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Ventricular Septal Rupture, Secondary to Myocardial Infarction
Ventricular Septal Rupture, Secondary to Myocardial Infarction* Roberto Lufschunowski, M.D.;Paolo Angelini, M.D.; Carlos De2 Rw, M.D.; Grady L. Hallman, M.D., F.C.C.P.;Denton A. Cooley, M.D., F.C.C.P.;and Robert D. Leachman, M.D., F.C.C.P.
We present our experience with 12 patients with operation for ventricular septal rupture following acute myocardial infarction. Clinically, two sets of symptoms are described. In the first, shock and severe failure occur shortly after the infarction. In the second, signs of moderate failure and a pansystolic murmur appear several days following the acute infarction. The two patients with shock shortly after infarction died during operation. The other ten patients survived the operation, although three died 11 days, 45 days, and 18 months afterward. The seven survivors are doing well after an average of 31 months. The surgical techniques used are discussed. These results compare favorably with the ominous natural course of this complication of acute infarction.
upture of the ventricular septum, one of the most dramatic complications of ischemic heart disease, has been recognized in autopsy material since the last century.' Only in recent years has the clinician shared with the pathologist a direct interest in this condition. The first clinical analysis was published in 1934,2with the first reported surgical repair in 1956.3 At present, sufficient cases have been collected to demonstrate the ominous natural prognosis of ventricular septal rupture. The diagnosis can be suspected with reasonable accuracy by clinical means and confirmed by simple hemodynamic procedures. A problem still unsolved is the optimal time for surgical repair. Previous s t ~ d i e s ~ favored ,~ a tendency to delay any surgical procedure until two months after the rupture. An earlier report from this institution3 described our first experience with this association, which has now increased with 11 more cases. This series consists of 12 patients, each of whom had operation for repair of the ventricular septal rupture, thus confirming the preoperative diagnosis. Since most of the patients were referred for surgical evaluation from other "From the Cardiology and Surgical Departments of St. Luke's Episcopal Hospital and the Texas Heart Institute, Houston. Manuscript received June 4; revision accepted August 27. Reprint requests: Dr. Leachman, Cardiology Department, St. Luke's Episcopal Hospital, Houston 77025
CHEST, VOL.
6 5 , NO. 1, JANUARY, 1974
institutions, our experience cannot be used to establish the actual incidence of ventricular septal rupture after myocardial infarction, since it is preselected. The majority (ten patients) were admitted not less than 25 days after infarction. Hemodynamic studies were performed in ten cases. Due to the critical condition of many of t h e s e ~ t i e n t s ,and also to the fact that the great majority were studied before coronary operation was performed at this institution, selective coronary angiography was done in only two cases. Retrograde arterial catheterization with left ventricular angiography was performed in six patients. Two patients died in the immediate period after operation. At the time of the patient's discharge, every case was re-evaluated clinically for evidence of residual murmurs.
Findings Of these 12 patients, there were 3 women and 9 men. The mean age was 59 years (range, 47-71 ). Every patient had a single episode of myocardial infarction. No one had a history of angina or cardiac murmurs. One had diabetes mellitus, one had gout and none had systemic hypertension. Clinical evidence of rupture of the ventricular septum appeared in ten cases before the fourth day following the acute myocardial infarction (Table 1). In patient 9 the clinical pattern changed two weeks after the infarction. Patient 7 was referred because of the onset of severe and progressive congestive heart failure, ten years after his only myocardial infarction. At operation, organized fibrous tissue was found surrounding large, multiple perforations of the lower septum, giving the macroscopic impression of old infarctions. The clinical course of these patients after ventricular septal rupture was a dramatic one, essentially because of the development of rapid and progressive congestive heart failure (nine cases), or low output syndrome, which in three
LUFSCHANOWSKI ET AL
60 patients evolved to severe shock (patients 2, 6, 12). Since these two clinical patterns are common in patients with severe myocardial infarction, an important clue at the bedside is the presence of a hyperdynamic heart, a finding which is rather atypical in severe ischemic heart disease. A harsh systolic murmur, frequently accompanied by a thrill, was found in all patients. The plane x-ray film of the chest only showed nonspecific signs such as cardiomegaly and pulmonary congestion. Increased pulmonary flow was usually difficult to recognize in roentgenograms because the signs of passive venous congestion predominated. The electrocardiogram did not offer specific patterns in ventricular septal rupture and only showed the localization of the infarcted area, frequently suggesting the presence of a ventricular aneurysm. In ten cases, there were electrocardiographic signs of inferior infarction and in nine cases, signs of anterior infarction. In seven cases, they were coexistent, so that in only five cases a single infarcted area was present. Cardiac catheterization was performed in all but two patients. In these ten cases, dye dilution curves consistent
with a left-to-right shunt at the ventricular level were obtained. The pulmonary blood flow was calculated to vary between two and five times systemic flow ( mean 2.7: 1). The pulmonary arterial wedge pressure was elevated in every patient, with a range of 17 to 45 mm Hg and a mean for the group of 24 mm Hg. The main pulmonary artery systolic pressure ranged between 44 and 100 mm Hg, with a mean for the group of 68 mm Hg. In only five cases retrograde arterial catheterization was performed and left ventricular angiograms were obtained. Selective coronary arteriography was performed in two cases. In one of them there was evidence of triple-vessel disease of severe degree and in the other the right coronary artery was completely occluded, the left coronary being essentially normal. Left ventriculography confirmed the presence of a ventricular septal defect, usually near the apex and always in the muscular septum. Aneurysm of the left ventricle was demonstrated in three cases in this group. The left ventricular phase of pulmonary angiograms was equally sensitive in detecting the presence of a ventricular septal defect. Findings at operation in these patients are described in Table 1.
Table 1 InkrvaIs
Hemdynumim
l M 49 4days
2mm
IWMI
CHF (class 4)
2.4:l
-
-
19513 2 em. VSD-pmterior RV y s no small pmterior aheurysm of LV
2 M 47 3days
&days
ASMI
Shock (class 4)
-
-
-
1958 3 c m VSD-anterior msaeive anterior infarct
RV yea ym persisting shock
3 M 52 5 days
2 mm
IWMI. LMI. APMI
CHF (class 41
2.5:l
25
59/22
1967 l c m VSD-inferior small inferior aneurysm
RV no
no
6 mm
IWMI, ASMI. RBBB
CHF 3.4:l (clan# 2-3)
17
29/16
1987 multiple small VSD'a (high-lat.) a m l l aneurysm
LV no RV
y s dive and well (class 1-2)
60 m a
5 M 53 2 days
I mo
ALMI, aneurysm
CHF ( c h 31 VF
5:l
18
W/15
1906 I.5cm VSD-apical anterolateral infarct
RV no
no
peraintingshock and vent. fib.
diedsame day
6 M 49 3days
I mo
IWMI
CHF Shock (class 41
2:l
17
4/13
1908 1.5 cm. VSDapical
RV yes no
satisfactory (class 2) VSD murmur
25 mm.
7 M W t
1
IWMI. ALMI
CHF (class 3)
2.5:l
20
70/20
1989 single VSD from LV RV no multiple VSD's from RV LV
n d dynamim by a t h . ; no VSD working without limibtions
died suddenly after 18 m a
R F
%days
IWMI, ASMI. aneurysm
CHF (class 3)
2:)
20
48/16
1969 2 c m VSD-anterior anterior aneurysm
LV
yee yes no murmur a t discharge (no late follow-up)
2 mm
IWMI, ASMI. aneurysm
CHF
2.3:l
25
75/20
1970 1 e m VSD-spical apical aneurysm
LV
yes yes nomurmurs ( c h 2)
1970 small VSD-&ria LV s m U pmterior aneurysm
4 F
88 I day
65 8&ya
9 M 71 12 days 10 F
feless 3)
60 3 days
2 mm
IWMI, true pasl.
CHF (class 3)
2.6:l
28
55/20
II M 69 Bdays
3 mm
APMI, IWMI. LAHB CHF (class 3)
2:l
45
100/40 1970 1 cm. VSD-npical apical aneurysm
12 M 59 s a m d a y
I day
ASMI, IWMI
-
-
Shock (class 4)
-
1971 3 c m VSD-eentral diffuse hypokineaia
no
yes no
persistent murmur. died after CHF and 45 days pulmonary infection died same &Y
hemdynamically 04 m a and clinically very f a v ~ b i (class e 1-2)
10 days
2/6 murmur (class 2)
LV
yes yes nomurmur (class 1-2)
20 mm.
LV
ym no
died after 11 days
murmur-rpnal failurelow outputven. fib.
Abbreviations: IWMI-inferior 411 myoardial infarction; ASMI=antermepbl myocardial infarction; LMI-lateral myocardial infarction; APMI=apical myocardial infarction; RBBB-right bundle h n c h block; ALMI-anterolateral myoeardi.1 infarction. Shunt: QP:@- pulmonary 0ow:systemic Bow.
CHEST, VOL. 65, NO. 1, JANUARY, 1974
VENTRICULAR SEPTAL RUPTURE Surgical Technique
Two patients were operated on as an emergency, because of progressive cardiogenic shock, nonresponsive to medical treatment. One of them had to be put on partial bypass before the cardiac procedure could be started (patient 8). Another had ventricular fibrillation during the induction of anesthesia and extracorporeal circulation was started immediately (patient 5 ). The approach to the ventricular septum was through a right ventriculotomy in five cases, left ventriculotomy in five, and combined in two. An Ivalon sponge was used as patching material in the first case, in 1956. In seven other cases, the patch was made of Dacron. In the remaining four cases only direct sutures were used. In the two patients (2, 12) operated on within the first five days after the infarction (one and two days after the appearance of signs of ventricular septal rupture), the defects were large, the infarcted areas were extensive and it was difficult to find healthy tissue for satisfactory suture of the patch. Ventricular aneurysms of the free wall of the left ventricle were excised in four of the seven patients when a left ventricular approach was used. In the remaining cases, with this type of ventriculotomy and in all of those in which a combined approach was used, the ventricle was entered through the infarcted area. In a single case, direct suture repair of the rupture was performed from both the right and the left sides of the septum (patient 7 ) . In patient 10, a fresh infarction involved the major part of the septum and of the anterior wall of the right and left ventricles. In this case, infarctectomy was performed on both sides of the septum and the free walls of the ventricles were resutured to the septum.
The immediate mortality at operation in this series was 17 percent ( 2 of 12). Two other patients died in the hospital before discharge, 11 and 45 days after operation, resulting in an overall hospital mortality of 33 percent. One of the two deaths at operation was that of an extremely ill patient who entered the surgical suite having an episode of ventricular fibrillation unresponsive to medical treatment. The second death occurred at operation in a patient who required emergency partial bypass with femoral venoarterial perfusion for treatment of progressive cardiogenic shock. In both of them, the left ventricular myocardium was diffusely and severely compromised and no effective contractions could be obtained after extracorporeal circulation was discontinued. The late hospital deaths were due to a moderately severe low output syndrome with secondary renal failure in patient 8, and progressive respiratory and cardiac failure in patient 11. An autopsy was obtained in three of these four cases and showed a satisfactory repair of the ventricular septal defect in one case (patient 5 ) , and a partial reopening of the ventricular septal defect in the other two. In patient 8 an abscess was found at the patch site.
CHEST, VOL. 65, NO. 1, JANUARY, 1974
Of the eight patients who left the hospital (average hospital stay of nine days after operation), only one had a class 2 (out of 6 ) systolic murmur, without thrill (patient 10). At one year of follow-up, which did not include hemodynamic studies, a great improvement in signs of congestive heart failure and cardiomegaly by x-ray film was found and correlated with the absence of significant functional limitations. In six of the remaining seven cases, follow-up clinical evaluation showed absence of signs of congestive heart failure on physical examination and x-ray film. Three of these patients are still partially limited by dyspnea on exertion (functional class 2 ) , and have been kept on digitalis and diuretic treatment. No one had experienced new episodes of myocardial infarction after an average 31-month period of observation (ranging from 10 to 50 months). Patient 7 had a smooth and favorable course for 18 months after operation when he suddenly died. No autopsy was obtained.
The natural history of ventricular septal rupture secondary to myocardial infarction has been already well described in the literature.04 Two extreme variants can be outlined for practical purposes. The first corresponds to a case of acute myocardial infarction, which eventually is complicated by severe and rapidly progressive congestive heart failure with low output syndrome. The shortterm prognosis of this clinical pattern is poor. The second variety is that of a stable acute myocardial infarction, with the clinical findings of a ventricular septal defect developing during the first few days and complicated by moderate congestive heart failure. Although between these two extremes, there are evidently many intermediate forms, this simplification should be kept in mind when handling an individual case of ventricular septal rupture. The diagnostic and therapeutic procedures will eventually vary according to these two different patterns. It is our opinion that in patients with severe acute compromise of the hemodynamic status, the diagnostic studies should be restricted to a few essential and rapid tests. Besides the electrocardiogram and x-ray film examination of the chest, a simple right heart catheterization is usually sufficient to confirm the diagnosis of left-toright shunt. The two patients in this series with the syndrome of cardiogenic shock initially, did not have catheterization and were transferred to the operating room as an emergency, a few hours after admission. On the other hand, in patients with a relatively smooth postinfarction course, and with signs of congestive heart failure responsive to medical treatment, it is advisable to wait for the optimal time for
LUFSCHANOWSKI ET AL
surgical repair, which usually is considered to be two to three months following the infarction. In our own experience, one month after the infarction the fibrous scar is already well developed, permitting a safe suturing of the defect (patients 2 , 3 , 5 ) .In these circumstances, hemodynamic studies should be performed and must include left and right heart catheterization, with selective coronary and left ventricular angiography. The surgical approach to the ventricular septal defect must be decided for the individual case. In general, it is safe to close this type of ventricular septal defect through a left ventricular approach, since it is easier to localize the rupture and to set the sutures of the pat~h.~JO This approach is also advised by the general principle that a communication between two cavities at different pressures should be closed from the high pressure side. In fact, the left surface of the septum is essentially smooth, while the right has trabeculations and recesses. A left ventriculotomy, on the other hand, can decrease the contractility of an already diseased left ventricle. Since a left ventriculotomy through healthy tissue should be avoided, this approach is best justified in those cases in which an infarcted area is present in the anterior or apical regions of the left ventricle. In cases with posterior or exclusively septal infarctions, the right ventriculotomy is probably more advantageous. Recently Shumaker" suggested an incision in the posterior wall of the right ventricle in posterior defects. The relationship between the ventricular septal rupture and the conduction system is not usually a problem, as the great majority of the perforations are found in the lower two thirds of the septum. The right ventriculotomy will produce a right-bundlebranch-block pattern of no real significance, as these are not true bundle lesions but only peripheral blocks, and atrioventricular conduction is essentially unaltered.12 The choice of using a patch versus direct suture of the defect is decided by the individual findings. When the ventricular septal defect is small and well circumscribed by resistant fibromuscular tissue, primary closure is consistently successful. Otherwise a patch, eventually combined with reinforcement of the tissue by direct sutures, should be used. In cases of very extensive perforations, the insertion of two patches, one on each side of the septum, might be necessary. Since the indication of ventricular septal rupture repair is heart failure, the elimination of the diastolic overload of the left ventricle is always beneficial. Other surgical procedures, such as aneurysmectomy, infarctectomy, plastic repair of the mitral valve and
aortocoronary bypass, can also be performed according to the individual situation. This multiplicity of approach not only will improve the late prognosis but also the risk at operation, especially in patients with operation during cardiogenic shock when the restoration of cardiac reserve is very important following the surgical trauma. We believe that diagnosis of postinfarction rupture of the interventricular septum is an almost unequivocal indication for surgical repair. The natural history of this complication of myocardial infarction has proved extremely ominous with a survival rate of only 10 to 20 percent two months after the perf ~ r a t i o n Our . ~ experience is not truly representative of the unselected population of ventricular septal ruptures because only a few patients were observed in our institution from the time of acute infarction. The majority were referred for surgical treatment at a later time. Several other patients not included in this series were referred as emergency cases in cardiogenic shock and died on admission or a few hours after admission, before surgical repair. Also with these limitations, it is interesting to note the absence of predisposing factors in our series. None of our patients had a history of hypertension, nor of multiple infarctions, two major risk factors for complications of myocardial necrosis. No specific review of these factors is available at present with regard to ventricular septal rupture, but they are expected to be similar to those of cardiac rupture,13 in which case hypertension and multiple infarctions have been thought to be causally related. Compared with the reported natural history, our surgical mortality is low in the patients operated in the postacute phase (one month after the infarction). Of the ten patients in this group, we had two deaths, one of a patient operated in 1956.3This was the first open-heart operation in our institution. The two patients treated as emergencies in the first few days after the infarction because of cardiogenic shock unresponsive to medical treatment, died in the immediate hours after operation with persistent low output syndrome and arrhythmias. This group is too small for significant conclusions but shows that the surgical risk is very high under these circumstances, especially if the shunt is not the main determinant of the poor performance of the heart. The review of the literature presented by Kitamura et all4 in 1971, showed that of 65 patients reported to have had ventricular septum repair, 21 were operated on within the first month after infarction. Of these, only five (30 percent) were alive at the time of the report. In summary, rupture of the ventricular septum secondary to myocardial infarction carries a grave prognosis. Surgery is nearly always indicated. When CHEST, VOL. 65, NO. 1, JANUARY, 1974
VENTRICULAR SEPTAL RUPTURE
the clinical course permits s d c i e n t time f o r proper h e a l i n g of the infarcted area, elective surgery can be p e r f o r m e d o n e to three m o n t h s after t h e infarction, a n d t h e results i n o u r experience a r e good. The p a t i e n t w h o s e clinical condition deteriorates shortly a f t e r the infarction and rupture represents a n obvious poor risk for a n y therapeutic intervention. Hopefully a m u l t i p l e approach combining closure of the defect w i t h excision of the infarcted a r e a a n d revascularization of the viable m y o c a r d i u m can offer a better outlook f o r these patients.
1 Latham PM: Lectures on Subjects Connected with Clinical Medicine, Comprising Diseases of the Heart (vol 2 ) . London, Longman, Brown, Green and Longmans, 1946, p 108 2 Sager RV: Coronary thrombosis: Perforation of infarcted interventricular septum. Arch Intern Med 53: 140, 1934 3 Cooley DA, Belmonte BA, Zeis LB, et al: Surgical repair of ruptured interventricular septum following acute myocardial infarction. Surgery 41:930, 1957 4 Friedberg CK: Diseases of the Heart. Philadelphia, Saunders Co., p 856, 1966 5 Davison T, Degenshein GA, Yuceoglu YZ, et al: Repair of ventricular septal defect following myocardial infarction. Ann Surg 160:33, 1964
6 Sanders RJ, Kern WH, Blount SG Jr: Perforation of the interventricular septum complicating myocardial infarction: A report of eight cases, one with cardiac catheterization. Am Heart J 51:736, 1956 7 Oyamada A, Queen FB: Spontaneous rupture of the interventricular septum following acute myocardial infarction with some clinicopathological observations on survival in five cases. Presented at Pan Pacific Pathology Congress, Tripler U.S. Army Hospital, 1961 8 Lee WY, Cardon L, Slodki SJ: Perforation of infarcted interventricular septum. Arch Intern Med 109:731, 1962 9 Kay JH, DuBmt C: Discussion of Iben AB, et al: Surgical treatment of post-infarction ventricular septal defects. Ann Thorac Surg 8:252, 1969 10 Javid H, Hunter JA, N a j d H, et al: Left ventricular approach for the repair of ventricular septal perforation and infarctectomy. J Thorac Cardiovasc Surg 63:14, 1972 11 Shumaker HB: Suggestions concerning operative management of postinfarction septal defects. J Thorac Cardiovasc Surg 64:452, 1972 12 Massig GK, James TN: Conduction and block in the right bundle branch. Real and imagined. Circulation 45:1, 1972 13 Lewis A, Burchell HB, Titus JL: Clinical and pathologic features of postinfarction cardiac rupture. Am J Cardiol 23:43, 1969 14 Kitamura S, Mendez A, Kay JH: Ventricular septal defect following myocardial infarction. Experience with surgical repair through a left ventriculotomy and review of literature. J Thorac Cardiovasc Surg 61: 186, 1971
ANNOUNCEMENTS Symposium: New Techniques in Chest Disease T h e New Jersey Chapter of the American College of Chest Physicians and the New Jersey Thoracic Society are co-sponsors of a Symposium on New Techniques in Chest Disease to be held February 27 in
Nutley, New Jersey a t the Hoffman-LaRoche Auditorium. Contact Mr. W. Stephen Jeffrey, American Lung Association of New Jersey, 2441 Route 22 West, Union 07083, for information.
Refresher Course in Cardiac Radiology A Refresher Course in Cardiac Radiology, presented by the North American Society for Cardiac Radiology, will be held a t the Royal Orleans Hotel, New Orleans,
CHEST, VOL. 65, NO. 1, JANUARY, 1974
March 6 9 . For information, write Erik Carlsson, M.D., University of California School of Medicine, San Francisco 94143.
We present our experience with 12 patients with operation for ventricular septal rupture following acute myocardial infarction. Clinically, two sets of symptoms are described. In the first, shock and severe failure occur shortly after the infarction. In the second, signs of moderate failure and a pansystolic murmur appear several days following the acute infarction. The two patients with shock shortly after infarction died during operation. The other ten patients survived the operation, although three died 11 days, 45 days, and 18 months afterward. The seven survivors are doing well after an average of 31 months. The surgical techniques used are discussed. These results compare favorably with the ominous natural course of this complication of acute infarction.
upture of the ventricular septum, one of the most dramatic complications of ischemic heart disease, has been recognized in autopsy material since the last century.' Only in recent years has the clinician shared with the pathologist a direct interest in this condition. The first clinical analysis was published in 1934,2with the first reported surgical repair in 1956.3 At present, sufficient cases have been collected to demonstrate the ominous natural prognosis of ventricular septal rupture. The diagnosis can be suspected with reasonable accuracy by clinical means and confirmed by simple hemodynamic procedures. A problem still unsolved is the optimal time for surgical repair. Previous s t ~ d i e s ~ favored ,~ a tendency to delay any surgical procedure until two months after the rupture. An earlier report from this institution3 described our first experience with this association, which has now increased with 11 more cases. This series consists of 12 patients, each of whom had operation for repair of the ventricular septal rupture, thus confirming the preoperative diagnosis. Since most of the patients were referred for surgical evaluation from other "From the Cardiology and Surgical Departments of St. Luke's Episcopal Hospital and the Texas Heart Institute, Houston. Manuscript received June 4; revision accepted August 27. Reprint requests: Dr. Leachman, Cardiology Department, St. Luke's Episcopal Hospital, Houston 77025
CHEST, VOL.
6 5 , NO. 1, JANUARY, 1974
institutions, our experience cannot be used to establish the actual incidence of ventricular septal rupture after myocardial infarction, since it is preselected. The majority (ten patients) were admitted not less than 25 days after infarction. Hemodynamic studies were performed in ten cases. Due to the critical condition of many of t h e s e ~ t i e n t s ,and also to the fact that the great majority were studied before coronary operation was performed at this institution, selective coronary angiography was done in only two cases. Retrograde arterial catheterization with left ventricular angiography was performed in six patients. Two patients died in the immediate period after operation. At the time of the patient's discharge, every case was re-evaluated clinically for evidence of residual murmurs.
Findings Of these 12 patients, there were 3 women and 9 men. The mean age was 59 years (range, 47-71 ). Every patient had a single episode of myocardial infarction. No one had a history of angina or cardiac murmurs. One had diabetes mellitus, one had gout and none had systemic hypertension. Clinical evidence of rupture of the ventricular septum appeared in ten cases before the fourth day following the acute myocardial infarction (Table 1). In patient 9 the clinical pattern changed two weeks after the infarction. Patient 7 was referred because of the onset of severe and progressive congestive heart failure, ten years after his only myocardial infarction. At operation, organized fibrous tissue was found surrounding large, multiple perforations of the lower septum, giving the macroscopic impression of old infarctions. The clinical course of these patients after ventricular septal rupture was a dramatic one, essentially because of the development of rapid and progressive congestive heart failure (nine cases), or low output syndrome, which in three
LUFSCHANOWSKI ET AL
60 patients evolved to severe shock (patients 2, 6, 12). Since these two clinical patterns are common in patients with severe myocardial infarction, an important clue at the bedside is the presence of a hyperdynamic heart, a finding which is rather atypical in severe ischemic heart disease. A harsh systolic murmur, frequently accompanied by a thrill, was found in all patients. The plane x-ray film of the chest only showed nonspecific signs such as cardiomegaly and pulmonary congestion. Increased pulmonary flow was usually difficult to recognize in roentgenograms because the signs of passive venous congestion predominated. The electrocardiogram did not offer specific patterns in ventricular septal rupture and only showed the localization of the infarcted area, frequently suggesting the presence of a ventricular aneurysm. In ten cases, there were electrocardiographic signs of inferior infarction and in nine cases, signs of anterior infarction. In seven cases, they were coexistent, so that in only five cases a single infarcted area was present. Cardiac catheterization was performed in all but two patients. In these ten cases, dye dilution curves consistent
with a left-to-right shunt at the ventricular level were obtained. The pulmonary blood flow was calculated to vary between two and five times systemic flow ( mean 2.7: 1). The pulmonary arterial wedge pressure was elevated in every patient, with a range of 17 to 45 mm Hg and a mean for the group of 24 mm Hg. The main pulmonary artery systolic pressure ranged between 44 and 100 mm Hg, with a mean for the group of 68 mm Hg. In only five cases retrograde arterial catheterization was performed and left ventricular angiograms were obtained. Selective coronary arteriography was performed in two cases. In one of them there was evidence of triple-vessel disease of severe degree and in the other the right coronary artery was completely occluded, the left coronary being essentially normal. Left ventriculography confirmed the presence of a ventricular septal defect, usually near the apex and always in the muscular septum. Aneurysm of the left ventricle was demonstrated in three cases in this group. The left ventricular phase of pulmonary angiograms was equally sensitive in detecting the presence of a ventricular septal defect. Findings at operation in these patients are described in Table 1.
Table 1 InkrvaIs
Hemdynumim
l M 49 4days
2mm
IWMI
CHF (class 4)
2.4:l
-
-
19513 2 em. VSD-pmterior RV y s no small pmterior aheurysm of LV
2 M 47 3days
&days
ASMI
Shock (class 4)
-
-
-
1958 3 c m VSD-anterior msaeive anterior infarct
RV yea ym persisting shock
3 M 52 5 days
2 mm
IWMI. LMI. APMI
CHF (class 41
2.5:l
25
59/22
1967 l c m VSD-inferior small inferior aneurysm
RV no
no
6 mm
IWMI, ASMI. RBBB
CHF 3.4:l (clan# 2-3)
17
29/16
1987 multiple small VSD'a (high-lat.) a m l l aneurysm
LV no RV
y s dive and well (class 1-2)
60 m a
5 M 53 2 days
I mo
ALMI, aneurysm
CHF ( c h 31 VF
5:l
18
W/15
1906 I.5cm VSD-apical anterolateral infarct
RV no
no
peraintingshock and vent. fib.
diedsame day
6 M 49 3days
I mo
IWMI
CHF Shock (class 41
2:l
17
4/13
1908 1.5 cm. VSDapical
RV yes no
satisfactory (class 2) VSD murmur
25 mm.
7 M W t
1
IWMI. ALMI
CHF (class 3)
2.5:l
20
70/20
1989 single VSD from LV RV no multiple VSD's from RV LV
n d dynamim by a t h . ; no VSD working without limibtions
died suddenly after 18 m a
R F
%days
IWMI, ASMI. aneurysm
CHF (class 3)
2:)
20
48/16
1969 2 c m VSD-anterior anterior aneurysm
LV
yee yes no murmur a t discharge (no late follow-up)
2 mm
IWMI, ASMI. aneurysm
CHF
2.3:l
25
75/20
1970 1 e m VSD-spical apical aneurysm
LV
yes yes nomurmurs ( c h 2)
1970 small VSD-&ria LV s m U pmterior aneurysm
4 F
88 I day
65 8&ya
9 M 71 12 days 10 F
feless 3)
60 3 days
2 mm
IWMI, true pasl.
CHF (class 3)
2.6:l
28
55/20
II M 69 Bdays
3 mm
APMI, IWMI. LAHB CHF (class 3)
2:l
45
100/40 1970 1 cm. VSD-npical apical aneurysm
12 M 59 s a m d a y
I day
ASMI, IWMI
-
-
Shock (class 4)
-
1971 3 c m VSD-eentral diffuse hypokineaia
no
yes no
persistent murmur. died after CHF and 45 days pulmonary infection died same &Y
hemdynamically 04 m a and clinically very f a v ~ b i (class e 1-2)
10 days
2/6 murmur (class 2)
LV
yes yes nomurmur (class 1-2)
20 mm.
LV
ym no
died after 11 days
murmur-rpnal failurelow outputven. fib.
Abbreviations: IWMI-inferior 411 myoardial infarction; ASMI=antermepbl myocardial infarction; LMI-lateral myocardial infarction; APMI=apical myocardial infarction; RBBB-right bundle h n c h block; ALMI-anterolateral myoeardi.1 infarction. Shunt: QP:@- pulmonary 0ow:systemic Bow.
CHEST, VOL. 65, NO. 1, JANUARY, 1974
VENTRICULAR SEPTAL RUPTURE Surgical Technique
Two patients were operated on as an emergency, because of progressive cardiogenic shock, nonresponsive to medical treatment. One of them had to be put on partial bypass before the cardiac procedure could be started (patient 8). Another had ventricular fibrillation during the induction of anesthesia and extracorporeal circulation was started immediately (patient 5 ). The approach to the ventricular septum was through a right ventriculotomy in five cases, left ventriculotomy in five, and combined in two. An Ivalon sponge was used as patching material in the first case, in 1956. In seven other cases, the patch was made of Dacron. In the remaining four cases only direct sutures were used. In the two patients (2, 12) operated on within the first five days after the infarction (one and two days after the appearance of signs of ventricular septal rupture), the defects were large, the infarcted areas were extensive and it was difficult to find healthy tissue for satisfactory suture of the patch. Ventricular aneurysms of the free wall of the left ventricle were excised in four of the seven patients when a left ventricular approach was used. In the remaining cases, with this type of ventriculotomy and in all of those in which a combined approach was used, the ventricle was entered through the infarcted area. In a single case, direct suture repair of the rupture was performed from both the right and the left sides of the septum (patient 7 ) . In patient 10, a fresh infarction involved the major part of the septum and of the anterior wall of the right and left ventricles. In this case, infarctectomy was performed on both sides of the septum and the free walls of the ventricles were resutured to the septum.
The immediate mortality at operation in this series was 17 percent ( 2 of 12). Two other patients died in the hospital before discharge, 11 and 45 days after operation, resulting in an overall hospital mortality of 33 percent. One of the two deaths at operation was that of an extremely ill patient who entered the surgical suite having an episode of ventricular fibrillation unresponsive to medical treatment. The second death occurred at operation in a patient who required emergency partial bypass with femoral venoarterial perfusion for treatment of progressive cardiogenic shock. In both of them, the left ventricular myocardium was diffusely and severely compromised and no effective contractions could be obtained after extracorporeal circulation was discontinued. The late hospital deaths were due to a moderately severe low output syndrome with secondary renal failure in patient 8, and progressive respiratory and cardiac failure in patient 11. An autopsy was obtained in three of these four cases and showed a satisfactory repair of the ventricular septal defect in one case (patient 5 ) , and a partial reopening of the ventricular septal defect in the other two. In patient 8 an abscess was found at the patch site.
CHEST, VOL. 65, NO. 1, JANUARY, 1974
Of the eight patients who left the hospital (average hospital stay of nine days after operation), only one had a class 2 (out of 6 ) systolic murmur, without thrill (patient 10). At one year of follow-up, which did not include hemodynamic studies, a great improvement in signs of congestive heart failure and cardiomegaly by x-ray film was found and correlated with the absence of significant functional limitations. In six of the remaining seven cases, follow-up clinical evaluation showed absence of signs of congestive heart failure on physical examination and x-ray film. Three of these patients are still partially limited by dyspnea on exertion (functional class 2 ) , and have been kept on digitalis and diuretic treatment. No one had experienced new episodes of myocardial infarction after an average 31-month period of observation (ranging from 10 to 50 months). Patient 7 had a smooth and favorable course for 18 months after operation when he suddenly died. No autopsy was obtained.
The natural history of ventricular septal rupture secondary to myocardial infarction has been already well described in the literature.04 Two extreme variants can be outlined for practical purposes. The first corresponds to a case of acute myocardial infarction, which eventually is complicated by severe and rapidly progressive congestive heart failure with low output syndrome. The shortterm prognosis of this clinical pattern is poor. The second variety is that of a stable acute myocardial infarction, with the clinical findings of a ventricular septal defect developing during the first few days and complicated by moderate congestive heart failure. Although between these two extremes, there are evidently many intermediate forms, this simplification should be kept in mind when handling an individual case of ventricular septal rupture. The diagnostic and therapeutic procedures will eventually vary according to these two different patterns. It is our opinion that in patients with severe acute compromise of the hemodynamic status, the diagnostic studies should be restricted to a few essential and rapid tests. Besides the electrocardiogram and x-ray film examination of the chest, a simple right heart catheterization is usually sufficient to confirm the diagnosis of left-toright shunt. The two patients in this series with the syndrome of cardiogenic shock initially, did not have catheterization and were transferred to the operating room as an emergency, a few hours after admission. On the other hand, in patients with a relatively smooth postinfarction course, and with signs of congestive heart failure responsive to medical treatment, it is advisable to wait for the optimal time for
LUFSCHANOWSKI ET AL
surgical repair, which usually is considered to be two to three months following the infarction. In our own experience, one month after the infarction the fibrous scar is already well developed, permitting a safe suturing of the defect (patients 2 , 3 , 5 ) .In these circumstances, hemodynamic studies should be performed and must include left and right heart catheterization, with selective coronary and left ventricular angiography. The surgical approach to the ventricular septal defect must be decided for the individual case. In general, it is safe to close this type of ventricular septal defect through a left ventricular approach, since it is easier to localize the rupture and to set the sutures of the pat~h.~JO This approach is also advised by the general principle that a communication between two cavities at different pressures should be closed from the high pressure side. In fact, the left surface of the septum is essentially smooth, while the right has trabeculations and recesses. A left ventriculotomy, on the other hand, can decrease the contractility of an already diseased left ventricle. Since a left ventriculotomy through healthy tissue should be avoided, this approach is best justified in those cases in which an infarcted area is present in the anterior or apical regions of the left ventricle. In cases with posterior or exclusively septal infarctions, the right ventriculotomy is probably more advantageous. Recently Shumaker" suggested an incision in the posterior wall of the right ventricle in posterior defects. The relationship between the ventricular septal rupture and the conduction system is not usually a problem, as the great majority of the perforations are found in the lower two thirds of the septum. The right ventriculotomy will produce a right-bundlebranch-block pattern of no real significance, as these are not true bundle lesions but only peripheral blocks, and atrioventricular conduction is essentially unaltered.12 The choice of using a patch versus direct suture of the defect is decided by the individual findings. When the ventricular septal defect is small and well circumscribed by resistant fibromuscular tissue, primary closure is consistently successful. Otherwise a patch, eventually combined with reinforcement of the tissue by direct sutures, should be used. In cases of very extensive perforations, the insertion of two patches, one on each side of the septum, might be necessary. Since the indication of ventricular septal rupture repair is heart failure, the elimination of the diastolic overload of the left ventricle is always beneficial. Other surgical procedures, such as aneurysmectomy, infarctectomy, plastic repair of the mitral valve and
aortocoronary bypass, can also be performed according to the individual situation. This multiplicity of approach not only will improve the late prognosis but also the risk at operation, especially in patients with operation during cardiogenic shock when the restoration of cardiac reserve is very important following the surgical trauma. We believe that diagnosis of postinfarction rupture of the interventricular septum is an almost unequivocal indication for surgical repair. The natural history of this complication of myocardial infarction has proved extremely ominous with a survival rate of only 10 to 20 percent two months after the perf ~ r a t i o n Our . ~ experience is not truly representative of the unselected population of ventricular septal ruptures because only a few patients were observed in our institution from the time of acute infarction. The majority were referred for surgical treatment at a later time. Several other patients not included in this series were referred as emergency cases in cardiogenic shock and died on admission or a few hours after admission, before surgical repair. Also with these limitations, it is interesting to note the absence of predisposing factors in our series. None of our patients had a history of hypertension, nor of multiple infarctions, two major risk factors for complications of myocardial necrosis. No specific review of these factors is available at present with regard to ventricular septal rupture, but they are expected to be similar to those of cardiac rupture,13 in which case hypertension and multiple infarctions have been thought to be causally related. Compared with the reported natural history, our surgical mortality is low in the patients operated in the postacute phase (one month after the infarction). Of the ten patients in this group, we had two deaths, one of a patient operated in 1956.3This was the first open-heart operation in our institution. The two patients treated as emergencies in the first few days after the infarction because of cardiogenic shock unresponsive to medical treatment, died in the immediate hours after operation with persistent low output syndrome and arrhythmias. This group is too small for significant conclusions but shows that the surgical risk is very high under these circumstances, especially if the shunt is not the main determinant of the poor performance of the heart. The review of the literature presented by Kitamura et all4 in 1971, showed that of 65 patients reported to have had ventricular septum repair, 21 were operated on within the first month after infarction. Of these, only five (30 percent) were alive at the time of the report. In summary, rupture of the ventricular septum secondary to myocardial infarction carries a grave prognosis. Surgery is nearly always indicated. When CHEST, VOL. 65, NO. 1, JANUARY, 1974
VENTRICULAR SEPTAL RUPTURE
the clinical course permits s d c i e n t time f o r proper h e a l i n g of the infarcted area, elective surgery can be p e r f o r m e d o n e to three m o n t h s after t h e infarction, a n d t h e results i n o u r experience a r e good. The p a t i e n t w h o s e clinical condition deteriorates shortly a f t e r the infarction and rupture represents a n obvious poor risk for a n y therapeutic intervention. Hopefully a m u l t i p l e approach combining closure of the defect w i t h excision of the infarcted a r e a a n d revascularization of the viable m y o c a r d i u m can offer a better outlook f o r these patients.
1 Latham PM: Lectures on Subjects Connected with Clinical Medicine, Comprising Diseases of the Heart (vol 2 ) . London, Longman, Brown, Green and Longmans, 1946, p 108 2 Sager RV: Coronary thrombosis: Perforation of infarcted interventricular septum. Arch Intern Med 53: 140, 1934 3 Cooley DA, Belmonte BA, Zeis LB, et al: Surgical repair of ruptured interventricular septum following acute myocardial infarction. Surgery 41:930, 1957 4 Friedberg CK: Diseases of the Heart. Philadelphia, Saunders Co., p 856, 1966 5 Davison T, Degenshein GA, Yuceoglu YZ, et al: Repair of ventricular septal defect following myocardial infarction. Ann Surg 160:33, 1964
6 Sanders RJ, Kern WH, Blount SG Jr: Perforation of the interventricular septum complicating myocardial infarction: A report of eight cases, one with cardiac catheterization. Am Heart J 51:736, 1956 7 Oyamada A, Queen FB: Spontaneous rupture of the interventricular septum following acute myocardial infarction with some clinicopathological observations on survival in five cases. Presented at Pan Pacific Pathology Congress, Tripler U.S. Army Hospital, 1961 8 Lee WY, Cardon L, Slodki SJ: Perforation of infarcted interventricular septum. Arch Intern Med 109:731, 1962 9 Kay JH, DuBmt C: Discussion of Iben AB, et al: Surgical treatment of post-infarction ventricular septal defects. Ann Thorac Surg 8:252, 1969 10 Javid H, Hunter JA, N a j d H, et al: Left ventricular approach for the repair of ventricular septal perforation and infarctectomy. J Thorac Cardiovasc Surg 63:14, 1972 11 Shumaker HB: Suggestions concerning operative management of postinfarction septal defects. J Thorac Cardiovasc Surg 64:452, 1972 12 Massig GK, James TN: Conduction and block in the right bundle branch. Real and imagined. Circulation 45:1, 1972 13 Lewis A, Burchell HB, Titus JL: Clinical and pathologic features of postinfarction cardiac rupture. Am J Cardiol 23:43, 1969 14 Kitamura S, Mendez A, Kay JH: Ventricular septal defect following myocardial infarction. Experience with surgical repair through a left ventriculotomy and review of literature. J Thorac Cardiovasc Surg 61: 186, 1971
ANNOUNCEMENTS Symposium: New Techniques in Chest Disease T h e New Jersey Chapter of the American College of Chest Physicians and the New Jersey Thoracic Society are co-sponsors of a Symposium on New Techniques in Chest Disease to be held February 27 in
Nutley, New Jersey a t the Hoffman-LaRoche Auditorium. Contact Mr. W. Stephen Jeffrey, American Lung Association of New Jersey, 2441 Route 22 West, Union 07083, for information.
Refresher Course in Cardiac Radiology A Refresher Course in Cardiac Radiology, presented by the North American Society for Cardiac Radiology, will be held a t the Royal Orleans Hotel, New Orleans,
CHEST, VOL. 65, NO. 1, JANUARY, 1974
March 6 9 . For information, write Erik Carlsson, M.D., University of California School of Medicine, San Francisco 94143.