Combined septal perforation and cardiac rupture after myocardial infarction

Volume 97,

Number 6

June 1989

THORACIC AND CARDIOVASCULAR SURGERY The Journal of

J

THORAC CARDIOVASC SURG

1989;97:815-20

Original Communications

Combined septal perforation and cardiac rupture after myocardial infarction Clinical features and surgical considerations of a correctable condition The combination of septal perforation and cardiac rupture after myocardial infarction has rarely been reported. This article describes two cases of successful surgical repair of this condition and reviews another three cases previously reported in the literature. The important clinical features were as foUows: (1) acute occlusion of a single dominant coronary artery; (2) renewed chest pain before perforation or rupture; (3) electromechanical dissociation at the time of frank rupture; (4) rupture through the left ventricular free waD; (5) in three patients both complications occurred within 3 days of the infarction, and in the other two patients they developed within three weeks. The main surgical considerations are as foUows: (1) femoral cannulation to prevent exsanguination before instituting cardiopulmonary bypass; (2) electricaUy induced fibriUation to avoid systemic embolism; (3) a left ventricular approach to repair the septal perforation foUowed by infarctectomy; (4) concomitant revascularization was unnecessary. In conclusion, combined septal perforation and cardiac rupture after myocardial infarction is a potentiaUy correctable condition that requires early diagnosis and prompt surgical intervention.

Dan J. Aravot, MD, Nazir Dhalla, FRCS, Nicholas R. Banner, MRCP, Andrew Mitchell, MRCP, and Alun Rees, FRCS, Barefield, Middlesex, England

Two anatomic complications that may follow myocardial infarction are perforation of the interventricular From the Thoracic and Cardiac Surgical Unit, Harefield Hospital, Harefield, Middlesex, England. Received for publication Feb. 25, 1988. Accepted for publication Nov. 2, 1988. Address for reprints: Dan J. Aravot, MD, Thoracic and Cardiac Surgical Unit, Harefield Hospital, Harefield, Uxbridge, Middlesex UB9 6JH, England.

septum and rupture of the ventricular free wall. Cardiac rupture occurs in 4% to 24% of all deaths from acute myocardial infarction, 1-7 and it is the second most common cause of death in coronary care units after myocardial power failure.' Antemortem diagnosis of this usually fatal complication is rarely made early enough to permit effective therapy.' Before 1981 only 10 cases had been reported in which the patient had undergone surgical repair of myocardial free wall rupture and survived to leave the hospital." Perforation of the 8 15

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Aravot et af.

Table I. Characteristics ofpatients with combination of septal perforation and cardiac rupture after MI Previous history of heart disease

Risk factors for ischemic heart disease

Site of MI

Septal perforation

Case

Year

Sex

Age (yr)

115

1959

M

56

No

No data

Posterior wall

48 hr after MI: Severe chest pain, pansystolic murmur

1981

M

66

No

No

Posterior wall

4 hr after MI: Severe chest pain, pansystolic murmur, VF-resus.

39

1983

F

61

No data

No data

Anterior

24 hr after MI: Heart failure, pansystolic murmur

4

1986

M

49

No

No

Anterior

5

1987

F

59

No

No

Anterior wall

4 days after MI: Severe chest pain, cardiac arrest-resus., pansystolic murmur 24 hr after MI: Severe chest pain, hypotension, pansystolic murmur

Cx, Circumflex; EMD, electromechanical dissociation; LAD, left anterior descending coronary artery; LV, left ventricle; MI, myocardial infarction; RCA, right coronary artery; resus., resuscitation; VF, ventricular fibrillation; VSD, ventricular septal defect.

interventricular septum after myocardial infarction occurs in I % to 1.3%10,11 of patients and is associated with a high early mortality." The severe hemodynamic consequences of this event may demand prompt surgical intervention despite unfavorable technical and medical factors. 12 The combination of cardiac rupture and septal perforation has rarely been reported" even though the two are related to the same pathogenic factors." We report two cases in which successful operations were performed and review another three cases reported in the literature, with emphasis on common clinical features and surgical considerations.

Case reports CASE 1. A 49-year-old man had an extensive acute anterior myocardial infarction. Four days later he experienced sudden onset of central chest pain followed by cardiac arrest and was resuscitated successfully. A systolic murmur was heard along the left sternal border, as well as a third heart sound. An echocardiogram showed an anteroapicalleft ventricular aneurysm with normal right ventricular size and a small to

moderate sized pericardial effusion. Cardiac catheterization performed on the ninth day after the myocardial infarction revealed no significant step-up in saturations, with a pulmonary artery saturation of only 52%. Left ventricular angiograms (right anterior oblique projection) showed a faint opacification of the pulmonary artery, but the site of the septal perforation could not be precisely defined. The coronary angiogram showed occlusion of the left anterior descending artery with no significant disease of the circumflex and right coronary arteries. He remained hemodynamically stable and inotropic support was discontinued 4 days later. On the twenty-first day after the infarction he had a further episodeof severe chest pain and collapsed. He was in sinus rhythm with no detectable cardiac output. After resuscitation a systolic blood pressure of 80 mm Hg and heart rate of 130 beats/min (in sinus rhythm) were recorded. Two hours later the patient had a further episode of apparent loss of cardiac output in the presence of sinus rhythm and was therfore transferred to the operating theater. The operation was performed through a median sternotomy. A substantial hemopericardium was found with a large clot surrounding a perforation of the infarcted anterior free wall of the left ventricle. Arterial cannulation was performed through the left femoral artery and venous cannulation through the venae cavae. On cardiopulmonary bypass the

Volume 97 Number 6

Combined septal perforation and cardiac rupture

June 1989

Angiographic findings

Cardiac rupture 60 hr after MI: EMD, death

8 hr after MI: Renewed chest pain, EMD, death

Apical VSD. aneurysm of anterior wall, occlusion of LAD

Incidental finding at operation 48 hr after MI

Anterior VSD, aneurysm of anterior wall, occlusion of LAD Anterior VSD, aneurysm of anterior wall, occlusion of LAD

21 days after MI: Renewed chest pain, EMD-resus., EMD-resus. Incidental finding at operation 20 days after MI

Postop. course

Acute thrombosis of dominant Cx, posterior rupture of LV wall, hemopericardium, posterior VSD Acute occlusion of dominant RCA, posterior rupture of LV wall, hemopericardium, posterior VSD

patient was systemically cooled to 25 C, and the heart was electricallyfibrillated and opened through the thinned out area of the infarct to expose the left ventricular chamber. A clot was carefully removed from the left ventricular cavity and the infarct was resected and trimmed back to the edges of normal-appearing myocardium. A perforation (I em in diameter) was found in the central portion of the interventricular septum toward the apex, which was closed with a Dacron patch by means of interrupted mattress sutures with Teflon pledgets. The free left ventricular wall was approximated with interrupted mattress sutures and reinforced by an overand-over layer. It was then possible to discontinue cardiopulmonary bypass. The postoperative course was uneventful. Eleven months later the patient is leading a normal and active life. Echocardiograms (including a Doppler study) obtained 6 months after the operation showed no residual shunting. A retrospective review of the original ventriculogram revealed that the ventricular cavity was small in relation to the cardiac shadow, and contrast material could be seen faintly opacifying the pericardial sac. CASE 2. A 59-year-old woman had an anterior transmural myocardial infarction. Twenty-two hours after admission she was found to be gray, sweating, and hypotensive. On auscultation a pansystolic murmur was heard which was maximal at the left sternal border. An echocardiogram showed a vigorous well-contracting left ventricle, and Doppler ultrasound showed 0

Operative findings

Autopsy

8 17

48 hr after MI: Hemopericardium rupture of anterior LV wall, apical VSD 21 days after M I: Rupture of anterior LV wall, central VSD 20 days after MI: Hemopericardium, rupture of anterior LV wall, anteroapical VSD

Bilateral lung infiltrates responded to medical therapy; asymptomatic

Uneventful recovery: asymptomatic 1 yr later Uneventful recovery; asymptomatic 4 mo later

evidence of a ventricular septal defect in the lower part of the anterior septum. No pericardial effusion was demonstrated. Cardiac catheterization was performed on the fourth day after the infarction. The left ventricular angiogram showed a large anteroapical aneurysm with opacification of the right ventricle and pulmonary artery. The left anterior descending artery was occluded and there was no significant disease in the other coronary arteries. The saturations obtained were as follows: right atrium, 60%; right ventricle, 88%; pulmonary artery, 73%; aorta, 95%. The patient's condition was stabilized with dopamine and dobutamine infusions. On the seventeenth day after admission, pulmonary edema developed, which responded to diuretics. An operation was performed 3 days after this episode. The heart was exposed through a median sternotomy and cardiac tamponade was relieved by incising the stretched pericardium, which improved the blood pressure from 80 to 100 mm Hg. On cardiopulmonary bypass, the patient was systemically cooled to 25° C and the heart was electrically fibrillated. A small perforation at the superior margin of the infarct involving the left ventricular free wall was found. The infarcted area was excised to expose the septal perforation, which was located at the anteroapical portion and was larger than 1.5 cm in diameter. The defect was patched and the free wall of the left ventricle closed. The patient was easily weaned from cardiopulmonary bypass. She had an unremarkable

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Aravot et al.

postoperative course. Six months later the patient was free of heart failure and entirely free of symptoms. Again, on retrospective review of the ventriculogram, opacification of the pericardia I sac was visible. Discussion The combination of septal perforation and ventricular rupture after acute myocardial infarction is rare. We have found only three other cases in the literature." 15. 16 Table I provides the data on these cases together with our patients. Clinical features. All five patients had occlusion of a single dominant vessel without any significant disease in the other coronary arteries. One had occlusion of a dominant circumflex artery, one had occlusion of a dominant right coronary artery (both had posterior wall myocardial infarction and rupture), and the other three had occlusion of the left anterior descending artery (with anterior wall myocardial infarction and rupture). Four patients had no previous history of heart disease and no known risk factors, and for all five patients it was the first myocardial infarction. These observations might lead to the speculation that acute occlusion superimposed on a previously noncritical coronary stenosis, with the consequent absence of an effective collateral circulation, resulted in extensive myocardial necrosis and subsequent perforation and rupture. London and London" described a higher prevalence of postmortem coronary thrombosis in patients with cardiac rupture (70% of 47 patients) than in patients having fatal myocardial infarction without rupture (29% of 200 patients). In an additional 6% of the patients with cardiac rupture, acute occlusion was caused by intimal hemorrhage or atheromatous debris. London and London" and others I. 7.17 reported that rupture usually occurs in the setting of the first infarction. Wessler, Zoll, and Schlesinger" demonstrated poor collateral circulation in the area of rupture in all of their 20 patients. Occlusion of only one coronary vessel may prevent impairment of a large portion of the myocardium and thereby may improve the chances of survival after surgical therapy. Renewed chest pain, before perforation or rupture, occurred in most cases reviewed. This phenomenon was found in 55% of 47 cases of cardiac rupture but in only 10% of 200 fatal cases of myocardial infarction without rupture.' Episodes of recurrent severe chest pain may result from slow leakage of blood into the pericardial sac before clinically evident cardiac tamponade." Dissmann and colleagues" reported electromechanical dissociation in 10 of 13 patients with cardiac rupture. This event occurred in one of our patients and two of those from the literature'<" who had frank cardiac rupture.

Thoracic and Cardiovascular Surgery

In all five patients the rupture occurred through the free wall of the left ventricle (two anteriorly and three posteriorly). Bates and associates' reviewed 1200 cases of cardiac rupture and found that more than 90% of cardiac ruptures occur in the left ventricle and usually in the junction of the infarcted and normal myocardium. In the three patients from the literature both perforation and rupture of the free wall occurred within 60 hours after the infarction. However, our two patients had a subacute course with the operation being performed 20 and 21 days after the infarction. This is consistent with the previous reports by O'Rourke," Van Tassel and Edwards," and Qureshi, Rissen, and Gray," who stated that cardiac rupture may have a subacute course. This gradual and episodic process may be comparable to the clinical course of arterial aneurysm, in which massive rupture is often preceded by minor episodes of bleeding.' This raises the possibility that' some cases can be diagnosed before the patient has an irreversible cardiovascular collapse and surgical treatment may be possible. Surgical considerations. Surgical treatment early after myocardial infarction presents a formidable technical challenge because of the friability of the infarcted and adjacent ischemic myocardium. Significant secondary problems include myocardial failure, electrical instability, and threat of recurrent infarction." The operative mortality rate of postinfarction septal defect has been reported to be 42%22: The shorter the interval between the infarction and the operation, the higher the mortality rate. Although delay in the operative treatment of postinfarction septal defect offers significant technical advantages, when septal perforation is combined with ventricular free wall rupture, early operation is mandatory. Three of the five patients whose cases were reviewed survived, which suggests that acceptable results may be obtained from early operation. In none of the patients was a preoperative diagnosis of left ventricular free wall rupture made. The first two patients (Table I) might have been saved by prompt surgical intervention. In the three patients who did survive, cardiac rupture was an incidental finding at the time of operation. In our two patients, opacification of the pericardium was identified only retrospectively, after the operative procedure. From our experience and the information in the literature, we believe the following factors should be considered when planning the operative procedure. Femoral cannulation will prevent exsanguination, and electrical fibrillation of the heart, once cardiopulmonary bypass has been established, may prevent dislodgment of mural thrombus. Surgical repair of postinfarction ventricular septal defects early after the infarction yielded unsatisfactory

Volume 97 Number 6 June 1989

results when the defect was exposed through a right ventriculotomy." Kitamura, Mendez, and Kay24 first demonstrated the efficacy of the left ventricular approach to postinfarction septal defects. They reported a shunt recurrence rate of 11% with the left ventricular approach, in contrast to 42% with the right ventricular approach. This observation suggests that it may be advisable to repair the septal defect through an incision in the infarcted left ventricle and then resect the infarcted muscle. The main technical advance that permitted early surgical repair of infarcted tissues was the introduction of Teflon felt strips for buttressing the necrotic myocardial tissues." These strips are essential for repair of both the septal perforation and the ventricular free wall rupture. Closure of the septal defect should be followed by infarctectomy. Javid and co-workers" reported on a series of 30 patients with septal defects and left ventricular aneurysms. Ten underwent repair of the septal defect without infarctectomy, and only two patients survived for more than 2 months after the operation. Seventeen of 20 patients who underwent both infarctectomy and repair of septal perforation recovered from the operation and lived 2 months or longer. When the infarction includes both ventricles and the septum, amputation of the entire apex of both the right and left ventricle, including the apical septal perforation, can be performed. 27 The necessity for concomitant coronary artery bypass grafting in the treatment of postinfarction mechanical complications is unsettled." However, in all five cases of combined septal perforation and cardiac rupture, there was occlusion of only one coronary artery and revascularization was unnecessary. In conclusion, from our experience with two cases and a review of the literature, we have found that the diagnosis of combined perforation of the interventricular septum and rupture of ventricular free wall is difficult to establish. However, if this condition is suspected before the patient has an irreversible cardiovascular collapse, satisfactory results may be obtained from surgical repair. REFERENCES I. Friedberg CK. General treatment of acute myocardial infarction. Circulation I969;40(Pt 2):IV252-60. 2. Griffiths GC, Hedge B, Oblath RW. Factors in myocardial rupture: an analysis of two hundred and four cases at Los Angeles County Hospital between 1924 and 1959. Am J Cardiol 1961 ;8:792-8. 3. Mundth ED. Rupture of the heart complicating myocardial infarction. Circulation 1972;46:427-9. 4. London RE, London SB. Rupture of the heart: a critical

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defect following myocardial infarction. Ann Thorac Surg 1979;27:580-9. 24. Kitamura S, Mendez A, Kay JH. Ventricular septal defect following myocardial infarction: experience with surgical repair through a left ventriculotomy and review of the literature. J THORAC CARDIOVASC SURG 1971; 61:186-99. 25. Loisance DY, Cachera JP, Poulain H, Aubry P, Juvin AM, Galey JJ. Ventricular septal defect after acute myocardial infarction: early repair. J THORAC CARDlOVASC SURG 1980;80:61-7.

The Journal of Thoracic and Cardiovascular Surgery

26. Javid H, Hunter JA, Najafi H, Dye WS, Julian oc. Left ventricular approach for the repair of ventricular septal perforation and infarctectomy. J THORAC CARDIOVASC SURG 1972;63:14-24. 27. Daggett WM, Burwell LR, Lawson DW, Austen WG. Resection of acute ventricular aneurysm and ruptured interventricular septum after myocardial infarction. N Engl J Med 1970;283:1507-8.

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