- Email: [email protected]
Postinfarction cardiac rupture
J THORAC
CARDIOVASC SURG
84:755-761, 1982
Postinfarction cardiac rupture This paper records an experience of 42 cases of cardiac rupture or syndromes simulating rupture. These include free wall rupture. hemopericardium without rupture. septal rupture associated with free wall rupture. pseudoaneurysm, and septal rupture. These groups constitute a series of syndromes with many features in common in terms of clinical presentation, difficulty in assessment. timing of operative intervention. and operative management. Free wall rupture, which can be simulated by hemopericardium without rupture, is not always rapidly fatal. Successful intervention was achieved in six of the /3 cases in the free wall group. Ventricular septal defect occurs less frequently than free wall rupture. is more easily diagnosed, and less frequently requires urgent surgical intervention. In 12 of the 14 cases of acute rupture, stabilization of the patient by conservative measures could not be achieved and operation was undertaken within / week of infarction, There were seven survivors, in four of whom the defect reopened. with successful reoperation in three. In the remaining 15 cases. stabilization by conservative measures was achieved and operation was delayed until at least 2 weeks after infarction. There were /4 survivors and only one instance of reopening of the defect.
H. M. Windsor, F.R.A.C.S., F.A.C.S., V. P. Chang, F.R.A.C.S., F.A.C.S., and M. X. Shanahan, F.R.A.C.S., Sydney, Australia
T
his paper records our experience with postinfarction rupture of the left ventricle, either into the pericardium (free wall rupture) or into the right ventricle (septal rupture). Early recognition of free wall rupture by Harvey! and Morgagni" and a report nearly 200 years later of 734 cases by Davenport" demonstrate the long-term awareness and frequency of occurrence. Recognition of septal defect by Latham" and a report by Lee, Cardon, and Slodki" indicate more recent recognition and less frequent occurrence. Since that time an extensive literature on the recognition and management of postinfarction septal rupture has been published,":" whereas reports on the recognition and management of the more common free wall rupture are rare. 9, 10 Our experience comprises 42 cases of cardiac rupture. This report includes previously reported cases. 11- 13 Because of the close relationship between the various syndromes, we have grouped them as follows: I. Free wall rupture 1. Free wall rupture alone (six cases), Table I 2. Free wall and associated septal ruptures (two cases) 3. Hemopericardium without rupture (three cases)
From St. Vincent's Hospital, University of New South Wales, Sydney, Australia. Received for publication Sept. 10, 1981. Accepted for publication Feb. 9, 1982. 0022-5223/82/110755+07$00.70/0
© 1982 The C. V. Mosby Co.
4. Pseudoaneurysm (two cases) II. Septal rupture 1. Acute (14 cases), Table II 2. Subacute (11 cases) 3. Chronic (four cases) All but one patient (Case 6, Table I) had some form of intervention.
Free wall rupture Clinical features. There were eight men and five women with an average age of 67 years. A feature of the history in all four groups was either protraction of the original pain or disappearance followed by recurrence of pain. This was noted in four of the six patients having free wall rupture, in one having combined free wall and septal rupture, in two having hemopericardium without rupture, and in both patients having pseudoaneurysm. Rupture occurred on an average of 4 days after the infarction, the longest interval being II days and the shortest 7 hours. In this latter instance (Case 6, Table I), the patient, a woman of 66 years, developed severe chest pain at 10:00 A.M, She developed neither shock nor cardiac failure. Her blood pressure remained at 160/100 mm Hg until 7 hours later, when she suddenly became profoundly hypotensive and died in 5 minutes. Autopsy revealed an anterolateral perforation with 300 ml of blood in the pericardium. The jugular venous pressure was raised in 11 patients and arterial paradox was recorded in four. Ten patients 755
The Journal of
756
Windsor, Chang, Shanahan
Thoracic and Cardiovascular Surgery
Table I. Free wall rupture Case No.
Sex, age, year M, 56, 1971
2
M, 61, 1972
3
F, 78, 1975
Clinical aspects Pain ~ disappearance of pain ~ recurrence of pain, day 10; cardiogenic shock, JVP 10 em H 20; arterial paradox Pain ~ disappearance of pain ~ recurrence of pain, day 3; cardiogenic shock, JVP 3 em H 20; arterial paradox Recurrent protracted pain; cardiogenic shock, JVP 6 em
Cardiac silhouette on chest film
Catheterization echo
Not enlarged
Double shadow
Ineffective counterpulsation; pericardiocentesis
Died day II after infarction. Autopsy: anterolateral rupture LAD 90% obstruction
Enlarged
Double shadow, leak of dye, cardiac arrest during catheterization
Ineffective counterpulsation; hemopericardium, cardiac rupture; infarctectomy
Recovery uneventful
Enlarged
Not done
Ineffective counterpulsation
Died day 10 after infarction. Autopsy: hemopericardium (100 ml); anterolateral rupture; LAD 90% obstruction Died day 2 after infarction. Autopsy: hemopericardium (200 ml); anterolateral rupture Recurrent postoperative ventricular fibrillation; discharged well on day 21 after operation
Management
H20
4
M, 66. 1975
Severe protracted pain; cardiogenic shock ,
Not enlarged
Not done
Ineffective counterpulsation
5
M, 57, 1980
Cardiogenic shock; JVP 8 em H 20; arterial paradox
Not enlarged
Coronary arteries defined; pericardial effusion on echo
6
F.66, 1981
Severe chest pain; no shock. BP 160/100 mm Hg
Not enlarged
Not done
Infarctectomy; thrombus on epicardial and endocardial aspects of rupture; septal necrosis; patch closure of VSD created by septal resection None
Result
Seven hours after onset of pain, sudden profound shock, bradycardia, and electromechanical dissociation; died. Autopsy: Anterolateral rupture; hemopericardium (300 ml)
Legend: J VP. Jugular venous pressure. LAD, Left anterior descending coronary artery. VSD. Ventricular septal defect. BP. Blood pressure.
were in cardiogenic shock when first seen and, as already stated, one was hypertensive. In both patients with combined free wall and septal rupture the signs of septal rupture predominated. Both were profoundly hypotensive and oliguric, with raised jugular venous pressures and pulmonary edema. In two of the patients with hemopericardium without rupture, the bleeding at operation was noted to be coming from the surface of the infarct. One of these two had a coincident acute ventricular septal defect. All three patients in the group were receiving heparin. The patients with pseudoaneurysms presented in characteristic fashion with left ventricular failure, cardiomegaly, and in one case an apical systolic murmur.
The cardiac silhouette on the chest x-ray film frequently was not enlarged. This was the case in four of the patients with free wall rupture, in both with combined free wall and septal rupture, and in two with hemopericardium without rupture. The silhouette was enlarged in the five other patients. A normal silhouette was accompanied by pulmonary edema in both patients having combined free wall and septal rupture. The electrocardiogram did not contribute to the diagnosis in any case, since bradycardia and electromechanical dissociation, when observed, were terminal events. Apart from the patients having pseudoaneurysm, both of whom had routine investigations, seven patients had cardiac catheterization, in one of whom it was done at
Volume84 Number 5 November, 1982
Postinfarction cardiac rupture
75 7
Table H. Acute VSD (operation within 1 week of infarction)
Sex. age, year
Infarctoperation interval (days)
Site of VSD
F, 64, 1972
5
Inferior
2
F, 52, 1972
6
3
F,56, 1973
4
Case No.
Catheterization
Management
Result
Shunt 2.5:1; LAD 100%, RCA 50%
Ineffective counterpulsation; infarctectomy and patch closure
Inferior
Shunt 4: I; LAD 100%, RCA 60%
5
Inferior
Not done
Ineffective counterpulsation; infarctectomy and patch closure; vein grafts to RCA and LCA Ineffective counterpulsation; infarctectomy and patch closure of VSD
M, 63,1973
3
Anterior
Shunt 3: I; LAD 90%
Ineffective counterpulsation; infarctectomy and patch closure of VSD
5
M, 55, 1973
5
Inferior
Not done
6
M,62,1975
3
Anterior
Shunt 2.5: I; LAD 90%
7
M,50, 1976
6
Anterior
Shunt 3: I; LAD 100%
8
M,60,1976
7
Anterior
Shunt 1.7: I; LAD 100%
9
M, 63, 1977
6
Inferior
Shunt 3: I
10
M, 66,1980
6
Inferior
II
M, 68,1980
4
Anterior
Bedside catheterization: Shunt 6: I; VF reverted Bedside catheterization
Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; infarctectomy and patch closure ofVSD Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; infarctectomy and patch closure of VSD with continuous suture Infarctectomy and patch closure of VSD; CABG x 4 (empirical) Infarctectomy and patch closure ofVSD
VSD reopened; refused reoperation; died 39 days after operation. Autopsy: extensive pneumonia and small bowel infarction VSD reopened; successfully closed at reoperation at 8 weeks Died day 3 after operation; Autopsy: Extensive infarction of right ventricle and septum; single localized lesion in midRCA Died of renal shutdown and respiratory failure. Autopsy: Extensive renal necrosis and pneumonia Uneventful recovery
12
M, 67,1981
3
Anterior
Not done
13
M,66, 1975
Inferior
Not done
14
M, 62,1976
Inferior
Not done
Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; no operation Ineffective counterpulsation; no operation
Renal shutdown, dialysis; discharged well 14 days after operation Died day 7 after operation; dissection of iliac artery and renal shutdown Died day 6 after operation; Autopsy: extensive residual necrosis of left ventricle VSD reopened; successfully closed at reoperation at 3 weeks; well Effective postoperative balloon support; discharged well 14 days after operation Effective postoperative balloon support; discharged well 16 days after operation VSD reopened; successfully closed at reoperation at 7 weeks; well Died on day of admission. Autopsy: Large inferior VSD with gross disease of RCA Died on day of admission. Autopsy: Large inferior VSD and thrombosis of RCA
Legend: Allpatients werein shock,oliguric,hadpulmonary edemaandcongestive cardiac failure, andwereunresponsive to conservative measures. VSD, Ventricular septal defect. LAD, Left anterior descending coronary artery. RCA,Rightcoronary artery. LCA, Left coronary artery. VF, Ventricular fibrillation. CABO,Coronary artery bypass graft.
the bedside. Double shadows were noted in two of these studies and leaks of dye into the pericardium were seen in two others. The coronary arteries were defined on only two occasions. Cardiac arrest occurred once during catheterization and necessitated urgent (success-
ful) surgical intervention (Case 2, Table I). On one occasion, catheterization was abandoned because of the desperate condition of the patient. It was not carried out in three of the patients having free wall rupture. In both patients having combined free wall and septal rupture
The Journal of
75 8 Windsor, Chang, Shanahan
Thoracic and Cardiovascular Surgery
the study defined the septal defect, and in one patient having pseudoaneurysm it defined the typical hourglass constriction at the neck. Echocardiography in more recent cases conclusively established the presence of a hemopericardium. Management. Intra-aortic balloon counterpulsation proved ineffective in all eight patients in whom it was used. Both patients in whom it was the only form of intervention died. Free wall rupture alone. Infarctectomy was carried out on two occasions, both patients surviving. Two patients died during balloon counterpulsation and one patient died of further tamponade after initial improvement following pericardiocentesis. Combined free wall and septal rupture. Infarctectomy and patch closure was carried out in both cases. The first patient survived 16 days and the second 3 days. Autopsy revealed bilateral pneumonia and portal thrombosis in the first patient and renal necrosis and acute pancreatitis in the second. Hemopericardium without rupture. Tamponade of a bleeding infarct was successful on one occasion and pericardiocentesis was successful on another occasion. Infarctectomy and patch closure of a septal defect was unsuccessful in one case. Pseudoaneurysm. Closure of the pseudoaneurysms presented no difficulty. One of these was a typical false aneurysm with a small ventricular opening and a blood-containing pericardial sac. The other was a pseudo- false aneurysm in that the ventricular opening was small and the blood was contained by distended epicardium with some thinned out muscle fibers.
Septal rupture Clinical features. Acute (14 cases) (Table II). The average age of the II men and three women in this group was 61 years. There was rarely difficulty in diagnosis. The history and signs of myocardial infarction, followed by the development of a pansystolic murmur, occurred in every case. All patients were in cardiogenic shock, oliguric, in congestive cardiac failure, and had pulmonary edema. All were unresponsive to supportive therapy including balloon counterpulsation. Cardiac catheterization, done at the bedside on two occasions, was carried out in 10 cases and not done in five. Ventricular fibrillation occurred in one case during the procedure, and catheterization had to be abandoned in one other. The shunts averaged 3: 1. The state of the coronary arteries was not significantly elucidated. The chest x-ray film showed obvious pulmonary congestion or edema with an enlarged cardiac silhou-
ette in most cases. There were eight inferior and six anterior ruptures. Rupture occurred within 2 days of the infarction in all patients, and all were operated upon within 7 days of infarction, the longest interval being 7 days and the shortest 3 days. Subacute (11 cases). The average age of the 10 men and one woman in this group was 63 years. We have chosen to make the distinction between the acute and subacute groups solely on the basis of the time interval between the infarction and operation. At the time of septal rupture the clinical state in the subacute group was little different from that in the acute group. All were in congestive cardiac failure, 10 had pulmonary edema, but only one was in cardiogenic shock. All responded to conservative supportive measures. The chest x-ray films showed varying degrees of cardiomegaly and pulmonary congestion or edema. Electrocardiography and echocardiography contributed no additional significant information. Cardiac catheterization was carried out in every case. The shunts averaged 3.1: 1. There were seven anterior and four inferior ruptures. The interval between the septal rupture and operation in this group averaged 12 weeks, the shortest interval being 2 weeks and the longest 28 weeks. Chronic (four cases). These patients all had small anterior defects with insignificant shunts. In all cases the operation was undertaken for other reasons, usually because of left ventricular aneurysm. Combinedfree wall and septal rupture. Both patients have been included in the "free wall rupture" group and in the "acute septal rupture" category. The chest x-ray film in both showed a normal cardiac silhouette and pulmonary edema. Cardiac catheterization in one case demonstrated a 5: I shunt. In the second the procedure had to be abandoned. The echocardiogram showed unequivocal evidence of pericardial effusion in one case. Operation was carried out 4 days and I day, respectively, from the time of infarction. Management. Balloon counterpulsation as a supportive preoperative measure was carried out in 14 patients, all of whom had either an acute rupture or a combined free wall and septal rupture. It was ineffective in all cases. Both patients in whom counterpulsation was the only form of intervention died, and it contributed to the death of one patient as a result of iliac artery dissection. It was not used in any of the patients with subacute or chronic rupture. Definitive operation was carried out in 12 patients who had an acute rupture, in both patients who had combined free wall and septal rupture, and in all 15 having subacute or chronic rup-
Volume 84 Number 5 November. 1982
ture. Twelve of the patients having an acute rupture had infarctectomy and patch closure. One of those having combined free wall and septal rupture had patch closure and the other had suture closure. Ten of the patients with a subacute rupture had patch closure and one had suture closure. All four patients with chronic rupture had suture closure. Results. Acute and combined free wall and septal ruptures. Seven of the 14 patients survived surgical therapy for an acute rupture (50%). However, since two patients died without operation on the day of admission while undergoing counterpulsation, seven of 12 patients survived operation. The septal defect reopened on four occasions, and in three of these successful closure was achieved at a second operation at 3, 7, and 8 weeks, respectively. All these patients are now well. The fourth patient refused reoperation and died 39 days after operation of extensive pneumonia. Postoperative balloon support was helpful in two of the survivors and renal dialysis in one. Neither of the patients having combined free wall and septal rupture survived. The difficulties in these two groups are highlighted by the wide range of autopsy findings, which included extensive pneumonia, residual necrosis of either the right or left ventricle, renal necrosis, bowel infarction, portal thrombosis, and pancreatitis. Subacute. Ten of 11 patients survived (91%). Death occurred in one patient who had longstanding chronic obstructive airways disease and prerenal failure. Chronic. All four patients survived. Discussion Free wall rupture. Autopsy studies indicate that the incidence of intrapericardial rupture following myocardial infarction is approximately 10%.14 Bates and associates," in an extensive review of 1,400 cases, found an incidence in some series as high as 14%. The rate appears to be higher in coroner's cases and also in mental patients. 16 Intrapericardial rupture is eight to ten times more common than rupture of the ventricular septum 17 and is, after cardiogenic shock and arrhythmia, the most important cause of sudden death. IS Wright and Alonso.!" in an analysis of 100 autopsies in patients who died of acute myocardial infarction, reported 11 instances of combined free wall and septal rupture. Lewis, Burchell, and Titus, 20 using the criteria of Mallory, White, and Sahedo-Salgar" to indicate infarct age, reported that 22% of ruptures occur within 12 hours but can be delayed for as long as 3 weeks. A number of factors make the assessment of this interval
Postinfarction cardiac rupture
759
difficult. It is not always easy to decide when the infarction occurred, especially in the older person with a silent infarct, nor is it always easy to decide when the shock of tamponade has been superimposed on cardiogenic shock. The longest interval in this series was 11 days and the shortest, 7 hours. Most ruptures are in the distribution of the left anterior descending artery and are associated with large transmural infarcts, which allow irregular dissection along endomysial planes. Poor collateral supply, absence of fibrosis, shearing at the periphery of the infarct due to a combination of paradoxical and normal movement, pericardial adherence, and heparin therapy all play a part in the rupture or in the production of hemopericardium. A rapid leak is poorly tolerated, as little as 100 to 150 ml being enough to cause a rapidly fatal tamponade (Case 6, Table I). Intrapericardial rupture, although much more common than ventricular septal rupture, is less frequently seen in the clinical setting: A septal defect is more easily diagnosed and causes gradual deterioration, whereas obscurity of signs and often rapidly fatal progress lead to less frequent recognition of the free wall rupture. We have been impressed by the sequence of chest pain, disappearance of pain, and recurrence or protraction of pain. 9. 12 This sequence occurred nine times but was most frequent in free wall ruptures. We agree with Bates and colleagues" that the chance of rupture is greatest in the elderly hypertensive patient who develops the recurrent/protracted pain syndrome in the days following his first myocardial infarction. The transition from cardiogenic shock following infarction to the shock of combined infarction and tamponade confused diagnosis in early cases. The misconception that balloon counterpulsation would relieve cardiogenic shock likewise confused diagnosis. The cardiac silhouette was normal in eight cases, probably because of the relatively indistensible pericardium and the small amount of blood required to cause tamponade, especially in an infarcted heart. The electrocardiogram was of no help in establishing the presence of a hemopericardium, bradycardia and electromechanical dissociation being agonal events. Cardiac catheterization was carried out nine times. It caused ventricular fibrillation in one case and had to be abandoned in another. However, only after angiography revealed a double shadow in one case and leak of dye in two others did we realize that hemopericardium was compounding the cardiogenic shock. It seems to us that catheterization is a dangerous and unwarranted investigation to be supplanted by a critical evaluation of
760
Windsor, Chang, Shanahan
the clinical state and sequential echocardiography. It can be argued that the absence of information regarding the state of the coronary arteries is a disadvantage, but this perhaps constitutes a lesser risk than a full catheter assessment in the presence of tamponade. Pericardiocentesis was used rarely. It is difficult to perform in a recumbent hypotensive patient whose pericardium contains no more than 150 ml. As a diagnostic measure in the acute situation it is inferior to echocardiography, and as a therapeutic measure it is neither as safe nor as effective as surgical intervention. The syndrome of hemopericardium without rupture closely resembled free wall rupture in every detail. In two cases we noted bleeding from the surface of the infarct and ascribed this to heparin therapy. The signs which suggest rupture or hemopericardium are as follows: (1) tamponade with jugular venous engorgement and pulsus paradoxus; (2) demonstration of a pericardial collection by echocardiography or nuclear scanning; (3) failure of balloon counterpulsation; (4) the presence of a double shadow or leak of dye on cardiac catheterization. A normal cardiac silhouette, absence of a double shadow, and good cardiac contractility do not exclude a hemopericardium. The pseudoaneurysms closely resembled the two types described by Stewart and colleagues. 22 Both had small ventricular openings. However, in one the blood was contained by a pericardial sac (false aneurysm) and in the other by a thinned out remnant of cardiac wall (pseudo-false aneurysm). Septal rupture. It is postulated that the higher pressure gradient between the left ventricle and the pericardium than between the right and left ventricles and the better septal collaterals are possible reasons for the less frequent occurrence of septal than free wall rupture. The high mortality is not surprising when one considers the extent of the infarct, poor ventricular performance due to muscle necrosis, akinesia, and aneurysm formation, the size of the shunt with the additional cardiac work it entails, the presence of extensive coronary artery disease, the involvement of the mitral mechanism, and the severe general disturbance of cardiogenic shock. About 66% of septal ruptures occur in the anterior region of the septum, 17% in the inferior region, and 13% in the middle region. In this series 19 were anterior and 13 were inferior. Inferior defects are usually large, may involve the papillary muscle, and may seriously interfere with the mitral mechanism. In this series papillary muscle infarction was noted in at least seven cases, but in no
The Journal of Thoracic and Cardiovascular Surgery
instance did it interfere with the mitral mechanism. Loisance and associates." in describing the massive septal necrosis that can occur in an inferior defect, point out that the hole in the left side of the septum is centrally placed and smaller than the hole in the right side, which is inferiorly placed. The massive necrosis can separate the septum into two layers, the right side sometimes having multiple holes. As in the case of free wall rupture, it is doubtful whether cardiac catheterization and arteriography were profitable in any of the seven cases in which they were carried out. Management and timing of operation. Stinson" called it "whimsical" to attempt stabilization by afterload reduction in order to achieve fibrosis of the margins of the defect and therefore a more favorable lesion to repair. By contrast, we found that the use of conservative measures to reduce afterload, together with aggressive medical management to control congestive cardiac failure, stabilized all 11 patients in the subacute group. Balloon counterpulsation was ineffective in the 12 patients with acute rupture in whom it was used and in both patients with combined free wall and septal rupture. Early operation was reserved for those in whom improvement could be neither initiated nor sustained. The decision to operate was based solely on failure to stabilize by supportive measures, a decision which must be reached as soon as possible after opening of the defect. Reports emphasize a virtual 100% mortality during the first week in patients who develop profound shock.F' Likewise they emphasize the high but somewhat lower mortality in similar patients operated upon in the first week." In short, if stabilization cannot be achieved early operation is imperative. On the other hand, reports confirm much better results if the operation can be delayed. 25 In this series of 12 patients operated upon for acute rupture, seven survived and the defect reopened in four; of 15 patients having subacute or chronic rupture, 14 survived and the defect reopened on one occasion. We consider the goal of stabilization a desirable one. Stinson'" has rightly questioned the wisdom of arteriography in acute septal defects and suggested revascularization on empirical grounds. This is our present policy. The ease with which the patch could be inserted in the case of subacute rupture contrasted with the difficulty of its insertion into the necrotic septum of the acute cases. The defect reopened on four occasions in
Volume 84 Number 5 November, 1982
the acute group, but in three of these it was closed successfully at a subsequent operation. In these cases the patient's condition was stabilized following the initial placement of the patch and remained stable until the second operation. The second operation in all three was technically much easier. In the subacute rupture group, one defect closed by suture technique reopened and necessitated subsequent patch closure. One further patient who had a 7 by 5 em patch inserted over a large defect with multiple openings has a small residual shunt. We have found consistently better suture holding properties if the operation was delayed for 2 weeks. This together with the low mortality and the lessened chance of reoperation persuaded us that the effort at stabilization is worthwhile. The experience gained in working on friable infarcted septum has influenced the development of our present technique, in which a large D-shaped Dacron patch is fashioned so that nearly the whole septum can be covered by the circular portion of the patch. This is then sutured to the viable septum in circumferential fashion with pledget-supported horizontal mattress sutures of 2-0 Tevdec. The highest sutures may have to be placed in the septum very close to the base of the mitral leaflets, passing through half thickness without transfixing the septum. The base of the patch protrudes outside the ventricle and is incorporated in the closure of the ventriculotomy, which is completed under Teflon strips. REFERENCES
2
3 4
5 6
7
Harvey W: Complete Works, R Willis, trans., London, 1847, Sydenham Society, p 127 Morgagni lB: The seats and causes of diseases investigated by anatomy, B Alexander, trans., Millar A, Cadell T, Letter 27, 1769 Davenport AB: Spontaneous heart rupture. A statistical summary. Am 1 Med 176:62, 1928 Latham PM: Lectures on Subjects Connected with Clinical Medicine Comprising Diseases of the Heart, Vol 2, London, 1845, Longmans, Brown, Green, and Longmans Lee WY, Cardon L, Siodki Sl: Perforation of infarcted intraventricular septum. Arch Intern Med 109:731, 1962 Iben AB, Papello OF, Stinson EB, Shumway NE: Surgical treatment of post infarction ventricular septal defects. Ann Thorac Surg 8:252, 1969 Crosby lK, Craver 1M, Crampton is. Schrank lP, Wellons HA: Resection of acute posterior ventricular aneurysm with repair of ventricular septal defect after acute myocardial infarction. 1 THORAC CARDIOVASC SURG 70:57, 1975
Postinfarction cardiac rupture
76 1
8 Daggett WM, Guyton RA, Mundth ED, Buckley Ml, McEnany MT, Gold HK, Leinback RC, Austen WG: Surgery for post-myocardial infarct ventricular septal defect. Ann Surg 186:206, 1977 9 London RE, London SB: Rupture of the heart. A critical analysis of 47 consecutive autopsy cases. Circulation 31:202, 1965 10 Fitzgibbon GM, Hooper GO, Heggtveit HA: Successful surgical treatment of postinfarction external cardiac rupture. 1 THORAC CARDIOVASC SURG 63:622, 1972 II 0 'Rourke MF: Subacute heart rupture following myocardial infarction. Lancet 2: 124, 1973 12 Windsor HM, Shanahan MX, Chang VP: Postinfarction cardiac rupture. Med 1 Aust 2:859, 1976 13 Windsor HM, Shanahan MX, Chang VP: Perforation of the interventricular septum complicating myocardial infarction. Med 1 Aust 1:587, 1978 14 Schechter DC: Inventory of surgical operations for cardiac structural sequels of myocardial infarction. NY State 1 Med 75: 1202, 1975 15 Bates RJ, Beutler S, Resnekov L, Anagnostopoulos CE: Cardiac rupture. Challenge in diagnosis and management. Am 1 Cardiol 40:429, 1977 16 letter WW, White PO: Rupture of the heart in patients in mental institutions. Ann Intern Med 21:793, 1944 17 Van Tassel RA, Edwards JE: Rupture of the heart complicating myocardial infarction. Analysis of 40 cases including nine examples of left ventricular false aneurysm. Chest 61: 104, 1972 18 Friedberg CK': General treatment of acute myocardial infarction. Circulation 39,40:Suppl 4:252, 1969 19 Wright IS, Alonso DR: Thromboembolic aspects ofmyocardial infarction. NY State 1 Med 79:317, 1979 20 Lewis Jl., Burchell HB, Titus lL: Clinical and pathologic features of postinfarction myocardial rupture. Am 1 CardioI23:43, 1969 21 Mallory GK, White PO, Sahedo-Salgar 1: The speed of healing of myocardial infarction. Am Heart 1 18:647, 1939 22 Stewart MD, Huddle R, Stuart I, Schreiner BF, DeWeese lA: False aneurysm and pseudo-false aneurysm of the left ventricle. Etiology, pathology, diagnosis and operative management. Ann Thorac Surg 31:259, 1981 23 Loisance DY, Cachera lP, Poulain H, Aubry P, luvin AM, Galey 11: Ventricular septal defect after acute myocardial infarction. 1 THORAC CARDIOVASC SURG 80:61, 1981 24 Stinson EB: Discussion of Naifeh JG, Grehl TM, Hurley El: Surgical treatment of post- myocardial infarction ventricular septal defects. 1 THORAC CARDIOVASC SURG 79:483, 1980 25 Brandt B, Wright CB, Ehrenhaft lL: Ventricular septal defect following myocardial infarction. Ann Thorac Surg 27:580, 1979
CARDIOVASC SURG
84:755-761, 1982
Postinfarction cardiac rupture This paper records an experience of 42 cases of cardiac rupture or syndromes simulating rupture. These include free wall rupture. hemopericardium without rupture. septal rupture associated with free wall rupture. pseudoaneurysm, and septal rupture. These groups constitute a series of syndromes with many features in common in terms of clinical presentation, difficulty in assessment. timing of operative intervention. and operative management. Free wall rupture, which can be simulated by hemopericardium without rupture, is not always rapidly fatal. Successful intervention was achieved in six of the /3 cases in the free wall group. Ventricular septal defect occurs less frequently than free wall rupture. is more easily diagnosed, and less frequently requires urgent surgical intervention. In 12 of the 14 cases of acute rupture, stabilization of the patient by conservative measures could not be achieved and operation was undertaken within / week of infarction, There were seven survivors, in four of whom the defect reopened. with successful reoperation in three. In the remaining 15 cases. stabilization by conservative measures was achieved and operation was delayed until at least 2 weeks after infarction. There were /4 survivors and only one instance of reopening of the defect.
H. M. Windsor, F.R.A.C.S., F.A.C.S., V. P. Chang, F.R.A.C.S., F.A.C.S., and M. X. Shanahan, F.R.A.C.S., Sydney, Australia
T
his paper records our experience with postinfarction rupture of the left ventricle, either into the pericardium (free wall rupture) or into the right ventricle (septal rupture). Early recognition of free wall rupture by Harvey! and Morgagni" and a report nearly 200 years later of 734 cases by Davenport" demonstrate the long-term awareness and frequency of occurrence. Recognition of septal defect by Latham" and a report by Lee, Cardon, and Slodki" indicate more recent recognition and less frequent occurrence. Since that time an extensive literature on the recognition and management of postinfarction septal rupture has been published,":" whereas reports on the recognition and management of the more common free wall rupture are rare. 9, 10 Our experience comprises 42 cases of cardiac rupture. This report includes previously reported cases. 11- 13 Because of the close relationship between the various syndromes, we have grouped them as follows: I. Free wall rupture 1. Free wall rupture alone (six cases), Table I 2. Free wall and associated septal ruptures (two cases) 3. Hemopericardium without rupture (three cases)
From St. Vincent's Hospital, University of New South Wales, Sydney, Australia. Received for publication Sept. 10, 1981. Accepted for publication Feb. 9, 1982. 0022-5223/82/110755+07$00.70/0
© 1982 The C. V. Mosby Co.
4. Pseudoaneurysm (two cases) II. Septal rupture 1. Acute (14 cases), Table II 2. Subacute (11 cases) 3. Chronic (four cases) All but one patient (Case 6, Table I) had some form of intervention.
Free wall rupture Clinical features. There were eight men and five women with an average age of 67 years. A feature of the history in all four groups was either protraction of the original pain or disappearance followed by recurrence of pain. This was noted in four of the six patients having free wall rupture, in one having combined free wall and septal rupture, in two having hemopericardium without rupture, and in both patients having pseudoaneurysm. Rupture occurred on an average of 4 days after the infarction, the longest interval being II days and the shortest 7 hours. In this latter instance (Case 6, Table I), the patient, a woman of 66 years, developed severe chest pain at 10:00 A.M, She developed neither shock nor cardiac failure. Her blood pressure remained at 160/100 mm Hg until 7 hours later, when she suddenly became profoundly hypotensive and died in 5 minutes. Autopsy revealed an anterolateral perforation with 300 ml of blood in the pericardium. The jugular venous pressure was raised in 11 patients and arterial paradox was recorded in four. Ten patients 755
The Journal of
756
Windsor, Chang, Shanahan
Thoracic and Cardiovascular Surgery
Table I. Free wall rupture Case No.
Sex, age, year M, 56, 1971
2
M, 61, 1972
3
F, 78, 1975
Clinical aspects Pain ~ disappearance of pain ~ recurrence of pain, day 10; cardiogenic shock, JVP 10 em H 20; arterial paradox Pain ~ disappearance of pain ~ recurrence of pain, day 3; cardiogenic shock, JVP 3 em H 20; arterial paradox Recurrent protracted pain; cardiogenic shock, JVP 6 em
Cardiac silhouette on chest film
Catheterization echo
Not enlarged
Double shadow
Ineffective counterpulsation; pericardiocentesis
Died day II after infarction. Autopsy: anterolateral rupture LAD 90% obstruction
Enlarged
Double shadow, leak of dye, cardiac arrest during catheterization
Ineffective counterpulsation; hemopericardium, cardiac rupture; infarctectomy
Recovery uneventful
Enlarged
Not done
Ineffective counterpulsation
Died day 10 after infarction. Autopsy: hemopericardium (100 ml); anterolateral rupture; LAD 90% obstruction Died day 2 after infarction. Autopsy: hemopericardium (200 ml); anterolateral rupture Recurrent postoperative ventricular fibrillation; discharged well on day 21 after operation
Management
H20
4
M, 66. 1975
Severe protracted pain; cardiogenic shock ,
Not enlarged
Not done
Ineffective counterpulsation
5
M, 57, 1980
Cardiogenic shock; JVP 8 em H 20; arterial paradox
Not enlarged
Coronary arteries defined; pericardial effusion on echo
6
F.66, 1981
Severe chest pain; no shock. BP 160/100 mm Hg
Not enlarged
Not done
Infarctectomy; thrombus on epicardial and endocardial aspects of rupture; septal necrosis; patch closure of VSD created by septal resection None
Result
Seven hours after onset of pain, sudden profound shock, bradycardia, and electromechanical dissociation; died. Autopsy: Anterolateral rupture; hemopericardium (300 ml)
Legend: J VP. Jugular venous pressure. LAD, Left anterior descending coronary artery. VSD. Ventricular septal defect. BP. Blood pressure.
were in cardiogenic shock when first seen and, as already stated, one was hypertensive. In both patients with combined free wall and septal rupture the signs of septal rupture predominated. Both were profoundly hypotensive and oliguric, with raised jugular venous pressures and pulmonary edema. In two of the patients with hemopericardium without rupture, the bleeding at operation was noted to be coming from the surface of the infarct. One of these two had a coincident acute ventricular septal defect. All three patients in the group were receiving heparin. The patients with pseudoaneurysms presented in characteristic fashion with left ventricular failure, cardiomegaly, and in one case an apical systolic murmur.
The cardiac silhouette on the chest x-ray film frequently was not enlarged. This was the case in four of the patients with free wall rupture, in both with combined free wall and septal rupture, and in two with hemopericardium without rupture. The silhouette was enlarged in the five other patients. A normal silhouette was accompanied by pulmonary edema in both patients having combined free wall and septal rupture. The electrocardiogram did not contribute to the diagnosis in any case, since bradycardia and electromechanical dissociation, when observed, were terminal events. Apart from the patients having pseudoaneurysm, both of whom had routine investigations, seven patients had cardiac catheterization, in one of whom it was done at
Volume84 Number 5 November, 1982
Postinfarction cardiac rupture
75 7
Table H. Acute VSD (operation within 1 week of infarction)
Sex. age, year
Infarctoperation interval (days)
Site of VSD
F, 64, 1972
5
Inferior
2
F, 52, 1972
6
3
F,56, 1973
4
Case No.
Catheterization
Management
Result
Shunt 2.5:1; LAD 100%, RCA 50%
Ineffective counterpulsation; infarctectomy and patch closure
Inferior
Shunt 4: I; LAD 100%, RCA 60%
5
Inferior
Not done
Ineffective counterpulsation; infarctectomy and patch closure; vein grafts to RCA and LCA Ineffective counterpulsation; infarctectomy and patch closure of VSD
M, 63,1973
3
Anterior
Shunt 3: I; LAD 90%
Ineffective counterpulsation; infarctectomy and patch closure of VSD
5
M, 55, 1973
5
Inferior
Not done
6
M,62,1975
3
Anterior
Shunt 2.5: I; LAD 90%
7
M,50, 1976
6
Anterior
Shunt 3: I; LAD 100%
8
M,60,1976
7
Anterior
Shunt 1.7: I; LAD 100%
9
M, 63, 1977
6
Inferior
Shunt 3: I
10
M, 66,1980
6
Inferior
II
M, 68,1980
4
Anterior
Bedside catheterization: Shunt 6: I; VF reverted Bedside catheterization
Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; infarctectomy and patch closure ofVSD Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; infarctectomy and patch closure of VSD with continuous suture Infarctectomy and patch closure of VSD; CABG x 4 (empirical) Infarctectomy and patch closure ofVSD
VSD reopened; refused reoperation; died 39 days after operation. Autopsy: extensive pneumonia and small bowel infarction VSD reopened; successfully closed at reoperation at 8 weeks Died day 3 after operation; Autopsy: Extensive infarction of right ventricle and septum; single localized lesion in midRCA Died of renal shutdown and respiratory failure. Autopsy: Extensive renal necrosis and pneumonia Uneventful recovery
12
M, 67,1981
3
Anterior
Not done
13
M,66, 1975
Inferior
Not done
14
M, 62,1976
Inferior
Not done
Ineffective counterpulsation; infarctectomy and patch closure of VSD Ineffective counterpulsation; no operation Ineffective counterpulsation; no operation
Renal shutdown, dialysis; discharged well 14 days after operation Died day 7 after operation; dissection of iliac artery and renal shutdown Died day 6 after operation; Autopsy: extensive residual necrosis of left ventricle VSD reopened; successfully closed at reoperation at 3 weeks; well Effective postoperative balloon support; discharged well 14 days after operation Effective postoperative balloon support; discharged well 16 days after operation VSD reopened; successfully closed at reoperation at 7 weeks; well Died on day of admission. Autopsy: Large inferior VSD with gross disease of RCA Died on day of admission. Autopsy: Large inferior VSD and thrombosis of RCA
Legend: Allpatients werein shock,oliguric,hadpulmonary edemaandcongestive cardiac failure, andwereunresponsive to conservative measures. VSD, Ventricular septal defect. LAD, Left anterior descending coronary artery. RCA,Rightcoronary artery. LCA, Left coronary artery. VF, Ventricular fibrillation. CABO,Coronary artery bypass graft.
the bedside. Double shadows were noted in two of these studies and leaks of dye into the pericardium were seen in two others. The coronary arteries were defined on only two occasions. Cardiac arrest occurred once during catheterization and necessitated urgent (success-
ful) surgical intervention (Case 2, Table I). On one occasion, catheterization was abandoned because of the desperate condition of the patient. It was not carried out in three of the patients having free wall rupture. In both patients having combined free wall and septal rupture
The Journal of
75 8 Windsor, Chang, Shanahan
Thoracic and Cardiovascular Surgery
the study defined the septal defect, and in one patient having pseudoaneurysm it defined the typical hourglass constriction at the neck. Echocardiography in more recent cases conclusively established the presence of a hemopericardium. Management. Intra-aortic balloon counterpulsation proved ineffective in all eight patients in whom it was used. Both patients in whom it was the only form of intervention died. Free wall rupture alone. Infarctectomy was carried out on two occasions, both patients surviving. Two patients died during balloon counterpulsation and one patient died of further tamponade after initial improvement following pericardiocentesis. Combined free wall and septal rupture. Infarctectomy and patch closure was carried out in both cases. The first patient survived 16 days and the second 3 days. Autopsy revealed bilateral pneumonia and portal thrombosis in the first patient and renal necrosis and acute pancreatitis in the second. Hemopericardium without rupture. Tamponade of a bleeding infarct was successful on one occasion and pericardiocentesis was successful on another occasion. Infarctectomy and patch closure of a septal defect was unsuccessful in one case. Pseudoaneurysm. Closure of the pseudoaneurysms presented no difficulty. One of these was a typical false aneurysm with a small ventricular opening and a blood-containing pericardial sac. The other was a pseudo- false aneurysm in that the ventricular opening was small and the blood was contained by distended epicardium with some thinned out muscle fibers.
Septal rupture Clinical features. Acute (14 cases) (Table II). The average age of the II men and three women in this group was 61 years. There was rarely difficulty in diagnosis. The history and signs of myocardial infarction, followed by the development of a pansystolic murmur, occurred in every case. All patients were in cardiogenic shock, oliguric, in congestive cardiac failure, and had pulmonary edema. All were unresponsive to supportive therapy including balloon counterpulsation. Cardiac catheterization, done at the bedside on two occasions, was carried out in 10 cases and not done in five. Ventricular fibrillation occurred in one case during the procedure, and catheterization had to be abandoned in one other. The shunts averaged 3: 1. The state of the coronary arteries was not significantly elucidated. The chest x-ray film showed obvious pulmonary congestion or edema with an enlarged cardiac silhou-
ette in most cases. There were eight inferior and six anterior ruptures. Rupture occurred within 2 days of the infarction in all patients, and all were operated upon within 7 days of infarction, the longest interval being 7 days and the shortest 3 days. Subacute (11 cases). The average age of the 10 men and one woman in this group was 63 years. We have chosen to make the distinction between the acute and subacute groups solely on the basis of the time interval between the infarction and operation. At the time of septal rupture the clinical state in the subacute group was little different from that in the acute group. All were in congestive cardiac failure, 10 had pulmonary edema, but only one was in cardiogenic shock. All responded to conservative supportive measures. The chest x-ray films showed varying degrees of cardiomegaly and pulmonary congestion or edema. Electrocardiography and echocardiography contributed no additional significant information. Cardiac catheterization was carried out in every case. The shunts averaged 3.1: 1. There were seven anterior and four inferior ruptures. The interval between the septal rupture and operation in this group averaged 12 weeks, the shortest interval being 2 weeks and the longest 28 weeks. Chronic (four cases). These patients all had small anterior defects with insignificant shunts. In all cases the operation was undertaken for other reasons, usually because of left ventricular aneurysm. Combinedfree wall and septal rupture. Both patients have been included in the "free wall rupture" group and in the "acute septal rupture" category. The chest x-ray film in both showed a normal cardiac silhouette and pulmonary edema. Cardiac catheterization in one case demonstrated a 5: I shunt. In the second the procedure had to be abandoned. The echocardiogram showed unequivocal evidence of pericardial effusion in one case. Operation was carried out 4 days and I day, respectively, from the time of infarction. Management. Balloon counterpulsation as a supportive preoperative measure was carried out in 14 patients, all of whom had either an acute rupture or a combined free wall and septal rupture. It was ineffective in all cases. Both patients in whom counterpulsation was the only form of intervention died, and it contributed to the death of one patient as a result of iliac artery dissection. It was not used in any of the patients with subacute or chronic rupture. Definitive operation was carried out in 12 patients who had an acute rupture, in both patients who had combined free wall and septal rupture, and in all 15 having subacute or chronic rup-
Volume 84 Number 5 November. 1982
ture. Twelve of the patients having an acute rupture had infarctectomy and patch closure. One of those having combined free wall and septal rupture had patch closure and the other had suture closure. Ten of the patients with a subacute rupture had patch closure and one had suture closure. All four patients with chronic rupture had suture closure. Results. Acute and combined free wall and septal ruptures. Seven of the 14 patients survived surgical therapy for an acute rupture (50%). However, since two patients died without operation on the day of admission while undergoing counterpulsation, seven of 12 patients survived operation. The septal defect reopened on four occasions, and in three of these successful closure was achieved at a second operation at 3, 7, and 8 weeks, respectively. All these patients are now well. The fourth patient refused reoperation and died 39 days after operation of extensive pneumonia. Postoperative balloon support was helpful in two of the survivors and renal dialysis in one. Neither of the patients having combined free wall and septal rupture survived. The difficulties in these two groups are highlighted by the wide range of autopsy findings, which included extensive pneumonia, residual necrosis of either the right or left ventricle, renal necrosis, bowel infarction, portal thrombosis, and pancreatitis. Subacute. Ten of 11 patients survived (91%). Death occurred in one patient who had longstanding chronic obstructive airways disease and prerenal failure. Chronic. All four patients survived. Discussion Free wall rupture. Autopsy studies indicate that the incidence of intrapericardial rupture following myocardial infarction is approximately 10%.14 Bates and associates," in an extensive review of 1,400 cases, found an incidence in some series as high as 14%. The rate appears to be higher in coroner's cases and also in mental patients. 16 Intrapericardial rupture is eight to ten times more common than rupture of the ventricular septum 17 and is, after cardiogenic shock and arrhythmia, the most important cause of sudden death. IS Wright and Alonso.!" in an analysis of 100 autopsies in patients who died of acute myocardial infarction, reported 11 instances of combined free wall and septal rupture. Lewis, Burchell, and Titus, 20 using the criteria of Mallory, White, and Sahedo-Salgar" to indicate infarct age, reported that 22% of ruptures occur within 12 hours but can be delayed for as long as 3 weeks. A number of factors make the assessment of this interval
Postinfarction cardiac rupture
759
difficult. It is not always easy to decide when the infarction occurred, especially in the older person with a silent infarct, nor is it always easy to decide when the shock of tamponade has been superimposed on cardiogenic shock. The longest interval in this series was 11 days and the shortest, 7 hours. Most ruptures are in the distribution of the left anterior descending artery and are associated with large transmural infarcts, which allow irregular dissection along endomysial planes. Poor collateral supply, absence of fibrosis, shearing at the periphery of the infarct due to a combination of paradoxical and normal movement, pericardial adherence, and heparin therapy all play a part in the rupture or in the production of hemopericardium. A rapid leak is poorly tolerated, as little as 100 to 150 ml being enough to cause a rapidly fatal tamponade (Case 6, Table I). Intrapericardial rupture, although much more common than ventricular septal rupture, is less frequently seen in the clinical setting: A septal defect is more easily diagnosed and causes gradual deterioration, whereas obscurity of signs and often rapidly fatal progress lead to less frequent recognition of the free wall rupture. We have been impressed by the sequence of chest pain, disappearance of pain, and recurrence or protraction of pain. 9. 12 This sequence occurred nine times but was most frequent in free wall ruptures. We agree with Bates and colleagues" that the chance of rupture is greatest in the elderly hypertensive patient who develops the recurrent/protracted pain syndrome in the days following his first myocardial infarction. The transition from cardiogenic shock following infarction to the shock of combined infarction and tamponade confused diagnosis in early cases. The misconception that balloon counterpulsation would relieve cardiogenic shock likewise confused diagnosis. The cardiac silhouette was normal in eight cases, probably because of the relatively indistensible pericardium and the small amount of blood required to cause tamponade, especially in an infarcted heart. The electrocardiogram was of no help in establishing the presence of a hemopericardium, bradycardia and electromechanical dissociation being agonal events. Cardiac catheterization was carried out nine times. It caused ventricular fibrillation in one case and had to be abandoned in another. However, only after angiography revealed a double shadow in one case and leak of dye in two others did we realize that hemopericardium was compounding the cardiogenic shock. It seems to us that catheterization is a dangerous and unwarranted investigation to be supplanted by a critical evaluation of
760
Windsor, Chang, Shanahan
the clinical state and sequential echocardiography. It can be argued that the absence of information regarding the state of the coronary arteries is a disadvantage, but this perhaps constitutes a lesser risk than a full catheter assessment in the presence of tamponade. Pericardiocentesis was used rarely. It is difficult to perform in a recumbent hypotensive patient whose pericardium contains no more than 150 ml. As a diagnostic measure in the acute situation it is inferior to echocardiography, and as a therapeutic measure it is neither as safe nor as effective as surgical intervention. The syndrome of hemopericardium without rupture closely resembled free wall rupture in every detail. In two cases we noted bleeding from the surface of the infarct and ascribed this to heparin therapy. The signs which suggest rupture or hemopericardium are as follows: (1) tamponade with jugular venous engorgement and pulsus paradoxus; (2) demonstration of a pericardial collection by echocardiography or nuclear scanning; (3) failure of balloon counterpulsation; (4) the presence of a double shadow or leak of dye on cardiac catheterization. A normal cardiac silhouette, absence of a double shadow, and good cardiac contractility do not exclude a hemopericardium. The pseudoaneurysms closely resembled the two types described by Stewart and colleagues. 22 Both had small ventricular openings. However, in one the blood was contained by a pericardial sac (false aneurysm) and in the other by a thinned out remnant of cardiac wall (pseudo-false aneurysm). Septal rupture. It is postulated that the higher pressure gradient between the left ventricle and the pericardium than between the right and left ventricles and the better septal collaterals are possible reasons for the less frequent occurrence of septal than free wall rupture. The high mortality is not surprising when one considers the extent of the infarct, poor ventricular performance due to muscle necrosis, akinesia, and aneurysm formation, the size of the shunt with the additional cardiac work it entails, the presence of extensive coronary artery disease, the involvement of the mitral mechanism, and the severe general disturbance of cardiogenic shock. About 66% of septal ruptures occur in the anterior region of the septum, 17% in the inferior region, and 13% in the middle region. In this series 19 were anterior and 13 were inferior. Inferior defects are usually large, may involve the papillary muscle, and may seriously interfere with the mitral mechanism. In this series papillary muscle infarction was noted in at least seven cases, but in no
The Journal of Thoracic and Cardiovascular Surgery
instance did it interfere with the mitral mechanism. Loisance and associates." in describing the massive septal necrosis that can occur in an inferior defect, point out that the hole in the left side of the septum is centrally placed and smaller than the hole in the right side, which is inferiorly placed. The massive necrosis can separate the septum into two layers, the right side sometimes having multiple holes. As in the case of free wall rupture, it is doubtful whether cardiac catheterization and arteriography were profitable in any of the seven cases in which they were carried out. Management and timing of operation. Stinson" called it "whimsical" to attempt stabilization by afterload reduction in order to achieve fibrosis of the margins of the defect and therefore a more favorable lesion to repair. By contrast, we found that the use of conservative measures to reduce afterload, together with aggressive medical management to control congestive cardiac failure, stabilized all 11 patients in the subacute group. Balloon counterpulsation was ineffective in the 12 patients with acute rupture in whom it was used and in both patients with combined free wall and septal rupture. Early operation was reserved for those in whom improvement could be neither initiated nor sustained. The decision to operate was based solely on failure to stabilize by supportive measures, a decision which must be reached as soon as possible after opening of the defect. Reports emphasize a virtual 100% mortality during the first week in patients who develop profound shock.F' Likewise they emphasize the high but somewhat lower mortality in similar patients operated upon in the first week." In short, if stabilization cannot be achieved early operation is imperative. On the other hand, reports confirm much better results if the operation can be delayed. 25 In this series of 12 patients operated upon for acute rupture, seven survived and the defect reopened in four; of 15 patients having subacute or chronic rupture, 14 survived and the defect reopened on one occasion. We consider the goal of stabilization a desirable one. Stinson'" has rightly questioned the wisdom of arteriography in acute septal defects and suggested revascularization on empirical grounds. This is our present policy. The ease with which the patch could be inserted in the case of subacute rupture contrasted with the difficulty of its insertion into the necrotic septum of the acute cases. The defect reopened on four occasions in
Volume 84 Number 5 November, 1982
the acute group, but in three of these it was closed successfully at a subsequent operation. In these cases the patient's condition was stabilized following the initial placement of the patch and remained stable until the second operation. The second operation in all three was technically much easier. In the subacute rupture group, one defect closed by suture technique reopened and necessitated subsequent patch closure. One further patient who had a 7 by 5 em patch inserted over a large defect with multiple openings has a small residual shunt. We have found consistently better suture holding properties if the operation was delayed for 2 weeks. This together with the low mortality and the lessened chance of reoperation persuaded us that the effort at stabilization is worthwhile. The experience gained in working on friable infarcted septum has influenced the development of our present technique, in which a large D-shaped Dacron patch is fashioned so that nearly the whole septum can be covered by the circular portion of the patch. This is then sutured to the viable septum in circumferential fashion with pledget-supported horizontal mattress sutures of 2-0 Tevdec. The highest sutures may have to be placed in the septum very close to the base of the mitral leaflets, passing through half thickness without transfixing the septum. The base of the patch protrudes outside the ventricle and is incorporated in the closure of the ventriculotomy, which is completed under Teflon strips. REFERENCES
2
3 4
5 6
7
Harvey W: Complete Works, R Willis, trans., London, 1847, Sydenham Society, p 127 Morgagni lB: The seats and causes of diseases investigated by anatomy, B Alexander, trans., Millar A, Cadell T, Letter 27, 1769 Davenport AB: Spontaneous heart rupture. A statistical summary. Am 1 Med 176:62, 1928 Latham PM: Lectures on Subjects Connected with Clinical Medicine Comprising Diseases of the Heart, Vol 2, London, 1845, Longmans, Brown, Green, and Longmans Lee WY, Cardon L, Siodki Sl: Perforation of infarcted intraventricular septum. Arch Intern Med 109:731, 1962 Iben AB, Papello OF, Stinson EB, Shumway NE: Surgical treatment of post infarction ventricular septal defects. Ann Thorac Surg 8:252, 1969 Crosby lK, Craver 1M, Crampton is. Schrank lP, Wellons HA: Resection of acute posterior ventricular aneurysm with repair of ventricular septal defect after acute myocardial infarction. 1 THORAC CARDIOVASC SURG 70:57, 1975
Postinfarction cardiac rupture
76 1
8 Daggett WM, Guyton RA, Mundth ED, Buckley Ml, McEnany MT, Gold HK, Leinback RC, Austen WG: Surgery for post-myocardial infarct ventricular septal defect. Ann Surg 186:206, 1977 9 London RE, London SB: Rupture of the heart. A critical analysis of 47 consecutive autopsy cases. Circulation 31:202, 1965 10 Fitzgibbon GM, Hooper GO, Heggtveit HA: Successful surgical treatment of postinfarction external cardiac rupture. 1 THORAC CARDIOVASC SURG 63:622, 1972 II 0 'Rourke MF: Subacute heart rupture following myocardial infarction. Lancet 2: 124, 1973 12 Windsor HM, Shanahan MX, Chang VP: Postinfarction cardiac rupture. Med 1 Aust 2:859, 1976 13 Windsor HM, Shanahan MX, Chang VP: Perforation of the interventricular septum complicating myocardial infarction. Med 1 Aust 1:587, 1978 14 Schechter DC: Inventory of surgical operations for cardiac structural sequels of myocardial infarction. NY State 1 Med 75: 1202, 1975 15 Bates RJ, Beutler S, Resnekov L, Anagnostopoulos CE: Cardiac rupture. Challenge in diagnosis and management. Am 1 Cardiol 40:429, 1977 16 letter WW, White PO: Rupture of the heart in patients in mental institutions. Ann Intern Med 21:793, 1944 17 Van Tassel RA, Edwards JE: Rupture of the heart complicating myocardial infarction. Analysis of 40 cases including nine examples of left ventricular false aneurysm. Chest 61: 104, 1972 18 Friedberg CK': General treatment of acute myocardial infarction. Circulation 39,40:Suppl 4:252, 1969 19 Wright IS, Alonso DR: Thromboembolic aspects ofmyocardial infarction. NY State 1 Med 79:317, 1979 20 Lewis Jl., Burchell HB, Titus lL: Clinical and pathologic features of postinfarction myocardial rupture. Am 1 CardioI23:43, 1969 21 Mallory GK, White PO, Sahedo-Salgar 1: The speed of healing of myocardial infarction. Am Heart 1 18:647, 1939 22 Stewart MD, Huddle R, Stuart I, Schreiner BF, DeWeese lA: False aneurysm and pseudo-false aneurysm of the left ventricle. Etiology, pathology, diagnosis and operative management. Ann Thorac Surg 31:259, 1981 23 Loisance DY, Cachera lP, Poulain H, Aubry P, luvin AM, Galey 11: Ventricular septal defect after acute myocardial infarction. 1 THORAC CARDIOVASC SURG 80:61, 1981 24 Stinson EB: Discussion of Naifeh JG, Grehl TM, Hurley El: Surgical treatment of post- myocardial infarction ventricular septal defects. 1 THORAC CARDIOVASC SURG 79:483, 1980 25 Brandt B, Wright CB, Ehrenhaft lL: Ventricular septal defect following myocardial infarction. Ann Thorac Surg 27:580, 1979