Rupture of the interventricular septum complicating myocardial infarction: Pathological analysis of 10 patients with clinically diagnosed perforations
Grover
M. Hutchins,
Baltimore,
M.D.
Md.
The development of interventricular septal defects within the necrotic myocardium of an infarct is a life-threatening but potentially correctable lesion. To examine the circumstances in which such myocardial ruptures occur the pathological findings in a group of patients with clinically diagnosed septal defects complicating myocardial infarcts were studied at autopsy after postmortem coronary arteriography. The results suggest that perforations of the interventricular septum tend to develop in large transmural first infarcts where coronary arteries adjacent to the occluded vessel also have significant obstructions. Materials
and
methods
Patients autopsied at The Johns Hopkins Hospital were included in this study if: (1) there was a clinically diagnosed ventricular septal defect complicating a myocardial infarct which was confirmed at autopsy, and (2) the heart had been studied following postmortem . coronary arteriography and formalin fixation in a distended state.’ Hearts obtained at autopsy were given coronary artery injections with a barium-gelatinpigment mass at 100 to 150 mm. Hg pressure. Following injection the intact heart was fixed From the Institutions,
Department Baltimore,
of Pathology, Maryland.
The
Supported by Grant P50-HL-17655-04 from Health, Public Health Service, Department Welfare. Received
for publication
Apr.
Accepted
for publication
May
Reprint requests to: Dr. Grover gy, The Johns Hopkins Hospital,
0002-8703/79/020165
Johns
Hopkins
Medical
The National Institutes of Health, Education
of and
5, 1978. 17, 1978. M. Hutchins, Baltimore,
+ 09$00.90/O
Department Md. 21205.
0 1979
The
of Patholo-
C. V. Mosby
Co.
overnight in-a distended state by formalin introduced into the cavities at 30 to 40 cm. H,O pressure while the heart was immersed in formalin. Following fixation stereoscopic radiographs were prepared of the intact heart and of the transverse sections into which it was sliced. The coronary arteries were transected at 2 to 3 mm. intervals and compared to the radiographs. Blocks of myocardium, at least 10 per heart, were removed for histological study from myocardial lesions, the area of septal perforation, and from other normal appearing areas. When myocardial necroses were encountered, any corresponding coronary artery lesions were sought and studied by serial histological sections.’ Blocks of the specialized conduction system containing sinoatria1 node atrioventricular node and its branches, His bundle and proximal left and right bundle branches were removed and examined by serial histological sections using a standard method..’ A curvature-thickness index (CTI) was determined for the right and left ventricular free walls and the interventricular septum as previously described.” Briefly, the curvature (l/r) of points in the mid-wall of each of the three ventricular segments was determined in the transverse (TX) and apex-to-base (AB) planes from the postmortem radiographs. A plastic overlay with etched lines of known curvature was matched to the radiograph. The wall thickness (t) was measured at the point where the curvatures were measured. The index was determined for each segment by the formula: CT1 = t (l/rTx + l/r,,). Assessments of age, type, and extent of coronary artery and myocardial lesions were made
American
Heart
Journal
165
Hutchins
1. Comparison of inferior-basilar and mid-apical septal ruptures complicating myocardial infarcts. A, Postmortem coronary arteriogram of heart with an inferior-septal myocardial infarct produced by occlusion of the right coronary artery (uertical arrour). The infarct has a septal perforation (horizontal arrou~). Injection mass has extravasated into the defect and the left ventricular cavity. The left coronary arterial tree shows significant obstructions. B, Transverse section of the ventricles at the level of the septal defect. The infarct involves the inferior wall of left (LV) and right (RV) ventricles and the inferior half of the interventricular septum (IL’S). C, Postmortem arteriogram of heart with an anterior-septal infarct caused by proximal occlusion of an unusually long left anterior descending coronary artery (LAD). The diagonal branch of the left and the right coronary arteries also have significant lesions. The septal rupture is at the arro(us. Compare the septal configuration to that shown in A. D, Transverse sections of ventricles. The probe passes through the septal defect. The infarct involves the entire septum and a large part of the anterior wall of the left ventricle. Fig.
from gross and microscopic examination.’ Infarct size was expressed as per cent of left ventricular surface area underlain by the infarct. The left ventricular surface area was calculated by measuring ventricular axes from the postmortem radiographs and considering the ventricle to be a prolate hemispheroid. Infarct area was measured directly on the specimen and considered to be an ellipse. The clinical information, autopsy findings, and results of pathological examination of the heart were then reviewed for each patient. Results
Among the 1,130 adult (16 years of age and over) hearts studied after postmortem arteriog166
raphy and fixation in distention there were 460 which had 768 pathologically demonstrated myocardial infarcts. The infarcts, defined as an area of myocardial necrosis or replacement fibrosis at least 3 cm. in one dimension and in the distribution of a coronary artery with an occlusive lesion, were attributable to atherosclerotic coronary artery lesions in 692 instances, to coronary artery thromboemboli in 71, and to other coronary artery obstructions such as surgical ligation or arteritis in five. Ten patients had septal ruptures in myocardial infarcts demonstrated at autopsy which had been clinically diagnosed. Two other patients, not included in this study, had septal ruptures produced by unsuccessful resuscitation efforts. February,
1979, Vol. 97, No. 2
Septal rupture
I. Septal rupture farct-clinical features
Table
Number Male:Female Age (years) Infarct to rupture (days) Rupture to death (days) Recurrent pain Murmur Hypotension Congestive heart failure Shunt demonstrated *Excludes 100 davs.
one patient
Clinical
features
after
myocardial
in-
Inferiorbasilar rupture
Midapical rupture
6 4:2 70 (58-82)
4 4:o 61 (51-75)
(0.5-t, 3 (0.5-g)* 4 (67%) 6 (100%) 6 (100%) 1(17%!
(2-i) 14 (0.552) 1(25%) 4 (100%) 4 (100%) 1(25%)
10 8:2 66 (51-82) 4 (0.5-7) 8 (l-52)* 5 (50%) 10 (100%) 10 (100%) 2 (20%)
6 (100%)
2/2 (100%)
8/8 (100%)
with operative
closure of rupture
II. Septal rupture farct-Pathologic findings Table
Total
who survived
Number of patients Heart weight (grams) Coronary artery Location Obstruction Obstruction
American
Heart
Journal
infarct
after myocardial
in-
Inferiorbasilar rupture
Midapical rupture
Normal hearts (4)
6
4
17
525
545
319
(380-690)
(50-650)
(227-430)
RCA 5-100% 1-Recanalized
LAD 3-100% 1-Recanalized
-
Transmural Inferiorseptal 26% (27-32) 6-first
Transmural Anteriorseptal 33% (28-39) 3-first l-third
-
lesions:
Infarcts: Location
Size Number
The ten patients with septal ruptures fell into two groups based on their morphological features: inferior-basilar and mid-apical defects (Fig. 1). The clinical features of the ruptures were similar both among the individual patients and in the two groups (Table I) and are considered together. The patients ranged in age from 51 to 82 years and eight were male. The interval from infarct to rupture varied from 0.5 to 7 days and averaged 4 days. Survival following rupture was one day or less in four patients, two days in two, and three days in one. Two patients survived for 9 and 52 days post-rupture. One patient who underwent operative closure of the defect lived for over 3 months thereafter. Pain, which in retrospect appeared to coincide with the development of the ventricular septal defect, was noted in five (50 per cent). The pain was severe and sometimes episodic. It may have been present also in other patients who were transferred to this hospital following appearance of the defect. A murmur was noted in all patients, usually loud and holosystolic, and two patients had thrills. In eight instances the clinical impression of septal defect was confirmed by right heart catheterization. A step-up in oxygen saturation at the right ventricular level was detected. Hypotension was present in every case and tended to increase in severity following onset of the septal rupture. In seven patients shock was the major cause of death. Symptoms or signs
after myocardial
-
Curvature-thickness Right ventricular free wall Interventricular septum Left ventricular free wall
indices 0.36 + 0.06*
0.36 i 0.03*
0.20 -+ 0.05
0.47 i 0.16*?
0.14 * 0.08*?
0.27 +- 0.06
0.88 f 0.16
0.64 z!z0.07
o.a1+
*Significantly tsignificantly
from normal (p < 0.001). from each other (p < 0.005)
different different
0.22
related to left-sided congestive heart failure were absent during the period immediately following rupture. In one case the pulmonary wedge pressure was 34 mm. Hg but pulmonary edema was not described. The two long-surviving patients developed left-sided heart failure but also had aneurysmal dilatation of the infarct which could have accounted for their pulmonary edema. Five patients were known to have hypertension, three had diabetes mellitus, and one had hypercholesterolemia. Pathologic
findings
There were six patients in whom an inferiorseptal infarct was complicated by a rupture (Table II). In five of the six hearts the right coronary artery was totally occluded by fresh thrombus overlying ulcerated atherosclerotic plaques and in the other, with long survival, there was recanalized thrombus. In each heart there were significant obstructions, greater than 75 per cent luminal narrowing,” in those vessels which 167
Hutchins
Fig. 2. Inferior-septal infarct caused by right coronary artery occlusion complicated by inferior-basilar septal rupture. A, Postmortem coronary arteriogram with right coronary occlusion (uertical arroul) and significant lesions in the left system. The septal defect (horizontal arrows) contains extravasated injection mass. B, Transverse section of the occluded right coronary artery showing admixed plaque debris, thrombus and blood. (Hematoxylin and eosin; original magnification x 16). C, Transverse section of ventricles with infarction of inferior half of septum and inferior right and left ventricles. The perforation is between the arrows. R, Disruption of endocardium (top) and surviving subendocardial muscle adjacent to the margin of the septal rupture. The appearance of the necrotic myocardium (bottom) is consistent with the history of a nine-day-old infarct (Hematoxylin and eosin; original magnification x 100).
would ordinarily supply collateral flow to the part of the right coronary system beyond the occlusipn. Such lesions were present in the proximal left anterior descending coronary artery in every case. The infarcts were large and transmural. The left ventricular surface area underlain by the infarct averaged 26 per cent. For comparison, the mean size of 457 sequentially observed unselected myocardial infarcts produced by fixed coronary artery obstructions, and studied by the same techniques employed here’ was 16 per cent + 12 per cent standard deviation with a range of 1 per cent to 84 per cent. Histological study of the infarcts showed coagulation necrosis with inflammatory and reparative reactions appropriate for their clinical age.“. ‘j Only trivial
168
amounts of contraction band necrosis, the form of injury occurring with reflow, were found and then, usually on the margins of the infarct. The defects in the septum varied from 0.75 to 3 cm. in diameter and were located in the basilar third of the septum close to its junction with the free wall and in the middle of the infarct (Fig. 2). There were four patients with anterior-septal infarcts complicated by a rupture (Figs. 3 and 4). In each instance an ulcerated atherosclerotic plaque in the proximal left anterior descending coronary artery had overlying thrombus. In three instances the thrombus completely occluded the lumen and in one, the longest survivor, there was recanalization. Study of the postmortem arteriograms showed that development of collateral flow
February,
1979, Vol. 97, No. 2
Septal
rupture
after
myocardial
infarct
Fig. 3. Anterior-septal infarct caused by occlusion of the left anterior descending coronary artery complicated by mid-apical septal rupture. A, Postmortem coronary arteriogram with proximal occlusion of a long LAD. The right and left diagonal coronary arteries have significant lesions. The septum has a convex to the left curvature in its basilar portion and a perforation (arrows) in the infarcted apical portion. B, Occlusive thrombus in the lumen of the LAD (Hematoxylin and eosin; original magnification x 16). C, Apex to base section of heart showing infarction of the apex and septal perforation (arrow). The basilar septum bulges into the left ventricular outflow tract. D. Endocardium and surviving subendocardial muscle (left) and infarcted myocardium with thin wavy fiber change on the right and subsiding acute inflammation consistent with the B-day clinical age of the infarct (Hematoxylin and eosin; original magnification X 250).
to the apical portion of the septum would have been poor in all of the hearts. Two hearts had exceptionally long LAD arteries which extended halfway up the posterior interventricular groove and thus supplied the entire apical half of the septum. In the other two hearts significant obstructions were present in both the right coronary arteries and LAD diagonal branches. One of these latter two hearts had small subendocardial infarcts in the right and diagonal coronary artery distributions. All of the other nine hearts in the study had only the one infarct that was complicated by septal rupture.
American
Heart
Journal
All four of the anterior-septal infarcts were transmural and involved on the average 33 per cent of the left ventricular surface area. Coagulation necrosis predominated in the necrotic myocardium with only trivial amounts of contraction band necrosis on the infarct margins. The septal defects were in the mid-apical portion of the septum in the approximate center of the myocardial infarct and ranged in size from 0.75 to 1.5 cm. in diameter. Configuration
of the
inter-ventricular
septum.
A curious feature of the two groups of cases was that within each group the interventricular
169
Hutchins
Fig. 4. The patient survived for 52 days following development of a mid-apical septal perforation in an anterior-septal myocardial infarct. A, Postmortem coronary arteriogram with recanalized proximal occlusion of an unusually long LAD coronary artery. The basilar septum is convex toward the left ventricular outflow tract and the apical septum has a healed infarct with a central perforation (lower arrows). The infarct has undergone aneurysmal dilatation. B, Transverse section of the recanalized organizing thrombus overlying an ulcerated atherosclerotic plaque in the LAD. The ends of the ruptured fibrous cap of the plaque are shown by the arrows. (Verhoeff-van Gieson elastic stain; original magnification x30). C, Transverse section of the ventricles viewed from the apical aspect. The healed transmural infarct involves the entire septum and the anterior left ventricle. The margins of the septal perforation are healed. D, The endocardium from an area adjacent to the septal defect shows well developed endocardial fibroelastosis at the top, surviving subendocardial muscle is in the middZe and the replacement fibrosis of the healed infarct is at the bottom. The histologic features are consistent with the clinical age of the infarct. (Verhoeff-van Gieson elastic stain; original magnification x 100).
septum (IVS) had a distinctive contour. In those hearts with anterior-septal infarcts and midapical ruptures the septum had its usual concave to the left curvature in the transverse plane. However, in the apex-to-base plane the septum was convex to the left, the reverse of the normal curvature, and produced a bulging of the basilar septum into the left ventricular outflow tract. In the hearts with inferior-septal infarcts and inferior-basilar ruptures the septum was of the
170
normal configuration but its curvature was greater than normal. Comparison of the curvature-thickness indices for the right and left ventricular free wall and IVS with the same determinations from a group of normal hearts prepared and studied in the same manner showed highly significant differences for right ventricle and septum. The septal indices are also significantly different for the two infarct groups. The right ventricular free wall
February,
1979, Vol. 97, No. 2
Septal rupture after myocardial infarct
Fig. 5. A, Histological section of conducting system from a patient with an inferior-septal infarct and inferior-basilar rupture. The necrosis extends to the top of the interventricular septum (ZVS) adjacent to the central fibrous body (CFB). The atrioventricular node (AVN) and interatrial septum (ZAS) show no necrosis. MV = mitral valve. B, Patient with an anterior-septal infarct and mid-apical septal rupture. The interventricular septum at this basilar level and the specialized conducting system including the atrioventricular node, His bundle, and proximal right (RB) and left (LB) bundle branches show no necrosis. MS = membranous septum. (Both Hematoxylin and eosin; original magnification x 10)
indices were significantly greater than normal in both groups of hearts with infarcts, probably secondary to the volume overload induced by the rupture. The left ventricular free wall indices showed no significant differences. Correlation tion system
of electrocardiograms studies. There
and conduc-
was no specific pattern of electrocardiographic changes that characterized these patients. In each instance the position of the original infarct was detected on the initial electrocardiogram. Histologic study of the conducting system showed normal sinoatrial nodes in all patients. There was no interruption or necrosis of the atrioventricular node or its approaches, the His bundle or proximal left or right bundle branches in any patient. In the six patients with inferior septal infarcts the septal necrosis did not extend far enough anteriorly to involve the myocardium adjacent to the bundle branches (Fig. 5). Despite the presence of occlusion of the right coronary artery with potential ischemia of the atrioventricular node, none showed necrosis. One patient had a terminal widening of QRS complexes and one other had a 2:l AV block. In the patients with anterior-septal infarcts the bundle branches passed adjacent to the infarcted myocardium of the septum. The conducting fibers themselves did not show necrosis, probably
American Heart Journal
because of their proximity to the blood within the ventricular cavity. Of the four patients with anterior-septal infarcts one had terminal bradycardia, one developed complete heart block, and a third had left anterior hemiblock and right bundle branch block. As noted, these conduction disturbances were apparently explained by ischemic destruction of the working myocardium itself rather than the specialized conduction system. Discussion
The study shows that patients who develop septal rupture as a complication of myocardial infarction commonly have pain during the period when the defect is developing. If the pain arises from the site of perforation it is probably originating within the surviving endocardial or immediately subendocardial tissues, since the remainder of the wall is necrotic. With creation of the defect a murmur, usually loud and holosystolic, is present and frequently a thrill as well. All of the patients developed hypotension which was usually severe and progressive. Left-sided congestive heart failure was absent in the immediate postrupture period and when it appeared later was explainable by aneurysmal dilatation of the left ventricle. Diagnosis of septal defect was established or confirmed in the eight patients studied
171
Hutchins
by right heart catheterization demonstration of an oxygen step-up in the right ventricle. Pathologic studies showed two patterns of septal rupture. Six patients had right coronary artery occlusions with inferior-septal infarcts and inferior-basilar defects. The other four patients had occlusions of the left anterior descending coronary artery producing anterior-septal infarcts and mid-apical ruptures. In all 10 hearts the infarcts were large and transmural and in nine they were the only infarct. The pattern of coronary artery disease was such that possible collateral blood flow to the ischemic zone was inhibited by significant obstructions in the major adjacent arteries. Consistent with this is the observation that the infarcts had mainly coagulation necrosis. Contraction band necrosis, the development of which is dependent on reflow into transiently ischemic areas,’ was trivial and confined to the margins of the infarcts. The factors mentioned, transmural necrosis and poor or absent collateral flow, must be of importance in the pathogenesis of the septal rupture. Another potentially significant factor is the distinctive configuration of the interventricular septum in the two groups of cases. The curvature-thickness indices (CT11 of the three components of the ventricular walls correlate with the pressure producing capacity of the wall segment.’ In the hearts with inferior-basilar ruptures the septal CTI’s, determined at points not involved by the infarct, were significantly greater than those seen in normal hearts. It is possible that greater than usual curvatures in these septa may have contributed to perforation of their necrotic portions. In contrast, the hearts with anterior-septal infarcts had septal CTI’s significantly less than those seen in normal hearts. Examination of the radiographs showed an unusual distortion of the normal septal configuration with the apex to base contour reversed so as to be convex toward the left ventricle rather than the usual concavity. This reversal of contour is probably attributable to the fact that the entire apical portion of septum is involved in the infarct. The appearance of the left ventricle suggests that an element of subaortic outflow obstruction may have been introduced by the altered geometry. If true, the consequent elevation of intracavitary pressure may have contributed to these midapical perforations.
172
Septal perforation is a relatively uncommon complication of myocardial infarcts. The 1.3 per cent of infarcts with rupture observed here is similar to the experience of others.“. !’ Occurrence of the complication may be suspected from the development of a new murmur with concomitant hypoperfusion. The slight or absent early congestive failure seen in these patients may be a useful sign in distinguishing septal perforation from ruptured papillary muscle. Diagnosis may be established by right heart catheterization or by echocardiography.“’ Surgical treatment of septal rupture is feasible.“, I.’ Current reports have emphasized the desirability of early operation in these clinically unstable and usually worsening patients.‘:, ‘,! Coles and colleagues’” have noted the importance of distinguishing high and low defects, corresponding to the inferior-basilar and mid-apical of this report, because of the differences in surgical approach. The sparing of specialized conducting tissues noted in these patients is in contrast to James’ experience’” with five patients with posterior infarcts, all of whom showed necrosis in the atrioventricular node. It is indeed surprising that the six patients in this study with right coronary artery occlusions and large transmural inferiorseptal infarcts would not have shown more clinical evidence of atrioventricular node ischemia. Instead, among the four patients with anteriorseptal infarcts one had complete heart block and another developed left anterior hemiblock and right bundle branch block. These disturbances appeared to be explained by destruction of the working myocardium rather than by necrosis of the conducting fibers themselves. The patients studied here show a uniform pathologic picture in that septal perforations complicate large transmural infarcts produced by total coronary artery occlusion and there is little opportunity for development of collateral blood flow. Two morphologic types of septal rupture are seen: An inferior-basilar defect with right coronary occlusion and inferior-septal infarcts and a mid-apical defect with left anterior descending occlusion and an anterior-septal infarct. A subsidiary factor leading to the septal defect may be the configuration of the interventricular septum. With inferior-basilar defects the septum has greater than normal curvature suggesting possi-
February,
1979, Vol. 97, No. 2
Septal rupture
ble increased tension in the infarcted portion. Mid-apical ruptures are associated with a leftward convexity of the basilar septum causing it to protrude into the outflow tract. Any outflow tract obstruction could produce rupture of the apical septum by increased intracavitary pressure. Since the defects usually occur several days after infarction, survival for a few more days brings the patient to a period when reparative reactions have begun in the area of the infarct. The onset of the healing process by this time suggests that surgical intervention would be technically possible. The severe life-threatening hypotension found in these patients is in accord with clinical studies suggesting treatment by early operative intervention. Summary
Among 768 myocardial infarcts in 480 hearts studied after postmortem coronary arteriography and formalin fixation in a distended state, there were 10 infarcts (1.3 per cent) complicated by perforation of the interventricular septum. Infarcts with rupture were large (average 28 per cent of left ventricular surface area), transmural, usually first infarcts, produced by complete occlusion of a coronary artery, and had little opportunity to receive collateral blood flow because of either significant obstructions of adjacent arteries or the pattern of coronary artery distribution. Six hearts had inferior-basilar defects in inferior-septal infarcts and four had mid-apical defects in anterior-septal infarcts. Development of septal rupture may relate to alterations of septal configuration: more curved than normal with inferior-basilar ruptures and bulging into the outflow tract with mid-apical ruptures. Pain was a common feature (50 per cent) of the development of the septal defect. A loud holosystolic murmur and severe hypotension were noted in all cases. Left-sided congestive heart failure was absent in the early post-rupture period. Diagnosis was established by right heart catheterization in the eight patients studied. Post-rupture survival without operation varied from 0.5 to 52 days (average 8 days) and the interval from infarct to rupture ranged from 0.5
American
Heart
Journal
ufter myocardial
infarct
to 7 days (average 4 days). The clinical course and pathologic findings in these patients support the desirability of early operative intervention in septal ruptures complicating infarcts. REFERENCES 1.
Hutchins, G. M., and Anaya, 0. A.: Measurements of cardiac size, chamber volumes and valve orifices at autopsy, Johns Hopkins Med. J. 133:96, 1973. 2. Ridolfi. R. L.. and Hutchins. G. M.: The relationship between coronary lesions and myocardial infarcts. Ulceration of atherosclerotic plaques precipitating coronary thrombosis, AM. HEART J. 93:468, 1977. 3. Ridolfi, R. L., Bulkley, B. H., and Hutchins, G. M.: The conduction system in cardiac amyloidosis: Clinical and pathological features of 23 patients, Am. J. Med. 62:677, 1977. 4. Hutchins, G. M., Bulkley, B. H., Moore, G. W., Piasio, M. A., and Lohr, F. T.: Shape of the human cardiac ventricles, Am. J. Cardiol. 41:646, 1978. 5. Hutchins, G. M., Bulkley, B. H., Ridolfi, R. L., Griffith, L. S. C., Lohr. F. T.. and Piasio. M. A.: Correlation of coronary arteriograms and left ventriculograms with postmortem studies, Circulation 56:32, 1977. 6. Hutchins, G. M., and Bannayan, G. A.: Development of endocardial fibroelastosis following myocardial infarction, Arch. Pathol. 91:113, 1971. 7. Hutchins, G. M., and Bulkley, B. H.: Correlation of myocardial contraction band necrosis and vascular patency: a study of coronary artery bypass graft anastomoses at branch-points, Lab. Invest. 36:642, 1977. 8. Edmondson. H. A., and Hoxie. H. J.: Hypertension and cardiac rupture. A clinical and pathologic study of seventy-two cases, in thirteen of which rupture of the interventricular septum occurred, AM. HEART J. 24:719, 1942. 9. Longo, E. A., and Cohen, L. S.: Rupture of interventricular septum in acute myocardial infarction AM. HEART J. 92%. 1976. 10. DeJoseph, R. L., Seides, S. F., Lindner. A., and Damato, A. N.: Echocardioaranhic findings of ventricular septal rupture in acute myocardial infarction, Am. J. Cardiol. 36:346, 1975. 11. Cooley, D. A., Belmonte, B. Z., Zeis, L. B., and Schnur, S.: Surgical repair of ruptured interventricular septum following acute myocardial infarction, Surgery 41:930, 1957. 12. Hill, J. D., Lary, D., Kerth, W. d., and Gerbode, F.: Acquired ventricular septal defects. J. Thorac. Cardiovast. Surg. 70:440, 1975. 13. Kaplan, M. A., Harris, C. N., Kay, J. H., Parker, D. P., and Magidson, 0.: Postinfarctional ventricular septal rupture. Clinical approach and surgical results, Chest 69:734, 1976. 14. Coles, J. C., Sandoval, W. G., and Mullangi, C.: Surgical repair of acute ventricular septal defect complicating myocardial infarction, Can. J. Surg. 19:143, 1976. 15. James, T. N.: De Subitaneis Mortibus. XXIV. Ruptured interventricular septum and heart block, Circulation 55:934, 1977.
173
Grover
M. Hutchins,
Baltimore,
M.D.
Md.
The development of interventricular septal defects within the necrotic myocardium of an infarct is a life-threatening but potentially correctable lesion. To examine the circumstances in which such myocardial ruptures occur the pathological findings in a group of patients with clinically diagnosed septal defects complicating myocardial infarcts were studied at autopsy after postmortem coronary arteriography. The results suggest that perforations of the interventricular septum tend to develop in large transmural first infarcts where coronary arteries adjacent to the occluded vessel also have significant obstructions. Materials
and
methods
Patients autopsied at The Johns Hopkins Hospital were included in this study if: (1) there was a clinically diagnosed ventricular septal defect complicating a myocardial infarct which was confirmed at autopsy, and (2) the heart had been studied following postmortem . coronary arteriography and formalin fixation in a distended state.’ Hearts obtained at autopsy were given coronary artery injections with a barium-gelatinpigment mass at 100 to 150 mm. Hg pressure. Following injection the intact heart was fixed From the Institutions,
Department Baltimore,
of Pathology, Maryland.
The
Supported by Grant P50-HL-17655-04 from Health, Public Health Service, Department Welfare. Received
for publication
Apr.
Accepted
for publication
May
Reprint requests to: Dr. Grover gy, The Johns Hopkins Hospital,
0002-8703/79/020165
Johns
Hopkins
Medical
The National Institutes of Health, Education
of and
5, 1978. 17, 1978. M. Hutchins, Baltimore,
+ 09$00.90/O
Department Md. 21205.
0 1979
The
of Patholo-
C. V. Mosby
Co.
overnight in-a distended state by formalin introduced into the cavities at 30 to 40 cm. H,O pressure while the heart was immersed in formalin. Following fixation stereoscopic radiographs were prepared of the intact heart and of the transverse sections into which it was sliced. The coronary arteries were transected at 2 to 3 mm. intervals and compared to the radiographs. Blocks of myocardium, at least 10 per heart, were removed for histological study from myocardial lesions, the area of septal perforation, and from other normal appearing areas. When myocardial necroses were encountered, any corresponding coronary artery lesions were sought and studied by serial histological sections.’ Blocks of the specialized conduction system containing sinoatria1 node atrioventricular node and its branches, His bundle and proximal left and right bundle branches were removed and examined by serial histological sections using a standard method..’ A curvature-thickness index (CTI) was determined for the right and left ventricular free walls and the interventricular septum as previously described.” Briefly, the curvature (l/r) of points in the mid-wall of each of the three ventricular segments was determined in the transverse (TX) and apex-to-base (AB) planes from the postmortem radiographs. A plastic overlay with etched lines of known curvature was matched to the radiograph. The wall thickness (t) was measured at the point where the curvatures were measured. The index was determined for each segment by the formula: CT1 = t (l/rTx + l/r,,). Assessments of age, type, and extent of coronary artery and myocardial lesions were made
American
Heart
Journal
165
Hutchins
1. Comparison of inferior-basilar and mid-apical septal ruptures complicating myocardial infarcts. A, Postmortem coronary arteriogram of heart with an inferior-septal myocardial infarct produced by occlusion of the right coronary artery (uertical arrour). The infarct has a septal perforation (horizontal arrou~). Injection mass has extravasated into the defect and the left ventricular cavity. The left coronary arterial tree shows significant obstructions. B, Transverse section of the ventricles at the level of the septal defect. The infarct involves the inferior wall of left (LV) and right (RV) ventricles and the inferior half of the interventricular septum (IL’S). C, Postmortem arteriogram of heart with an anterior-septal infarct caused by proximal occlusion of an unusually long left anterior descending coronary artery (LAD). The diagonal branch of the left and the right coronary arteries also have significant lesions. The septal rupture is at the arro(us. Compare the septal configuration to that shown in A. D, Transverse sections of ventricles. The probe passes through the septal defect. The infarct involves the entire septum and a large part of the anterior wall of the left ventricle. Fig.
from gross and microscopic examination.’ Infarct size was expressed as per cent of left ventricular surface area underlain by the infarct. The left ventricular surface area was calculated by measuring ventricular axes from the postmortem radiographs and considering the ventricle to be a prolate hemispheroid. Infarct area was measured directly on the specimen and considered to be an ellipse. The clinical information, autopsy findings, and results of pathological examination of the heart were then reviewed for each patient. Results
Among the 1,130 adult (16 years of age and over) hearts studied after postmortem arteriog166
raphy and fixation in distention there were 460 which had 768 pathologically demonstrated myocardial infarcts. The infarcts, defined as an area of myocardial necrosis or replacement fibrosis at least 3 cm. in one dimension and in the distribution of a coronary artery with an occlusive lesion, were attributable to atherosclerotic coronary artery lesions in 692 instances, to coronary artery thromboemboli in 71, and to other coronary artery obstructions such as surgical ligation or arteritis in five. Ten patients had septal ruptures in myocardial infarcts demonstrated at autopsy which had been clinically diagnosed. Two other patients, not included in this study, had septal ruptures produced by unsuccessful resuscitation efforts. February,
1979, Vol. 97, No. 2
Septal rupture
I. Septal rupture farct-clinical features
Table
Number Male:Female Age (years) Infarct to rupture (days) Rupture to death (days) Recurrent pain Murmur Hypotension Congestive heart failure Shunt demonstrated *Excludes 100 davs.
one patient
Clinical
features
after
myocardial
in-
Inferiorbasilar rupture
Midapical rupture
6 4:2 70 (58-82)
4 4:o 61 (51-75)
(0.5-t, 3 (0.5-g)* 4 (67%) 6 (100%) 6 (100%) 1(17%!
(2-i) 14 (0.552) 1(25%) 4 (100%) 4 (100%) 1(25%)
10 8:2 66 (51-82) 4 (0.5-7) 8 (l-52)* 5 (50%) 10 (100%) 10 (100%) 2 (20%)
6 (100%)
2/2 (100%)
8/8 (100%)
with operative
closure of rupture
II. Septal rupture farct-Pathologic findings Table
Total
who survived
Number of patients Heart weight (grams) Coronary artery Location Obstruction Obstruction
American
Heart
Journal
infarct
after myocardial
in-
Inferiorbasilar rupture
Midapical rupture
Normal hearts (4)
6
4
17
525
545
319
(380-690)
(50-650)
(227-430)
RCA 5-100% 1-Recanalized
LAD 3-100% 1-Recanalized
-
Transmural Inferiorseptal 26% (27-32) 6-first
Transmural Anteriorseptal 33% (28-39) 3-first l-third
-
lesions:
Infarcts: Location
Size Number
The ten patients with septal ruptures fell into two groups based on their morphological features: inferior-basilar and mid-apical defects (Fig. 1). The clinical features of the ruptures were similar both among the individual patients and in the two groups (Table I) and are considered together. The patients ranged in age from 51 to 82 years and eight were male. The interval from infarct to rupture varied from 0.5 to 7 days and averaged 4 days. Survival following rupture was one day or less in four patients, two days in two, and three days in one. Two patients survived for 9 and 52 days post-rupture. One patient who underwent operative closure of the defect lived for over 3 months thereafter. Pain, which in retrospect appeared to coincide with the development of the ventricular septal defect, was noted in five (50 per cent). The pain was severe and sometimes episodic. It may have been present also in other patients who were transferred to this hospital following appearance of the defect. A murmur was noted in all patients, usually loud and holosystolic, and two patients had thrills. In eight instances the clinical impression of septal defect was confirmed by right heart catheterization. A step-up in oxygen saturation at the right ventricular level was detected. Hypotension was present in every case and tended to increase in severity following onset of the septal rupture. In seven patients shock was the major cause of death. Symptoms or signs
after myocardial
-
Curvature-thickness Right ventricular free wall Interventricular septum Left ventricular free wall
indices 0.36 + 0.06*
0.36 i 0.03*
0.20 -+ 0.05
0.47 i 0.16*?
0.14 * 0.08*?
0.27 +- 0.06
0.88 f 0.16
0.64 z!z0.07
o.a1+
*Significantly tsignificantly
from normal (p < 0.001). from each other (p < 0.005)
different different
0.22
related to left-sided congestive heart failure were absent during the period immediately following rupture. In one case the pulmonary wedge pressure was 34 mm. Hg but pulmonary edema was not described. The two long-surviving patients developed left-sided heart failure but also had aneurysmal dilatation of the infarct which could have accounted for their pulmonary edema. Five patients were known to have hypertension, three had diabetes mellitus, and one had hypercholesterolemia. Pathologic
findings
There were six patients in whom an inferiorseptal infarct was complicated by a rupture (Table II). In five of the six hearts the right coronary artery was totally occluded by fresh thrombus overlying ulcerated atherosclerotic plaques and in the other, with long survival, there was recanalized thrombus. In each heart there were significant obstructions, greater than 75 per cent luminal narrowing,” in those vessels which 167
Hutchins
Fig. 2. Inferior-septal infarct caused by right coronary artery occlusion complicated by inferior-basilar septal rupture. A, Postmortem coronary arteriogram with right coronary occlusion (uertical arroul) and significant lesions in the left system. The septal defect (horizontal arrows) contains extravasated injection mass. B, Transverse section of the occluded right coronary artery showing admixed plaque debris, thrombus and blood. (Hematoxylin and eosin; original magnification x 16). C, Transverse section of ventricles with infarction of inferior half of septum and inferior right and left ventricles. The perforation is between the arrows. R, Disruption of endocardium (top) and surviving subendocardial muscle adjacent to the margin of the septal rupture. The appearance of the necrotic myocardium (bottom) is consistent with the history of a nine-day-old infarct (Hematoxylin and eosin; original magnification x 100).
would ordinarily supply collateral flow to the part of the right coronary system beyond the occlusipn. Such lesions were present in the proximal left anterior descending coronary artery in every case. The infarcts were large and transmural. The left ventricular surface area underlain by the infarct averaged 26 per cent. For comparison, the mean size of 457 sequentially observed unselected myocardial infarcts produced by fixed coronary artery obstructions, and studied by the same techniques employed here’ was 16 per cent + 12 per cent standard deviation with a range of 1 per cent to 84 per cent. Histological study of the infarcts showed coagulation necrosis with inflammatory and reparative reactions appropriate for their clinical age.“. ‘j Only trivial
168
amounts of contraction band necrosis, the form of injury occurring with reflow, were found and then, usually on the margins of the infarct. The defects in the septum varied from 0.75 to 3 cm. in diameter and were located in the basilar third of the septum close to its junction with the free wall and in the middle of the infarct (Fig. 2). There were four patients with anterior-septal infarcts complicated by a rupture (Figs. 3 and 4). In each instance an ulcerated atherosclerotic plaque in the proximal left anterior descending coronary artery had overlying thrombus. In three instances the thrombus completely occluded the lumen and in one, the longest survivor, there was recanalization. Study of the postmortem arteriograms showed that development of collateral flow
February,
1979, Vol. 97, No. 2
Septal
rupture
after
myocardial
infarct
Fig. 3. Anterior-septal infarct caused by occlusion of the left anterior descending coronary artery complicated by mid-apical septal rupture. A, Postmortem coronary arteriogram with proximal occlusion of a long LAD. The right and left diagonal coronary arteries have significant lesions. The septum has a convex to the left curvature in its basilar portion and a perforation (arrows) in the infarcted apical portion. B, Occlusive thrombus in the lumen of the LAD (Hematoxylin and eosin; original magnification x 16). C, Apex to base section of heart showing infarction of the apex and septal perforation (arrow). The basilar septum bulges into the left ventricular outflow tract. D. Endocardium and surviving subendocardial muscle (left) and infarcted myocardium with thin wavy fiber change on the right and subsiding acute inflammation consistent with the B-day clinical age of the infarct (Hematoxylin and eosin; original magnification X 250).
to the apical portion of the septum would have been poor in all of the hearts. Two hearts had exceptionally long LAD arteries which extended halfway up the posterior interventricular groove and thus supplied the entire apical half of the septum. In the other two hearts significant obstructions were present in both the right coronary arteries and LAD diagonal branches. One of these latter two hearts had small subendocardial infarcts in the right and diagonal coronary artery distributions. All of the other nine hearts in the study had only the one infarct that was complicated by septal rupture.
American
Heart
Journal
All four of the anterior-septal infarcts were transmural and involved on the average 33 per cent of the left ventricular surface area. Coagulation necrosis predominated in the necrotic myocardium with only trivial amounts of contraction band necrosis on the infarct margins. The septal defects were in the mid-apical portion of the septum in the approximate center of the myocardial infarct and ranged in size from 0.75 to 1.5 cm. in diameter. Configuration
of the
inter-ventricular
septum.
A curious feature of the two groups of cases was that within each group the interventricular
169
Hutchins
Fig. 4. The patient survived for 52 days following development of a mid-apical septal perforation in an anterior-septal myocardial infarct. A, Postmortem coronary arteriogram with recanalized proximal occlusion of an unusually long LAD coronary artery. The basilar septum is convex toward the left ventricular outflow tract and the apical septum has a healed infarct with a central perforation (lower arrows). The infarct has undergone aneurysmal dilatation. B, Transverse section of the recanalized organizing thrombus overlying an ulcerated atherosclerotic plaque in the LAD. The ends of the ruptured fibrous cap of the plaque are shown by the arrows. (Verhoeff-van Gieson elastic stain; original magnification x30). C, Transverse section of the ventricles viewed from the apical aspect. The healed transmural infarct involves the entire septum and the anterior left ventricle. The margins of the septal perforation are healed. D, The endocardium from an area adjacent to the septal defect shows well developed endocardial fibroelastosis at the top, surviving subendocardial muscle is in the middZe and the replacement fibrosis of the healed infarct is at the bottom. The histologic features are consistent with the clinical age of the infarct. (Verhoeff-van Gieson elastic stain; original magnification x 100).
septum (IVS) had a distinctive contour. In those hearts with anterior-septal infarcts and midapical ruptures the septum had its usual concave to the left curvature in the transverse plane. However, in the apex-to-base plane the septum was convex to the left, the reverse of the normal curvature, and produced a bulging of the basilar septum into the left ventricular outflow tract. In the hearts with inferior-septal infarcts and inferior-basilar ruptures the septum was of the
170
normal configuration but its curvature was greater than normal. Comparison of the curvature-thickness indices for the right and left ventricular free wall and IVS with the same determinations from a group of normal hearts prepared and studied in the same manner showed highly significant differences for right ventricle and septum. The septal indices are also significantly different for the two infarct groups. The right ventricular free wall
February,
1979, Vol. 97, No. 2
Septal rupture after myocardial infarct
Fig. 5. A, Histological section of conducting system from a patient with an inferior-septal infarct and inferior-basilar rupture. The necrosis extends to the top of the interventricular septum (ZVS) adjacent to the central fibrous body (CFB). The atrioventricular node (AVN) and interatrial septum (ZAS) show no necrosis. MV = mitral valve. B, Patient with an anterior-septal infarct and mid-apical septal rupture. The interventricular septum at this basilar level and the specialized conducting system including the atrioventricular node, His bundle, and proximal right (RB) and left (LB) bundle branches show no necrosis. MS = membranous septum. (Both Hematoxylin and eosin; original magnification x 10)
indices were significantly greater than normal in both groups of hearts with infarcts, probably secondary to the volume overload induced by the rupture. The left ventricular free wall indices showed no significant differences. Correlation tion system
of electrocardiograms studies. There
and conduc-
was no specific pattern of electrocardiographic changes that characterized these patients. In each instance the position of the original infarct was detected on the initial electrocardiogram. Histologic study of the conducting system showed normal sinoatrial nodes in all patients. There was no interruption or necrosis of the atrioventricular node or its approaches, the His bundle or proximal left or right bundle branches in any patient. In the six patients with inferior septal infarcts the septal necrosis did not extend far enough anteriorly to involve the myocardium adjacent to the bundle branches (Fig. 5). Despite the presence of occlusion of the right coronary artery with potential ischemia of the atrioventricular node, none showed necrosis. One patient had a terminal widening of QRS complexes and one other had a 2:l AV block. In the patients with anterior-septal infarcts the bundle branches passed adjacent to the infarcted myocardium of the septum. The conducting fibers themselves did not show necrosis, probably
American Heart Journal
because of their proximity to the blood within the ventricular cavity. Of the four patients with anterior-septal infarcts one had terminal bradycardia, one developed complete heart block, and a third had left anterior hemiblock and right bundle branch block. As noted, these conduction disturbances were apparently explained by ischemic destruction of the working myocardium itself rather than the specialized conduction system. Discussion
The study shows that patients who develop septal rupture as a complication of myocardial infarction commonly have pain during the period when the defect is developing. If the pain arises from the site of perforation it is probably originating within the surviving endocardial or immediately subendocardial tissues, since the remainder of the wall is necrotic. With creation of the defect a murmur, usually loud and holosystolic, is present and frequently a thrill as well. All of the patients developed hypotension which was usually severe and progressive. Left-sided congestive heart failure was absent in the immediate postrupture period and when it appeared later was explainable by aneurysmal dilatation of the left ventricle. Diagnosis of septal defect was established or confirmed in the eight patients studied
171
Hutchins
by right heart catheterization demonstration of an oxygen step-up in the right ventricle. Pathologic studies showed two patterns of septal rupture. Six patients had right coronary artery occlusions with inferior-septal infarcts and inferior-basilar defects. The other four patients had occlusions of the left anterior descending coronary artery producing anterior-septal infarcts and mid-apical ruptures. In all 10 hearts the infarcts were large and transmural and in nine they were the only infarct. The pattern of coronary artery disease was such that possible collateral blood flow to the ischemic zone was inhibited by significant obstructions in the major adjacent arteries. Consistent with this is the observation that the infarcts had mainly coagulation necrosis. Contraction band necrosis, the development of which is dependent on reflow into transiently ischemic areas,’ was trivial and confined to the margins of the infarcts. The factors mentioned, transmural necrosis and poor or absent collateral flow, must be of importance in the pathogenesis of the septal rupture. Another potentially significant factor is the distinctive configuration of the interventricular septum in the two groups of cases. The curvature-thickness indices (CT11 of the three components of the ventricular walls correlate with the pressure producing capacity of the wall segment.’ In the hearts with inferior-basilar ruptures the septal CTI’s, determined at points not involved by the infarct, were significantly greater than those seen in normal hearts. It is possible that greater than usual curvatures in these septa may have contributed to perforation of their necrotic portions. In contrast, the hearts with anterior-septal infarcts had septal CTI’s significantly less than those seen in normal hearts. Examination of the radiographs showed an unusual distortion of the normal septal configuration with the apex to base contour reversed so as to be convex toward the left ventricle rather than the usual concavity. This reversal of contour is probably attributable to the fact that the entire apical portion of septum is involved in the infarct. The appearance of the left ventricle suggests that an element of subaortic outflow obstruction may have been introduced by the altered geometry. If true, the consequent elevation of intracavitary pressure may have contributed to these midapical perforations.
172
Septal perforation is a relatively uncommon complication of myocardial infarcts. The 1.3 per cent of infarcts with rupture observed here is similar to the experience of others.“. !’ Occurrence of the complication may be suspected from the development of a new murmur with concomitant hypoperfusion. The slight or absent early congestive failure seen in these patients may be a useful sign in distinguishing septal perforation from ruptured papillary muscle. Diagnosis may be established by right heart catheterization or by echocardiography.“’ Surgical treatment of septal rupture is feasible.“, I.’ Current reports have emphasized the desirability of early operation in these clinically unstable and usually worsening patients.‘:, ‘,! Coles and colleagues’” have noted the importance of distinguishing high and low defects, corresponding to the inferior-basilar and mid-apical of this report, because of the differences in surgical approach. The sparing of specialized conducting tissues noted in these patients is in contrast to James’ experience’” with five patients with posterior infarcts, all of whom showed necrosis in the atrioventricular node. It is indeed surprising that the six patients in this study with right coronary artery occlusions and large transmural inferiorseptal infarcts would not have shown more clinical evidence of atrioventricular node ischemia. Instead, among the four patients with anteriorseptal infarcts one had complete heart block and another developed left anterior hemiblock and right bundle branch block. These disturbances appeared to be explained by destruction of the working myocardium rather than by necrosis of the conducting fibers themselves. The patients studied here show a uniform pathologic picture in that septal perforations complicate large transmural infarcts produced by total coronary artery occlusion and there is little opportunity for development of collateral blood flow. Two morphologic types of septal rupture are seen: An inferior-basilar defect with right coronary occlusion and inferior-septal infarcts and a mid-apical defect with left anterior descending occlusion and an anterior-septal infarct. A subsidiary factor leading to the septal defect may be the configuration of the interventricular septum. With inferior-basilar defects the septum has greater than normal curvature suggesting possi-
February,
1979, Vol. 97, No. 2
Septal rupture
ble increased tension in the infarcted portion. Mid-apical ruptures are associated with a leftward convexity of the basilar septum causing it to protrude into the outflow tract. Any outflow tract obstruction could produce rupture of the apical septum by increased intracavitary pressure. Since the defects usually occur several days after infarction, survival for a few more days brings the patient to a period when reparative reactions have begun in the area of the infarct. The onset of the healing process by this time suggests that surgical intervention would be technically possible. The severe life-threatening hypotension found in these patients is in accord with clinical studies suggesting treatment by early operative intervention. Summary
Among 768 myocardial infarcts in 480 hearts studied after postmortem coronary arteriography and formalin fixation in a distended state, there were 10 infarcts (1.3 per cent) complicated by perforation of the interventricular septum. Infarcts with rupture were large (average 28 per cent of left ventricular surface area), transmural, usually first infarcts, produced by complete occlusion of a coronary artery, and had little opportunity to receive collateral blood flow because of either significant obstructions of adjacent arteries or the pattern of coronary artery distribution. Six hearts had inferior-basilar defects in inferior-septal infarcts and four had mid-apical defects in anterior-septal infarcts. Development of septal rupture may relate to alterations of septal configuration: more curved than normal with inferior-basilar ruptures and bulging into the outflow tract with mid-apical ruptures. Pain was a common feature (50 per cent) of the development of the septal defect. A loud holosystolic murmur and severe hypotension were noted in all cases. Left-sided congestive heart failure was absent in the early post-rupture period. Diagnosis was established by right heart catheterization in the eight patients studied. Post-rupture survival without operation varied from 0.5 to 52 days (average 8 days) and the interval from infarct to rupture ranged from 0.5
American
Heart
Journal
ufter myocardial
infarct
to 7 days (average 4 days). The clinical course and pathologic findings in these patients support the desirability of early operative intervention in septal ruptures complicating infarcts. REFERENCES 1.
Hutchins, G. M., and Anaya, 0. A.: Measurements of cardiac size, chamber volumes and valve orifices at autopsy, Johns Hopkins Med. J. 133:96, 1973. 2. Ridolfi. R. L.. and Hutchins. G. M.: The relationship between coronary lesions and myocardial infarcts. Ulceration of atherosclerotic plaques precipitating coronary thrombosis, AM. HEART J. 93:468, 1977. 3. Ridolfi, R. L., Bulkley, B. H., and Hutchins, G. M.: The conduction system in cardiac amyloidosis: Clinical and pathological features of 23 patients, Am. J. Med. 62:677, 1977. 4. Hutchins, G. M., Bulkley, B. H., Moore, G. W., Piasio, M. A., and Lohr, F. T.: Shape of the human cardiac ventricles, Am. J. Cardiol. 41:646, 1978. 5. Hutchins, G. M., Bulkley, B. H., Ridolfi, R. L., Griffith, L. S. C., Lohr. F. T.. and Piasio. M. A.: Correlation of coronary arteriograms and left ventriculograms with postmortem studies, Circulation 56:32, 1977. 6. Hutchins, G. M., and Bannayan, G. A.: Development of endocardial fibroelastosis following myocardial infarction, Arch. Pathol. 91:113, 1971. 7. Hutchins, G. M., and Bulkley, B. H.: Correlation of myocardial contraction band necrosis and vascular patency: a study of coronary artery bypass graft anastomoses at branch-points, Lab. Invest. 36:642, 1977. 8. Edmondson. H. A., and Hoxie. H. J.: Hypertension and cardiac rupture. A clinical and pathologic study of seventy-two cases, in thirteen of which rupture of the interventricular septum occurred, AM. HEART J. 24:719, 1942. 9. Longo, E. A., and Cohen, L. S.: Rupture of interventricular septum in acute myocardial infarction AM. HEART J. 92%. 1976. 10. DeJoseph, R. L., Seides, S. F., Lindner. A., and Damato, A. N.: Echocardioaranhic findings of ventricular septal rupture in acute myocardial infarction, Am. J. Cardiol. 36:346, 1975. 11. Cooley, D. A., Belmonte, B. Z., Zeis, L. B., and Schnur, S.: Surgical repair of ruptured interventricular septum following acute myocardial infarction, Surgery 41:930, 1957. 12. Hill, J. D., Lary, D., Kerth, W. d., and Gerbode, F.: Acquired ventricular septal defects. J. Thorac. Cardiovast. Surg. 70:440, 1975. 13. Kaplan, M. A., Harris, C. N., Kay, J. H., Parker, D. P., and Magidson, 0.: Postinfarctional ventricular septal rupture. Clinical approach and surgical results, Chest 69:734, 1976. 14. Coles, J. C., Sandoval, W. G., and Mullangi, C.: Surgical repair of acute ventricular septal defect complicating myocardial infarction, Can. J. Surg. 19:143, 1976. 15. James, T. N.: De Subitaneis Mortibus. XXIV. Ruptured interventricular septum and heart block, Circulation 55:934, 1977.
173
