endocarditis involving the aortic valve with secondary infection of the mitral-aortic intervalvular fibrosa, the j u n c t i o n a l zone between the aortic a n d mitral valve. Perforation of this zone resulted in the f o r m a t i o n of a false a n e u r y s m interposed between the aorta a n d left atrium, and its s u b s e q u e n t r u p t u r e led to cardiac t a m p o n a d e a n d death. C a s e Report
From the Department of Pathology, Henderson General Hospital, Chedoke Hospitals and McMaster University, Hamilton, Ontario, Canada. Manuscript accepted December 11, 1972. Address for reprints: Ali H. Qizilbash, MD, Department of Pathology, Henderson General Hospital, 711 Concession St., Hamilton, Ontario, Canada LSV IC3
110
July 1973
Clinical history: The patient, a 17 year old Caucasian boy, was well until the summer of 1971, when fatigue and intermittent fever developed. In the interval between the onset of the illness and admission to the hospital on November 12, 1971, he lost approximately 15 lb in weight. During the 2 weeks before admission he had developed a nonproductive cough and noted some discomfort in the region of the left Achilles tendon. There was no past history of rheumatic fever, and he had no antecedent cardiovascular symptoms. On physical examination he appeared pale and ill. On admission, temperature was 38.5 C and pulse rate 90 beats/min; rhythm was sinus, and blood pressure was 140/70 mm Hg. A short systolic ejection murmur heard in the aortic area was not transmitted to the neck; no diastolic murmur was noted. The splenic tip was just palpable. There were no other positive physical findings; the optic fundi appeared normal, and no splinter hemorrhages or Osler nodes were observed. Laboratory studies on admission revealed the following values: hemoglobin 11.2 g/100 ml and white blood cell count 11,600 mm 3, with 69 percent neutrophils, 11 percent bands, 1 percent eosinophils, 11 percent lymphocytes and 3 percent monocytes. Sedimentation rate was 81 mm in 1 hour, and platelet count was 430,000/mm 3. The blood showed no specific changes other than a shift to the left in the neutrophils. Urinalysis revealed 2 to 3 erythrocytes/high power field. Results of serum biochemistry studies were within normal limits, and the electrocardiogram revealed no abnormality.
The American Journal of CARDIOLOGY
Volume 32
FALSE ANEURYSM OF LEFT VENTRICLE--QIZILBASH
FIGURE 2. Internal view of the left ventricular cavity showing the bicuspid aortic valve. Slight thickening and nodulation is present along the commissure. A triangular defect (arrow) representing the opening of the false aneurysm into the left ventricle is seen just below the junction of the 2 valves. The anterior leaflet of the mitral valve appears normal. The opening of this aneurysm is situated in the mitral-aortic intervalvular fibrosa, the junctional zone between the mitral and aortic valves•
FIGURE 1. Gross photograph of the heart viewed anteriorly. Note the large oval shaped false aneurysm (arrow) lying between the aorta and the left atrial appendage.
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The combination of fever, heart murmur, splenomegaly and microscopic hematuria suggested infective endocarditis. Blood cultures revealed a growth of streptococci (streptococcus viridans). Other studies performed on admission included antistreptolysin O titer, latex fixation and lupus erythematosus cell tests, all of which were noncontributory. The serum albumin level was depressed at 3.17 g/100 ml. Serum globulin values were alpha~ globulin 0.4, alpha2 (slightly increased) 1.20, beta globulin (slightly increased)
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1.25, and gamma globulin (marginally increased) 1.16 g/ 100 ml. Course in hospital: On November 19, intravenous penicillin therapy was initiated. At this time the patient's oral temperature was 38.5 C; on the following day it became normal and remained normal. On November 28, a painful tender swelling developed over the medial side of the right ankle, and an aortic diastolic murmur was heard in addition to the previously noted systolic murmur. On
July 1973
The A m e r i c a n Journal of CARDIOLOGY
Volume 32
111
FALSE ANEURYSM OF LEFT VENTRICLE--QlZlLBASH AND SCHWARTZ
I~IGURE 4. Gross appearance of the heart through the posterior aortic cusp. Patient's heart on the left, normal heart on right. Note the large aneurysmal sac lying between the aorta and the left atrium in the space normally occupied by a wedge of epicardial fatty tissue. The opening of the sac (arrow, left) into the ventricular cavity is in the region of the mitral-aorta intervalvular fibrosa (arrow, right). A -- aorta; LA = left atrium; MV = mitral valve; S = aneurysmal sac; X = epicardial wedge.
FIGURE 5. Gross specimen through the aneurysmal sac (left) compared with the normal sac (right), showing the perforation of the mitral-aortic intervalvular fibrosa (arrow). A = aorta; AC = aneurysmal cavity; LA --- wall of left atrium; MAiVF = mitral-aortic intervalvular fibrosa; PL = posterior leaflet, aortic valve.
FIGURE 6. Left, histologic section of the false aneurysm lying between the aorta and the wall of the left atrium in the region normally occupied by an epicardial wedge of fatty tissue. Right, normal histologic section through the posterior leaflet of aortic valve. (Elastic stain X3, reduced by 24 percent.) A = aorta; LA = wall of left atrium; MAIVF = mitral-aortic intervalvular fibrosa; MV = anterior leaflet, mitral valve; PL = posterior leaflet, aortic valve; X = epicardial wedge of fatty tissue.
112
July 1973
The American Journal of CARDIOLOGY
Volume 32
FALSE ANEURYSM OF LEFT VENTRICLE--QIZILBASH AND SCHWARTZ
December 14, the patient experienced epigastric distress and vomited some coffee ground-like material. Surgical consultation was obtained but no specific findings were noted, and the patient's condition stabilized without explanation. The possibility of a mesenteric embolus was considered. A chest X-ray film obtained on December 18 revealed an increase in cardiac size and a cardiothoracic ratio of 15.7/30.4. A previous film obtained on November 29 had shown normal heart size and a cardiothoracic ratio of 13/29.4. The patient was afebrile and asymptomatic, but cardiac arrest occurred the following day, and attempts at resuscitation were unsuccessful. Autopsy findings: The body was that of a 17 year old, well developed Caucasian boy, weighing 135 lb. The pericardial cavity contained approximately 700 ml of fresh blood mixed with a few clots. The source of this blood was a ruptured false aneurysm at the base of the left ventricle, between the aorta and the left atrium, and adherent to the adjoining structures (Fig. 1). The aneurysmal sac was oval and measured 5 by 3 cm. The heart weighed 300 g. The tricuspid, pulmonary and mitral valves were normal. The aortic valve was bicuspid; both cusps were slightly thickened and showed some nodulation near the commissures. A triangular defect measuring 1 cm across the base lay immediately below the junction of the 2 cusps. It represented the mouth of the aneurysm, which had smooth and glistening edges (Fig. 2). The uppermost part of the aneurysmal wall was only 0.2 cm thick; it had a ragged tear, approximately 0.5 cm long, representing the site of rupture and hemorrhage. The lining of the sac was generally smooth with a few grayish to yellow streaks and thickened plaques on the surface. Microscopically, the wall of the aneurysm consisted of rather vascular cellular connective tissue containing neutrophils, lymphocytes, plasma cells and histiocytes (Fig. 3A). The sac was adherent to the epicardial surface of the left atrium and the adventitia of the ascending aorta, being attached by newly formed fibrous tissue rich in small capillaries and inflammatory cells. A few small arteries and arterioles were also present; they showed marked luminal narrowing due to muscular and intimal hyperplasia. There were numerous aggregates of hemosiderin pigment within the wall of the aneurysmal sac, indicative of old hemorrhage (Fig. 3B). The lining of the sac was composed of fibrin-staining material. The aortic valve showed organization of fibrinous exudate on the surface. No bacteria were noted. Examination of the remainder of the heart revealed no abnormality. The coronary ostia were patent and normally located in the sinuses of Valsalva. There was no evidence of thrombosis or stenosis of the coronary arteries. No stigmata of rheumatic heart disease were seen. Additional autopsy findings were congestive enlargement of the spleen (weight 440 g) and healed focal "embolic" glomerulonephritis.
Comment False a n e u r y s m s of the left ventricle are rare and have been described after t r a u m a , 2 m y o c a r d i a l infarction, 3 a n d infections. 1,4,5 Occasionally, these m a y be of congenital origin. 6 T h e false a n e u r y s m in our p a t i e n t occurred in a site rare for this l e s i o n - - t h e m i t r a l - a o r t i c i n t e r v a l v u l a r fibrosa, 6,7 the junctional zone of the aortic a n d mitral valves. To a p p r e c i a t e the f o r m a t i o n and a n a t o m i c relations of the a n e u r y s m , it is essential to e x a m i n e a similar site in the n o r m a l heart (Fig. 4 to 6). Normally, the left half of the posterior (noncoronary) aortic cusp a n d the a d j a c e n t third of the left aortic cusp are continuous with the anterior leaflet of the m i t r a l valve. This area is the only p a r t of the aortic wall t h a t is not connected with the ventricular p o r tion of the heart; instead, the aorta is connected with the base of the anterior m i t r a l leaflet. This j u n c t i o n a l zone between the 2 valves is f o r m e d by fibrous tissue called the mitral-aortic intervalvular fibrosa.2,6 T h e site is covered by a wedge of epicardial f a t t y tissue s e p a r a t i n g the outflow t r a c t of the left ventricle from the pericardial cavity. Infection with s u b s e q u e n t perforation of this area could easily result in (1) h e m o r r h a g e and infection extending into' the epicardial wedge with evagination of the structures, a n d (2) f o r m a t i o n of a false a n e u r y s m between the a o r t a and the left a t r i u m . Cases similar to ours have previously been described.l,~.6 T h e histologic a p p e a r a n c e of the aneur y s m a l sac in each of these cases was similar to t h a t reported in our patient, t h a t is, vascular connective tissue c o n t a i n e d i n f l a m m a t o r y cells with evidence of prior hemorrhage, t h e r e b y suggesting t h a t infection and slow h e m o r r h a g e in the epicardial wedge resulted in f o r m a t i o n of the false a n e u r y s m . E v e n t u a l ly, as in our patient, the false a n e u r y s m m a y r u p t u r e into the pericardial cavity, because of the high level of pressure in the left ventricle. Our p a t i e n t had a congenital bicuspid aortic valve, and the possibility exists t h a t a congenital weakness in the area of the mitral-aortic intervalvular fibrosa resulted in perforation. Although this possibility c a n n o t definitely be excluded, the histologic a p p e a r ance of the a n e u r y s m a l sac suggests an i n f l a m m a t o r y basis for the perforation at the intervalvular fibrosa.
Acknowledgment We gratefully acknowledge the valuable advice and comments of Dr. Jesse E. Edwards and the secretarial assistance of Mrs. Hilda Parkinson.
References 1. Pirani CL: Erosive (mycotic) aneurysm of the heart with rupture. Arch Path (Chicago) 36:579-586, 1943 2. Pitts HH, Purvis GS: Ruptured traumatic aneurysm in a child. Canad Med Ass J 57:165-166, 1947 3. Cone RB, Hawley RL: Pseudoaneurysm of the heart following infarction. Arch Path (Chicago) 77:166-171, 1964 4. Medalia LS, Drapiewski JF: Congenital defects of the aortic vestibule complicated by bacterial endocarditis with perforation and death from cardiac tamponade. Amer Heart J 31:103-106, 1946
5. Chesler E, Korns ME, Porter GE, et ah False aneurysm of the left ventricle secondary to bacterial endocarditis with perforation of the mitral-aortic intervalvular fibrosa. Circulation 37:518-523, 1968 6. Edwards JE, Burchell HB: The pathological anatomy of deficiencies between the aortic roof and the heart including aortic sinus aneurysms. Thorax 12:125-139, 1957 7. Gross L, Kugel MA: Topographic anatomy and histology of the valves in the human heart. Amer J Path 7:445-473, 1931
July 1973
The American Journal of CARDIOLOGY
Vo|ume 32
113
A case of subacute bacterial endocarditis occurring in a congenital bicuspid aortic valve in a 17 year old boy is presented. The infection secondarily involved the mitral-aortic intervalvular fibrosa, the junctional zone between the mitral and aortic valves. Perforation of this zone, with extension of infection and blood into the epicardial wedge overlying the fibrosa, resulted in the formation of a false aneurysm situated at the base of the left ventricle between the aorta and the left atrium. Rupture of the aneurysm with hemorrhage into the pericardial cavity resulted in death from cardiac tamponade.
R u p t u r e of the heart due to an erosive m y c o t i c a n e u r y s m into the pericardial cavity is rare. Available reports suggest t h a t the frequency of this cause of cardiac r u p t u r e is a little less t h a n 1 percent of t h a t of all other causes of rupture. 1 In this report we describe a case of s u b a c u t e bacterial endocarditis involving the aortic valve with secondary infection of the mitral-aortic intervalvular fibrosa, the j u n c t i o n a l zone between the aortic a n d mitral valve. Perforation of this zone resulted in the f o r m a t i o n of a false a n e u r y s m interposed between the aorta a n d left atrium, and its s u b s e q u e n t r u p t u r e led to cardiac t a m p o n a d e a n d death. C a s e Report
From the Department of Pathology, Henderson General Hospital, Chedoke Hospitals and McMaster University, Hamilton, Ontario, Canada. Manuscript accepted December 11, 1972. Address for reprints: Ali H. Qizilbash, MD, Department of Pathology, Henderson General Hospital, 711 Concession St., Hamilton, Ontario, Canada LSV IC3
110
July 1973
Clinical history: The patient, a 17 year old Caucasian boy, was well until the summer of 1971, when fatigue and intermittent fever developed. In the interval between the onset of the illness and admission to the hospital on November 12, 1971, he lost approximately 15 lb in weight. During the 2 weeks before admission he had developed a nonproductive cough and noted some discomfort in the region of the left Achilles tendon. There was no past history of rheumatic fever, and he had no antecedent cardiovascular symptoms. On physical examination he appeared pale and ill. On admission, temperature was 38.5 C and pulse rate 90 beats/min; rhythm was sinus, and blood pressure was 140/70 mm Hg. A short systolic ejection murmur heard in the aortic area was not transmitted to the neck; no diastolic murmur was noted. The splenic tip was just palpable. There were no other positive physical findings; the optic fundi appeared normal, and no splinter hemorrhages or Osler nodes were observed. Laboratory studies on admission revealed the following values: hemoglobin 11.2 g/100 ml and white blood cell count 11,600 mm 3, with 69 percent neutrophils, 11 percent bands, 1 percent eosinophils, 11 percent lymphocytes and 3 percent monocytes. Sedimentation rate was 81 mm in 1 hour, and platelet count was 430,000/mm 3. The blood showed no specific changes other than a shift to the left in the neutrophils. Urinalysis revealed 2 to 3 erythrocytes/high power field. Results of serum biochemistry studies were within normal limits, and the electrocardiogram revealed no abnormality.
The American Journal of CARDIOLOGY
Volume 32
FALSE ANEURYSM OF LEFT VENTRICLE--QIZILBASH
FIGURE 2. Internal view of the left ventricular cavity showing the bicuspid aortic valve. Slight thickening and nodulation is present along the commissure. A triangular defect (arrow) representing the opening of the false aneurysm into the left ventricle is seen just below the junction of the 2 valves. The anterior leaflet of the mitral valve appears normal. The opening of this aneurysm is situated in the mitral-aortic intervalvular fibrosa, the junctional zone between the mitral and aortic valves•
FIGURE 1. Gross photograph of the heart viewed anteriorly. Note the large oval shaped false aneurysm (arrow) lying between the aorta and the left atrial appendage.
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....
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..:~-.>.:...:.-.-..:. FIGURE 3. Photomicrographs of the wall of the aneurysmal sac A, the wall is composed of vascular connective tissue containing inflammatory cells. The sac is lined by fibrinous material (top) which has begun to organize. B, wall of sac showing aggregates of hemosiderin pigment• (Hematoxylin-eosin X300 (A) and 750 (B), reduced by 50 percent.)
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The combination of fever, heart murmur, splenomegaly and microscopic hematuria suggested infective endocarditis. Blood cultures revealed a growth of streptococci (streptococcus viridans). Other studies performed on admission included antistreptolysin O titer, latex fixation and lupus erythematosus cell tests, all of which were noncontributory. The serum albumin level was depressed at 3.17 g/100 ml. Serum globulin values were alpha~ globulin 0.4, alpha2 (slightly increased) 1.20, beta globulin (slightly increased)
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1.25, and gamma globulin (marginally increased) 1.16 g/ 100 ml. Course in hospital: On November 19, intravenous penicillin therapy was initiated. At this time the patient's oral temperature was 38.5 C; on the following day it became normal and remained normal. On November 28, a painful tender swelling developed over the medial side of the right ankle, and an aortic diastolic murmur was heard in addition to the previously noted systolic murmur. On
July 1973
The A m e r i c a n Journal of CARDIOLOGY
Volume 32
111
FALSE ANEURYSM OF LEFT VENTRICLE--QlZlLBASH AND SCHWARTZ
I~IGURE 4. Gross appearance of the heart through the posterior aortic cusp. Patient's heart on the left, normal heart on right. Note the large aneurysmal sac lying between the aorta and the left atrium in the space normally occupied by a wedge of epicardial fatty tissue. The opening of the sac (arrow, left) into the ventricular cavity is in the region of the mitral-aorta intervalvular fibrosa (arrow, right). A -- aorta; LA = left atrium; MV = mitral valve; S = aneurysmal sac; X = epicardial wedge.
FIGURE 5. Gross specimen through the aneurysmal sac (left) compared with the normal sac (right), showing the perforation of the mitral-aortic intervalvular fibrosa (arrow). A = aorta; AC = aneurysmal cavity; LA --- wall of left atrium; MAiVF = mitral-aortic intervalvular fibrosa; PL = posterior leaflet, aortic valve.
FIGURE 6. Left, histologic section of the false aneurysm lying between the aorta and the wall of the left atrium in the region normally occupied by an epicardial wedge of fatty tissue. Right, normal histologic section through the posterior leaflet of aortic valve. (Elastic stain X3, reduced by 24 percent.) A = aorta; LA = wall of left atrium; MAIVF = mitral-aortic intervalvular fibrosa; MV = anterior leaflet, mitral valve; PL = posterior leaflet, aortic valve; X = epicardial wedge of fatty tissue.
112
July 1973
The American Journal of CARDIOLOGY
Volume 32
FALSE ANEURYSM OF LEFT VENTRICLE--QIZILBASH AND SCHWARTZ
December 14, the patient experienced epigastric distress and vomited some coffee ground-like material. Surgical consultation was obtained but no specific findings were noted, and the patient's condition stabilized without explanation. The possibility of a mesenteric embolus was considered. A chest X-ray film obtained on December 18 revealed an increase in cardiac size and a cardiothoracic ratio of 15.7/30.4. A previous film obtained on November 29 had shown normal heart size and a cardiothoracic ratio of 13/29.4. The patient was afebrile and asymptomatic, but cardiac arrest occurred the following day, and attempts at resuscitation were unsuccessful. Autopsy findings: The body was that of a 17 year old, well developed Caucasian boy, weighing 135 lb. The pericardial cavity contained approximately 700 ml of fresh blood mixed with a few clots. The source of this blood was a ruptured false aneurysm at the base of the left ventricle, between the aorta and the left atrium, and adherent to the adjoining structures (Fig. 1). The aneurysmal sac was oval and measured 5 by 3 cm. The heart weighed 300 g. The tricuspid, pulmonary and mitral valves were normal. The aortic valve was bicuspid; both cusps were slightly thickened and showed some nodulation near the commissures. A triangular defect measuring 1 cm across the base lay immediately below the junction of the 2 cusps. It represented the mouth of the aneurysm, which had smooth and glistening edges (Fig. 2). The uppermost part of the aneurysmal wall was only 0.2 cm thick; it had a ragged tear, approximately 0.5 cm long, representing the site of rupture and hemorrhage. The lining of the sac was generally smooth with a few grayish to yellow streaks and thickened plaques on the surface. Microscopically, the wall of the aneurysm consisted of rather vascular cellular connective tissue containing neutrophils, lymphocytes, plasma cells and histiocytes (Fig. 3A). The sac was adherent to the epicardial surface of the left atrium and the adventitia of the ascending aorta, being attached by newly formed fibrous tissue rich in small capillaries and inflammatory cells. A few small arteries and arterioles were also present; they showed marked luminal narrowing due to muscular and intimal hyperplasia. There were numerous aggregates of hemosiderin pigment within the wall of the aneurysmal sac, indicative of old hemorrhage (Fig. 3B). The lining of the sac was composed of fibrin-staining material. The aortic valve showed organization of fibrinous exudate on the surface. No bacteria were noted. Examination of the remainder of the heart revealed no abnormality. The coronary ostia were patent and normally located in the sinuses of Valsalva. There was no evidence of thrombosis or stenosis of the coronary arteries. No stigmata of rheumatic heart disease were seen. Additional autopsy findings were congestive enlargement of the spleen (weight 440 g) and healed focal "embolic" glomerulonephritis.
Comment False a n e u r y s m s of the left ventricle are rare and have been described after t r a u m a , 2 m y o c a r d i a l infarction, 3 a n d infections. 1,4,5 Occasionally, these m a y be of congenital origin. 6 T h e false a n e u r y s m in our p a t i e n t occurred in a site rare for this l e s i o n - - t h e m i t r a l - a o r t i c i n t e r v a l v u l a r fibrosa, 6,7 the junctional zone of the aortic a n d mitral valves. To a p p r e c i a t e the f o r m a t i o n and a n a t o m i c relations of the a n e u r y s m , it is essential to e x a m i n e a similar site in the n o r m a l heart (Fig. 4 to 6). Normally, the left half of the posterior (noncoronary) aortic cusp a n d the a d j a c e n t third of the left aortic cusp are continuous with the anterior leaflet of the m i t r a l valve. This area is the only p a r t of the aortic wall t h a t is not connected with the ventricular p o r tion of the heart; instead, the aorta is connected with the base of the anterior m i t r a l leaflet. This j u n c t i o n a l zone between the 2 valves is f o r m e d by fibrous tissue called the mitral-aortic intervalvular fibrosa.2,6 T h e site is covered by a wedge of epicardial f a t t y tissue s e p a r a t i n g the outflow t r a c t of the left ventricle from the pericardial cavity. Infection with s u b s e q u e n t perforation of this area could easily result in (1) h e m o r r h a g e and infection extending into' the epicardial wedge with evagination of the structures, a n d (2) f o r m a t i o n of a false a n e u r y s m between the a o r t a and the left a t r i u m . Cases similar to ours have previously been described.l,~.6 T h e histologic a p p e a r a n c e of the aneur y s m a l sac in each of these cases was similar to t h a t reported in our patient, t h a t is, vascular connective tissue c o n t a i n e d i n f l a m m a t o r y cells with evidence of prior hemorrhage, t h e r e b y suggesting t h a t infection and slow h e m o r r h a g e in the epicardial wedge resulted in f o r m a t i o n of the false a n e u r y s m . E v e n t u a l ly, as in our patient, the false a n e u r y s m m a y r u p t u r e into the pericardial cavity, because of the high level of pressure in the left ventricle. Our p a t i e n t had a congenital bicuspid aortic valve, and the possibility exists t h a t a congenital weakness in the area of the mitral-aortic intervalvular fibrosa resulted in perforation. Although this possibility c a n n o t definitely be excluded, the histologic a p p e a r ance of the a n e u r y s m a l sac suggests an i n f l a m m a t o r y basis for the perforation at the intervalvular fibrosa.
Acknowledgment We gratefully acknowledge the valuable advice and comments of Dr. Jesse E. Edwards and the secretarial assistance of Mrs. Hilda Parkinson.
References 1. Pirani CL: Erosive (mycotic) aneurysm of the heart with rupture. Arch Path (Chicago) 36:579-586, 1943 2. Pitts HH, Purvis GS: Ruptured traumatic aneurysm in a child. Canad Med Ass J 57:165-166, 1947 3. Cone RB, Hawley RL: Pseudoaneurysm of the heart following infarction. Arch Path (Chicago) 77:166-171, 1964 4. Medalia LS, Drapiewski JF: Congenital defects of the aortic vestibule complicated by bacterial endocarditis with perforation and death from cardiac tamponade. Amer Heart J 31:103-106, 1946
5. Chesler E, Korns ME, Porter GE, et ah False aneurysm of the left ventricle secondary to bacterial endocarditis with perforation of the mitral-aortic intervalvular fibrosa. Circulation 37:518-523, 1968 6. Edwards JE, Burchell HB: The pathological anatomy of deficiencies between the aortic roof and the heart including aortic sinus aneurysms. Thorax 12:125-139, 1957 7. Gross L, Kugel MA: Topographic anatomy and histology of the valves in the human heart. Amer J Path 7:445-473, 1931
July 1973
The American Journal of CARDIOLOGY
Vo|ume 32
113