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Ruptured papillary muscle after acute myocardial infarction
Ruptured papillary muscle after acute myocardial infarction James S. Robinson, M.B., B.S., M.R.A.C.P.* Mary M. Stannard, M.B., B.S.** Michael Long, M.B., B.S.*** Victoria, Australia
A
lthough first described by M&rat’ in 1803, only 81 cases of ruptured papillary muscle have been reported.1-g This rare clinical entity is usually the result of acute myocardial infarction. The diagnosis was made at autopsy in most of the reported cases; only 12 cases were diagnosed before death. Two additional cases of ruptured papillary muscle after acute myocardial infarction are now reported. In one patient the diagnosis of ruptured papillary muscle was made on the day on which the rupture occurred, 5 days before death; in the other patient the diagnosis was made at autopsy. Case reports Case 1. E.P., a 77-year-old man, was admitted to the continuous electrocardiographic monitoring service’” with a 12-hour history of severe, crushing, retrosternal chest pain. He was confused and there was marked pallor, the blood pressure was 150/80 mm. Hg, and the jugular venous pressure was elevated 3 cm. On auscultation there was a split first heart sound, but no murmurs. These findings were confirmed by phonocardiogram (see Fig. 1). Examination of the chest revealed bilateral rhles and crepitations. An electrocardiogram (see Fig. 2) showed a nodal tachycardia at a rate of 1.50 per minute, the changes of posterior myocardial in-
farction, and marked S-T segment depression in the anterior chest leads. Because carotid sinus massage had no effect on the tachycardia, he was given 0.75 mg. of digoxin intramuscularly, and 0.25 mg. of digoxin orally every 8 hours. Chlorothiazide, 500 mg. twice daily, was begun, but anticoagulant therapy was not employed. Serum glutamic-oxalacetic transaminase was estimated every 12 hours, and blood urea and urinary output were measured daily (see Fig. 3). The day after admission the erythrocyte sedimentation rate was 42 mm. in 1 hour, hemoglobin 15.3 Gm. per 100 ml., white cells 10,000 per cubic millimeter, serum cholesterol 2.50 mg. per 100 ml., and total serum lipids 720 mg. per 100 ml. Over the next 4 days his clinical condition improved, the tachycardia was controlled, and the signs of cardiac failure cleared. However, in spite of a good urinary volume, with a fixed specific gravity of 1.010, the blood urea continued to rise (see Fig. 3). Daily electrocardiograms showed persistence of the S-T segment depression in the anterior chest leads; it was considered that these changes were due to associated subendocardial infarction (see Fig. 4). A moderately loud, Grade 2 (4), pansystolic murmur, maximal at the left sternal edge and well conducted to the left axilla and infrascapular region, was detected on the fifth day after admission (see phonocardiogram Fig. 1). A systolic thrill was not palpable. The diagnosis of ruptured papillary muscle was made. After this complication there was no significant change in the blood pressure, or heart rate, and pulmonary edema did not appear. However, his clinical condition deteriorated, associated
From the Cardiac Department and Department of Morbid Anatomy, Received for publication Aug. 17, 1964. *Research Assistant, Cardiac Department, Royal Melbourne Hospital, National Heart Foundation of Australia. Present address: Royal **Cardiology Registrar. -Pathology Registrar.
233
Royal
Melbourne
Hospital,
Victoria,
in receipt of Grant-in-Aid G-162 Perth Hospital, Western Australia.
Australia. from
the
234
Robinson,
Stannard,
and Long
Fig. 1. Case 1. The phonocardiogram recorded on May 15, 1964, at the time of the patient’s admission to hospital shows a split first heart sound. ‘The second recording. obtained on May 20, shows a pansyqstolic murmur. l’he recordings were made at the left sternal edee in the hfth intercostaI space. Paler speed = 100 mm. per second.
avl
Fig.
2. Case
1. Electrocardiogram
recorded
on admission,
May
15, 1964.
Ruptured
papillary
muscle
after acute myocardial
Fig. 3. Case 1. There was a progressive rise in blood SGOT from a peak measured level of 197 units.
urea,
and
infurctiorr
235
a fall in
avr
Fig.
4. Case
1. Electrocardiogram
with a progressive rise in blood urea to 615 mg. per 100 ml., and the development of bronrhopneumonia. Death occurred 10 days after his admission to hospital. AUTOPSY. The heart was slightly enlarged, weighing 400 grams. Two centimeters from its origin, the right coronary artery u-as completely obstructed by antemortem thrombus. The circumflex branch of the left coronary artery was obliterated at its origin by calcified atheroma and organized thrombus. There
recorded
on May
20, 1964.
were calcified plaques of atheroma in the wall of the anterior descending branch of the left coronary artery, but its lumen was patent. Transmural infarction involved the posterior superior aspect of the left ventricle, and spread inferiorly, becoming mainly subendocardial to involve the entire left posterior papillary muscle. Complete rupture of the left posterior papillary muscle had occurred, 3 mm. above its base (see Fig. 5). Apart from excess mobility of the aortic cusp of the mitral
236
Robinson,
Stannard,
and Long
Fig. 5. Case 1. The papillary muscle.
valve, all cardiac valves were ventricular septum was intact. Both kidneys were contracted irregular surfaces; the renal wide. Microscopically, both changes of nephrosclerosis. Case 2. L.B., a 61-year-old
normal,
arrow
indicates
and the inter-
and showed scarred cortices were 3 mm. kidneys showed the man,
presented
to his
the base of the ruptured
left posterior
medical practitioner with a 2-week history of pain between the scapulae, and shortness of breath. A systolic murmur was audible and there were r%les at both lung bases. The patient initially refused admission to hospital, but later that day consented because of increasing shortness of breath. On his arrival at the casualty department, acute pulmonary edema was present, and he was acutely dyspneic and unable to give a medical history. There was gross central cyanosis, the radial p&e was impalpable, and the jugular venous pressure was elevated 8 cm. There were loud coarse r%les throughout the chest, and the heart sounds were inaudible. Before a standard electrocardiogram could be recorded, cardiac arrest occurred and attempted resuscitation faiIed. AUTOPSY. The heart was enlarged, weighing 430 grams. All branches of the left coronary artery were patent, whereas the posterior interventricular branch of the right coronary artery was occluded by a thrombus. Infarction of the posterior wall of the left ventricIe extended from the endocardial surface to just beneath the epicardial surface; the infarcted zone was yellow and softened. The process spread inferiorly, involving the left posterior papillary muscle, which had ruptured completely, 1.5 cm. above its base. The separated portion, which measured 1.2 cm., had passed through a space between its attached chordae tendineae, thus twisting the chordae (see Fig. 6).
Discussion
Fig. 6. Case 2. The arrow indicates the basal segment of the ruptured papillary muscle. The separated portion has passed through a space between the chordae tendineae, twisting the chordae.
When a systolic murmur suddenly develops after acute myocardial infarction, the differential diagnosis will include: ruptured papillary muscle, perforation of the interventricular septum, infarction of a
l'olume
70
Number
2
Ruptured
papillary
papillary muscle without rupture, and left ventricular failure with functional mitral incompetence. With rupture of a papillary muscle, the pansystolic murmur of mitral incompetence would be expected. In about 60 per cent of the reported cases of ruptured papillary muscle a systolic murmur was detected.4 In some cases the murmur may not be heard because of the sudden death of the patient after the rupture, or, as in Case 2, the heart sounds and murmur may be obscured by the loud r%les of acute pulmonary edema. In only 2 of the reported cases was a systolic thrill palpable.2J The left posterior papillary muscle is the muscle most commonly involved, and this is usually associated with the electrocardiographic changes of posterior myocardial infarction.4 Perforation of the interventricular septum is accompanied in 95 per cent of the cases by the development of a pansystolic murmur, maximal at the left sternal edge in the fourth or fifth intercostal space, and a systolic thrill is palpable in over 50 per cent of the cases.5 In 75 per cent of the cases of ruptured septum the electrocardiogram shows the changes of anterior myocardial infarction.4 Rupture of the interventricular septum is usually followed rapidly by severe congestive cardiac failure with hepatic engorgement. During the last 18 months, we have observed 3 patients with myocardial infarction and rupture of the interventricular septum. In each case, after rupture there was a rapid and progressive rise in serum glutamic-oxalacetic transaminase to levels above 700 units. Presumably this was derived from both myocardial and hepatic damage. Infarction of a papillary muscle without rupture can lead to a systolic murmur.11 In this condition it is postulated that the damaged papillary muscle fails to contract during the ejection phase of ventricular systole, and then the attached segments of the mitral valve cusps will evert into the left atrium. The murmur produced is not pansystolic, but is of a crescendo-decrescendo quality and begins after the first heart sound. Acute pulmonary edema does not commonly follow this complication of myocardial infarctional Functional mitral incompetence second-
muscle after acute myocardial
infarction
237
ary to left ventricular failure will cause a pansystolic murmur. This murmur develops gradually, and it will increase progressively in intensity. Burch and associate+ suggest that in some cases of left ventricular failure the genesis of this pansystolic murmur may be dependent on papillary muscle dysfunction, rather than dilatation of the atrioventricular ring. In Case 1, the association of acute posterior myocardial infarction and subendocardial infarction, with a sudden onset of the pansystolic murmur of mitral incompetence, and the absence of a systolic thrill, led to the diagnosis of ruptured papillary muscle. The serum glutamicoxalacetic transaminase did not rise after the development of this murmur, which was unlike our previous experience with ruptured interventricular septum. When rupture of a papillary muscle follows myocardial infarction, there is usually a sudden onset of pulmonary edema, and death ensues.3 The typical clinical course of ruptured papillary muscle is illustrated by Case 2. In Case 1, sudden deterioration of the circulatory state did not occur ; instead, death was due to renal failure. Breneman and Drake5 have reported 2 patients with myocardial infarction who survived for 10 and 14 months after rupture of the left posterior papillary muscle. Cooley and associates13 have discussed the possibility of reparative surgery for ruptured papillary muscle after acute myocardial infarction. They suggest that surgery should be delayed until at least 6 weeks after the acute episode. Summary
TWO casesof rupture of the left posterior papillary muscle after acute myocardial infarction are reported. The diagnostic features of this uncommon complication of myocardial infarction are discussed, We wish to thank Dr. GraemeSlotnan for helpful criticism and Mr. Roy Ingles for preparation of the photographs. We are indebted to Dr. A. E. Prendergast and Mr. Brian Davie, F.R.A.C.S., who supplied the clinical details of the second case. REFERENCES 1. M&at, F. V.: Observations sur une l&ion organique du coeur par rupture d’une des colonnes charnues du ventricle gauche, J. de M&d., Chir., Pharm., Paris 6587, 1803.
238
2.
Robinson,
Stannard,
and Long
Hope, R. B., and Askey, J. M.: Necrosis of a cardiac papillary muscle following infarction with incomplete rupture, AM. HEART J. 44:306, 1952. 3. Hackel, D. B., and Kaufman, N.: Papillary muscle rupture due to a myocardial abscess, Ann. Int. Med 38:824, 1952. 4. Sanders, R. J,, Neubuerger, K. ‘I., and Ravin, ~1.: Rupture of papillary muscles: Occurrence of rupture of the posterior muscles in posterior myorardial infarction, Dis. Chest 31:316. 19.57. \5 Breneman, G. M., and Drake, E. H.: Ruptured papillary muscle following myocardial infarction with long s~lr\ival,CircLllation 25:862,1962. 6. Lundberg, S., and Soderstriim, J.: Perforation of the inten~entriculx septum in myocardial infarction, Arta med. Scandinav. 172 :413, 1962. 7. Hansen, J. : Spontaneous rupture of a papillary .\cta nied. scandinnx~. muscle of the heart, 172:531, 1962.
8. 9. 10.
11.
12.
13.
Beaghler, R. L., and Laurain, A. K.: Rupture of a cardiac papillary muscle, Arch. Path. 76:609. 1963. Case Records of the Massachusetts General Hospital, New England J. Med. 270:98, 1964. Robinson, J. S., Sloman, G., and McRae, C.: Continuous electrocardiographic monitoring in the early stages after acute myocardial infarction, M.J. Australia lA27. 1964. Burch, G. E:, DeF’asquale, N. I’., and Phillips, I. H. : Clinical manifestations of papillary muscle dvsfunction, .Irch. Int. Med. il2:112; 1963. Phillips. J. H.. Bruch. G. I?., and DePasquale, N. I’.: ‘The syndrome of papillary muscle dysf unction, :1nn. Int. Med. 59:508, 1963. Cooley, D. A., Henly, it:. S.. .Amad, K. H., and Chapman, I>. W.: \:entricular aneurysm following rnyocardinl infarction: Results of surgical treatment, Ann. Surg. lSO:595. 1959.
A
lthough first described by M&rat’ in 1803, only 81 cases of ruptured papillary muscle have been reported.1-g This rare clinical entity is usually the result of acute myocardial infarction. The diagnosis was made at autopsy in most of the reported cases; only 12 cases were diagnosed before death. Two additional cases of ruptured papillary muscle after acute myocardial infarction are now reported. In one patient the diagnosis of ruptured papillary muscle was made on the day on which the rupture occurred, 5 days before death; in the other patient the diagnosis was made at autopsy. Case reports Case 1. E.P., a 77-year-old man, was admitted to the continuous electrocardiographic monitoring service’” with a 12-hour history of severe, crushing, retrosternal chest pain. He was confused and there was marked pallor, the blood pressure was 150/80 mm. Hg, and the jugular venous pressure was elevated 3 cm. On auscultation there was a split first heart sound, but no murmurs. These findings were confirmed by phonocardiogram (see Fig. 1). Examination of the chest revealed bilateral rhles and crepitations. An electrocardiogram (see Fig. 2) showed a nodal tachycardia at a rate of 1.50 per minute, the changes of posterior myocardial in-
farction, and marked S-T segment depression in the anterior chest leads. Because carotid sinus massage had no effect on the tachycardia, he was given 0.75 mg. of digoxin intramuscularly, and 0.25 mg. of digoxin orally every 8 hours. Chlorothiazide, 500 mg. twice daily, was begun, but anticoagulant therapy was not employed. Serum glutamic-oxalacetic transaminase was estimated every 12 hours, and blood urea and urinary output were measured daily (see Fig. 3). The day after admission the erythrocyte sedimentation rate was 42 mm. in 1 hour, hemoglobin 15.3 Gm. per 100 ml., white cells 10,000 per cubic millimeter, serum cholesterol 2.50 mg. per 100 ml., and total serum lipids 720 mg. per 100 ml. Over the next 4 days his clinical condition improved, the tachycardia was controlled, and the signs of cardiac failure cleared. However, in spite of a good urinary volume, with a fixed specific gravity of 1.010, the blood urea continued to rise (see Fig. 3). Daily electrocardiograms showed persistence of the S-T segment depression in the anterior chest leads; it was considered that these changes were due to associated subendocardial infarction (see Fig. 4). A moderately loud, Grade 2 (4), pansystolic murmur, maximal at the left sternal edge and well conducted to the left axilla and infrascapular region, was detected on the fifth day after admission (see phonocardiogram Fig. 1). A systolic thrill was not palpable. The diagnosis of ruptured papillary muscle was made. After this complication there was no significant change in the blood pressure, or heart rate, and pulmonary edema did not appear. However, his clinical condition deteriorated, associated
From the Cardiac Department and Department of Morbid Anatomy, Received for publication Aug. 17, 1964. *Research Assistant, Cardiac Department, Royal Melbourne Hospital, National Heart Foundation of Australia. Present address: Royal **Cardiology Registrar. -Pathology Registrar.
233
Royal
Melbourne
Hospital,
Victoria,
in receipt of Grant-in-Aid G-162 Perth Hospital, Western Australia.
Australia. from
the
234
Robinson,
Stannard,
and Long
Fig. 1. Case 1. The phonocardiogram recorded on May 15, 1964, at the time of the patient’s admission to hospital shows a split first heart sound. ‘The second recording. obtained on May 20, shows a pansyqstolic murmur. l’he recordings were made at the left sternal edee in the hfth intercostaI space. Paler speed = 100 mm. per second.
avl
Fig.
2. Case
1. Electrocardiogram
recorded
on admission,
May
15, 1964.
Ruptured
papillary
muscle
after acute myocardial
Fig. 3. Case 1. There was a progressive rise in blood SGOT from a peak measured level of 197 units.
urea,
and
infurctiorr
235
a fall in
avr
Fig.
4. Case
1. Electrocardiogram
with a progressive rise in blood urea to 615 mg. per 100 ml., and the development of bronrhopneumonia. Death occurred 10 days after his admission to hospital. AUTOPSY. The heart was slightly enlarged, weighing 400 grams. Two centimeters from its origin, the right coronary artery u-as completely obstructed by antemortem thrombus. The circumflex branch of the left coronary artery was obliterated at its origin by calcified atheroma and organized thrombus. There
recorded
on May
20, 1964.
were calcified plaques of atheroma in the wall of the anterior descending branch of the left coronary artery, but its lumen was patent. Transmural infarction involved the posterior superior aspect of the left ventricle, and spread inferiorly, becoming mainly subendocardial to involve the entire left posterior papillary muscle. Complete rupture of the left posterior papillary muscle had occurred, 3 mm. above its base (see Fig. 5). Apart from excess mobility of the aortic cusp of the mitral
236
Robinson,
Stannard,
and Long
Fig. 5. Case 1. The papillary muscle.
valve, all cardiac valves were ventricular septum was intact. Both kidneys were contracted irregular surfaces; the renal wide. Microscopically, both changes of nephrosclerosis. Case 2. L.B., a 61-year-old
normal,
arrow
indicates
and the inter-
and showed scarred cortices were 3 mm. kidneys showed the man,
presented
to his
the base of the ruptured
left posterior
medical practitioner with a 2-week history of pain between the scapulae, and shortness of breath. A systolic murmur was audible and there were r%les at both lung bases. The patient initially refused admission to hospital, but later that day consented because of increasing shortness of breath. On his arrival at the casualty department, acute pulmonary edema was present, and he was acutely dyspneic and unable to give a medical history. There was gross central cyanosis, the radial p&e was impalpable, and the jugular venous pressure was elevated 8 cm. There were loud coarse r%les throughout the chest, and the heart sounds were inaudible. Before a standard electrocardiogram could be recorded, cardiac arrest occurred and attempted resuscitation faiIed. AUTOPSY. The heart was enlarged, weighing 430 grams. All branches of the left coronary artery were patent, whereas the posterior interventricular branch of the right coronary artery was occluded by a thrombus. Infarction of the posterior wall of the left ventricIe extended from the endocardial surface to just beneath the epicardial surface; the infarcted zone was yellow and softened. The process spread inferiorly, involving the left posterior papillary muscle, which had ruptured completely, 1.5 cm. above its base. The separated portion, which measured 1.2 cm., had passed through a space between its attached chordae tendineae, thus twisting the chordae (see Fig. 6).
Discussion
Fig. 6. Case 2. The arrow indicates the basal segment of the ruptured papillary muscle. The separated portion has passed through a space between the chordae tendineae, twisting the chordae.
When a systolic murmur suddenly develops after acute myocardial infarction, the differential diagnosis will include: ruptured papillary muscle, perforation of the interventricular septum, infarction of a
l'olume
70
Number
2
Ruptured
papillary
papillary muscle without rupture, and left ventricular failure with functional mitral incompetence. With rupture of a papillary muscle, the pansystolic murmur of mitral incompetence would be expected. In about 60 per cent of the reported cases of ruptured papillary muscle a systolic murmur was detected.4 In some cases the murmur may not be heard because of the sudden death of the patient after the rupture, or, as in Case 2, the heart sounds and murmur may be obscured by the loud r%les of acute pulmonary edema. In only 2 of the reported cases was a systolic thrill palpable.2J The left posterior papillary muscle is the muscle most commonly involved, and this is usually associated with the electrocardiographic changes of posterior myocardial infarction.4 Perforation of the interventricular septum is accompanied in 95 per cent of the cases by the development of a pansystolic murmur, maximal at the left sternal edge in the fourth or fifth intercostal space, and a systolic thrill is palpable in over 50 per cent of the cases.5 In 75 per cent of the cases of ruptured septum the electrocardiogram shows the changes of anterior myocardial infarction.4 Rupture of the interventricular septum is usually followed rapidly by severe congestive cardiac failure with hepatic engorgement. During the last 18 months, we have observed 3 patients with myocardial infarction and rupture of the interventricular septum. In each case, after rupture there was a rapid and progressive rise in serum glutamic-oxalacetic transaminase to levels above 700 units. Presumably this was derived from both myocardial and hepatic damage. Infarction of a papillary muscle without rupture can lead to a systolic murmur.11 In this condition it is postulated that the damaged papillary muscle fails to contract during the ejection phase of ventricular systole, and then the attached segments of the mitral valve cusps will evert into the left atrium. The murmur produced is not pansystolic, but is of a crescendo-decrescendo quality and begins after the first heart sound. Acute pulmonary edema does not commonly follow this complication of myocardial infarctional Functional mitral incompetence second-
muscle after acute myocardial
infarction
237
ary to left ventricular failure will cause a pansystolic murmur. This murmur develops gradually, and it will increase progressively in intensity. Burch and associate+ suggest that in some cases of left ventricular failure the genesis of this pansystolic murmur may be dependent on papillary muscle dysfunction, rather than dilatation of the atrioventricular ring. In Case 1, the association of acute posterior myocardial infarction and subendocardial infarction, with a sudden onset of the pansystolic murmur of mitral incompetence, and the absence of a systolic thrill, led to the diagnosis of ruptured papillary muscle. The serum glutamicoxalacetic transaminase did not rise after the development of this murmur, which was unlike our previous experience with ruptured interventricular septum. When rupture of a papillary muscle follows myocardial infarction, there is usually a sudden onset of pulmonary edema, and death ensues.3 The typical clinical course of ruptured papillary muscle is illustrated by Case 2. In Case 1, sudden deterioration of the circulatory state did not occur ; instead, death was due to renal failure. Breneman and Drake5 have reported 2 patients with myocardial infarction who survived for 10 and 14 months after rupture of the left posterior papillary muscle. Cooley and associates13 have discussed the possibility of reparative surgery for ruptured papillary muscle after acute myocardial infarction. They suggest that surgery should be delayed until at least 6 weeks after the acute episode. Summary
TWO casesof rupture of the left posterior papillary muscle after acute myocardial infarction are reported. The diagnostic features of this uncommon complication of myocardial infarction are discussed, We wish to thank Dr. GraemeSlotnan for helpful criticism and Mr. Roy Ingles for preparation of the photographs. We are indebted to Dr. A. E. Prendergast and Mr. Brian Davie, F.R.A.C.S., who supplied the clinical details of the second case. REFERENCES 1. M&at, F. V.: Observations sur une l&ion organique du coeur par rupture d’une des colonnes charnues du ventricle gauche, J. de M&d., Chir., Pharm., Paris 6587, 1803.
238
2.
Robinson,
Stannard,
and Long
Hope, R. B., and Askey, J. M.: Necrosis of a cardiac papillary muscle following infarction with incomplete rupture, AM. HEART J. 44:306, 1952. 3. Hackel, D. B., and Kaufman, N.: Papillary muscle rupture due to a myocardial abscess, Ann. Int. Med 38:824, 1952. 4. Sanders, R. J,, Neubuerger, K. ‘I., and Ravin, ~1.: Rupture of papillary muscles: Occurrence of rupture of the posterior muscles in posterior myorardial infarction, Dis. Chest 31:316. 19.57. \5 Breneman, G. M., and Drake, E. H.: Ruptured papillary muscle following myocardial infarction with long s~lr\ival,CircLllation 25:862,1962. 6. Lundberg, S., and Soderstriim, J.: Perforation of the inten~entriculx septum in myocardial infarction, Arta med. Scandinav. 172 :413, 1962. 7. Hansen, J. : Spontaneous rupture of a papillary .\cta nied. scandinnx~. muscle of the heart, 172:531, 1962.
8. 9. 10.
11.
12.
13.
Beaghler, R. L., and Laurain, A. K.: Rupture of a cardiac papillary muscle, Arch. Path. 76:609. 1963. Case Records of the Massachusetts General Hospital, New England J. Med. 270:98, 1964. Robinson, J. S., Sloman, G., and McRae, C.: Continuous electrocardiographic monitoring in the early stages after acute myocardial infarction, M.J. Australia lA27. 1964. Burch, G. E:, DeF’asquale, N. I’., and Phillips, I. H. : Clinical manifestations of papillary muscle dvsfunction, .Irch. Int. Med. il2:112; 1963. Phillips. J. H.. Bruch. G. I?., and DePasquale, N. I’.: ‘The syndrome of papillary muscle dysf unction, :1nn. Int. Med. 59:508, 1963. Cooley, D. A., Henly, it:. S.. .Amad, K. H., and Chapman, I>. W.: \:entricular aneurysm following rnyocardinl infarction: Results of surgical treatment, Ann. Surg. lSO:595. 1959.