Papillary muscle rupture complicating acute myocardial infarction

Papillary muscle rupture complicating acute myocardial infarction

Papillary Muscle Rupture Complicating Acute Myocardial Infarction Treatment With Mitral Valve Replacement and Coronary Bypass Surgery David L. Nunley...

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Papillary Muscle Rupture Complicating Acute Myocardial Infarction Treatment With Mitral Valve Replacement and Coronary Bypass Surgery

David L. Nunley, MD, Portland, Oregon Albert Starr, MD, Portland, Oregon

Complete rupture of a papillary muscle occurs infrequently after acute myocardial infarction, but is typically associated with acute left ventricular failure, pulmonary edema, and relentless clinical deterioration. The early mortality rate after such an event is approximately 80 to 90 percent [I]. Surgery to restore competence to the mitral valve is imperative to alleviate the hemodynamic strain imposed by severe mitral insufficiency. Coronary bypass surgery in the setting of acute infarction may restore blood flow to partially ischemic areas of myocardium, prevent symptoms, and improve survival. Our experience with six such cases is described. Material

and Methods

From 1969 to 1980,717 mitral valve replacements were performed at The Oregon Health Sciences University and St. Vincent Medical Center. Of these, 64 patients also had concurrent coronary bypass surgery. Twenty patients were found to have pure mitral regurgitation on an ischemic basis, the majority being consequent to annular dilatation or papillary muscle dysfunction. Six patients were found to have complete or partial rupture of a papillary muscle; these cases form the basis for this report. Follow-up was achieved through regular questionnaires, telephone contact, and communication with referring physicians. Case Reports Case 1. A 64 year old diabetic man presented with a long history of cigarette smoking and hypertension. On June 10, 1973 he was hospitalized with an acute infarction of the inferior wall. Physical examination revealed a loud holosystolic murmur at the cardiac apex with radiation to the axilla, a third heart sound, and bibasilar rales. Chest roentgenography confirmed bilateral “butterfly” infiltrates consistent with pulmonary edema. This patient’s clinical status was New York Heart Association (NYHA) class IV. From the Division of CardiopulmonarySurgery, The Oregon Health Sciences University, and St. Vincent Medical Center, Portland, Oregon. Requests for reprints stwuld be aMessed to David L. Nunley, M). Division of Cardiopulmonary Surgery, The Oregon Health Sciences University, 3161 SW Sam Jackson Park Road, Portland, Oregon 97201. Presented at the 69th Annual Meeting of the North Pacific Surgical Association, Spokane, Washington, November 12 and 13. 1962.


Cardiac catheterization demonstrated an ejection fraction of 39 percent with a mean pulmonary artery pressure of 26 mm Hg, and 214 mitral regurgitation. Coronary angiography showed complete occlusion of the right coronary artery, a single 90 percent stenosis of t.he left anterior descending artery and multiple 90 percent narrowings of the circumflex vessel. The patient was treated with diuretics and vasodilators and taken to surgery on June 13 where the posterior papillary muscle as well as several chordae attaching to the anterior muscle were found to be ruptured. The mitral valve was replaced with a 6320 Starr-Edwards prosthesis, and coronary bypass surgery was performed to the left anterior descending and right coronary arteries after endarterectomy of the latter vessel. Cross-clamp time was 39 minutes for valve replacement. The patient became profoundly hypotensive shortly after decannulation and required open cardiac massage and reinstitution of cardiac bypass. He was eventually separated from the heart-lung machine but needed high doses of vasopressors to maintain his blood pressure. Renal failure subsequently developed. Peritoneal dialysis was begun, but on the 15th postoperative day, septic shock developed secondary to a Klebsiella pneumoniae bacteremia. He was stabilized with antibiotics and fluid resuscitation, but died 5 days later after a second episode of severe shock.

Case 2. A 70 year old woman suffered her first myocardial infarction in March 1973. Although no murmur was heard during this initial hospitalization, congestive heart failure developed shortly after her discharge and therapy with digoxin and diuretics was begun with marginal control of symptoms. She was readmitted in NYHA class IV condition in July 1973 and at that time, was noted to have a left ventricular heave, a loud pulmonary component of the second heart sound, a 516 blowing holosystolic apical murmur, and a third heart sound. Electrocardiography demonstrated remote inferior myocardial infarction. Angiographic study showed 90 percent stenoses of both the left anterior descending and right coronary arteries with a small, diffusely diseased circumflex system. Pulmonary artery wedge pressure was 15 mm Hg, and gross 4/4 mitral regurgitation was noted. She was taken to surgery where rupture of two of the apical heads of the posterior papillary muscle was found. A 6320 Starr-Edwards prosthesis was placed, and both the left anterior descending and the posterior descending arteries were grafted. Postoperatively, the patient experienced transient atrioventricular block,

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Papillary Muscle Rupture After Myocardial Infarction

but otherwise her course was unremarkable. She was discharged on the 15th postoperative day and died 7 years later from a noncardiac cause. Case 3. A 49 year old man was admitted to the hospital on April 16, 1978 in cardiogenic shock. Infarction of the inferior wall was confirmed by elevations of enzyme levels and electrocardiographic changes. On admission, a mitral insufficiency murmur was noted. Angiograms were immediately obtained; they demonstrated 3/4 mitral regurgitation with a pulmonary artery wedge pressure of 25 mm Hg and marked hypokinesis of the entire inferior wall. In addition, diffuse, severe occlusive disease was seen in both the left anterior descending and circumflex vessels with occlusion of the right coronary artery. Because of this patient’s precarious condition, surgery was deferred in the hope of gaining some improvement with medical treatment. However, he continued to deteriorate and was taken to surgery on April 19 on an emergent basis. In addition to an acute inferior wall infarct, complete rupture of the main trunk of the anterior papillary muscle was found. Saphenous vein grafts were placed to the left anterior descending and obtuse marginal arteries, and the valve was replaced using a 6400 Starr-Edwards prosthesis. Cardioplegia was used for myocardial protection; the longest single period of aortic cross-clamp was 30 minutes. This patient had multiple postoperative complications including adult respiratory distress syndrome, massive upper gastrointestinal hemorrhage requiring emergency antrectomy and vagotomy on the 22nd postoperative day, and empyema of the right side of the chest. These were all treated successfully and he was discharged after a 6 week hospital stay. He is currently alive and well. Case 4. A 70 year old woman sustained an infarction in 1968 from which she recovered uneventfully. In May 1978 she had a second infarction with complications of pulmonary edema and continued angina. Angiography revealed hypokinesis of the posterior inferior wall, 90 percent stenosis of the left anterior descending artery, occlusion of the circumflex artery, and nonvisualization of the right system. Left ventricular end-diastolic pressure was 40 mm Hg with a mean pulmonary artery pressure of 50 mm Hg and 4/4 mitral regurgitation. The patient suffered a cardiac arrest during catheterization and was resuscitated but remained comatose for nearly 8 hours before regaining consciousness. On June 2 she was taken to surgery where a massive inferolateral infarction was noted. The posterior papillary muscle was necrotic and the main trunk ruptured. A 6120 Starr-Edwards mitral prosthesis was implanted and coronary bypass surgery was performed to the left anterior descending artery. The exposure was very difficult due to a small left atrium. Cross-clamp time was 50 minutes. Intraaortic balloon pumping was required to wean the patient from cardiopulmonary bypass; this was continued for 5 days postoperatively. During this time, ischemic demarcation of both feet occurred as a consequence of poor cardiac output and severe peripheral vascular disease. The patient had intermittent periods of rapid atria1 fibrillation-flutter and during one of these episodes, a right hemiparesis and aphasia developed which were thought to represent an embolic stroke. Her hemodynamic status slowly improved and she was transferred to the referring hospital free from all forms of support on the 17th postoperative day. She did well and died 3 years later from a ruptured abdominal aortic aneurysm.

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Case 5. A 54 year old man had documented infarctions in February and again in August of 1975. He continued to have stable angina until he suffered a third infarction on December 4,1978. A 4/6 pansystolic murmur at the apex was noted on December 10, and an echocardiogram was obtained and interpreted as normal except for increased heart size. He was discharged with beta-blockers and diuretics, but heart failure developed shortly thereafter. His beta-blockers were then discontinued and he was given digoxin and readmitted in February 1979 for rapid atria1 fibrillation. At that time his clinical status was NYHA class III. The apical murmur was again noted, but he had no physical signs of congestive failure. Cardiac catheterization demonstrated 2/4 mitral regurgitation with a pulmonary artery wedge pressure of 15 mm Hg. Focal 90 percent stenoses were noted in the left anterior descending and circumflex vessels with occlusion of the right coronary artery. At operation on February 5, the annulus was dilated and one apical head of the anterior papillary muscle was ruptured with marked leaflet prolapse. Triple coronary bypass surgery was performed and the mitral valve was replaced with a 6400 Starr-Edwards prosthesis. His postoperative course was uncomplicated. The patient is currently alive and well. Case 6. A 69 year old diabetic woman sustained an inferolateral myocardial infarction in April 1979. She was hospitalized at another hospital where a new apical blowing murmur was first heard on May 20,1979. At that time the patient’s clinical status was NYHA class IV. She was transferred to St. Vincent Medical Center with severe pulmonary edema. On arrival she was already receiving nitroprusside and dopamine and had a blood pressure of 90 mm Hg. Catheterization revealed a left ventricular end-diastolic pressure of 25 mm Hg, a pulmonary wedge pressure of 27 mm Hg, and 4/4 mitral regurgitation. The right dominant system was normal, but there was a focal 95 percent stenosis of the left anterior descending artery with the circumflex vessels appearing small but not diseased. A large aneurysm involving the left ventricular inflow area was noted. At operation, complete disruption of the trunk of the anterior papillary muscle and a golfballsize aneurysm along the lateral wall were found. The aneurysm was excised, the mitral valve was replaced with a 6400 Starr-Edwards prosthesis, and a single vein graft, was performed to the left anterior descending artery. Postoperatively, the patient required balloon pump support for 2 days, after which time she was hemodynamically stable. Heart failure continued however, and she died 1 month later.

Comments The two papillary muscles of the left ventricle are derived from embryologic modification of the trabeculae carneae and range in appearance from discrete cylindrical muscle bellies to exaggerated trabeculations. They are located beneath the corresponding commissures of the mitral valve, and give attachment to the chordae tendinae from one of several apical heads that arise from the main muscle trunks. Each papillary muscle sends chordae to both leaflets. The anterior papillary muscle generally receives its primary blood supply from obtuse marginal branches of the left circumflex artery as well as col-


Nunley and Starr

Figure l.mpleie papillary muscle rupture affect& the main trunk of the posterior muscle. In this instance, a secondary posterlor trunk Is also present.

lateral flow from the left anterior descending vessel. The posterior descending artery provides blood to the posterior papillary muscle. This vessel may arise from either the right coronary or left circumflex artery, depending on which is dominant. Penetrating epicardial branches merge to form a subendocardial plexus. Because the papillary muscles are the thickest portion of the subendocardial muscle, they are the most vulnerable to ischemia [I]. Frank rupture of a papillary muscle occurs in 1 to 5 percent of myocardial infarctions, and is associated with a strikingly high mortality rate [2,3]. The clinical features are left ventricular failure, pulmonary edema, and shock, occurring 2 to 7 days after infarction. Death is immediate in a third of such patients, half die within 24 hours, and only a fifth survive beyond 7 days [2]. The hemodynamic burden imposed by the development of sudden massive mitral regurgitation causes ventricular overload and decompensation, particularly when it occurs in the setting of acute ischemic injury. The extent of myocardial infarction is typically not great in these patients [3] however, and residual ventricular function may be sufficient to sustain life for a variable length of time, depending on the degree of papillary muscle rupture. Complete disruption of the papillary muscle trunk (Figure 1) will cause loss of roughly half of the support to both leaflets, overwhelming regurgitation, and severe pulmonary edema or cardiogenic shock. Median survival is 3 days [3]. Lesser degrees of mitral regurgitation result when one or more apical heads are torn (Figure 2); the severity of heart failure is then dependent on intrinsic ventricular function [4].


F&re 2. Partlal mpture of the papMary muscle InvoMng an @cal head of the posterlor muscle.

Because of the less extensive collateral blood supply, rupture of the posterior papillary muscle occurs 6 to 12 times more frequently than does anterior muscle dehiscence [2]. The latter is generally seen after anterior or lateral wall injury, whereas posterior papillary muscle rupture is usually associated with inferior infarction. Ruptures classically occur an average of 4 days after myocardial infarction since the amount of collagen present in the infarcted tissue is at its lowest during the first week. Wei et al [3] noted that in patients who die in cardiogenic shock after complete rupture of the papillary muscle, the mean infarct size is modest (19 percent) and the perivalvular myocardium is invariably spared injury. These important morphological findings indicate the following: (1) Circulatory collapse in these patients is due to massive regurgitant flow through the mitral valve rather than ventricular power failure; thus early correction of the mechanical defect can be expected to markedly improve survival since left ventricular function is adequate in most cases. (2) Immediate valve replacement can be securely accomplished in the absence of perivalvular necrosis. The differential diagnosis of papillary muscle rupture includes papillary muscle dysfunction, ruptured chordae tendineae, annular dilatation, extension of infarction, and ventricular septal defect. The finding of a murmur of mitral insufficiency in the immediate postinfarction period is common and nonspecific, occurring in 56 percent of patients [5]. The clinical occurrence of a new murmur within the first week in addition to the sudden development of left heart failure requires further evaluation with echocardiographic or angiographic studies. Dilatation

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Papillary Muscle Rupture After Myocardial

of the left ventricle, mild degrees of left atria1 enlargement, and flail mitral leaflet are most often demonstrated by echocardiography in the patient with papillary muscle rupture. The finding of large “V” waves appearing in the pulmonary artery wedge tracing is a classic hemodynamic sign of mitral regurgitation, although chronic left atria1 dilatation from preexistent mitral valve disease can cause dampening of such pulsations [6]. Increased oxygen saturation of the right ventricle distinguishes postmyocardial infarction ventricular septal defect from papillary muscle rupture. Right anterior oblique views of the mitral valve are most useful for determining the degree of regurgitant flow. The extent of coronary artery disease is evaluated by selective coronary angiography. Since the early mortality rate is high in severely compromised patients with complete papillary muscle rupture, surgery should be performed as soon as the diagnosis is confirmed. Ruptures involving only a few apical heads usually are not as immediately fatal; longer periods of survival, albeit with severe functional impairment, may be possible as noted in Cases 3 and 5. Operation is mandatory before irreversible ventricular dysfunction supervenes. Valve replacement is generally preferred [4,7] although postinfarction papillary muscle repair has been described [8]. Concomitant coronary artery bypass grafting should be performed if angiographically indicated since ischemic heart disease remains the chief cause of death in these individuals [9]. The hemodynamic impairment seen in patients with papillary muscle rupture may predispose to extension of infarction as coronary perfusion is diminished; thus prompt revascularization may serve to limit infarct size and improve ventricular function. Our preferred treatment for either complete papillary muscle rupture or partial rupture with inadequate left ventricular function is immediate mitral valve replacement and coronary bypass surgery. Delayed valve replacement and coronary revascularization may be performed for partial rupture when ventricular reserve is satisfactory. Buckley et al [7] have reported successful mitral valve replacement with coronary bypass surgery in four individuals with rupture of “all or part of one papillary muscle.” All patients were supported by intraaortic balloon pumping preoperatively for 2 to 4 days. Morrow et al [4] described the clinical course of four patients, each of whom had rupture of only a single head of the involved papillary muscle. Although all patients displayed severe heart failure, operation was delayed for 3 to 15 months after the occurrence of infarction; only valve replacement was performed.

Volume 145, May 1983


Summarv _ Six cases of complete or partial rupture of the papillary muscle after acute myocardial infarction are presented. All cases were treated by mitral valve replacement and concomitant coronary bypass surgery. An average delay of 3 days between rupture and operation occurred in the four patients with rupture of the main muscle trunk. The operative mortality rate was 50 percent. Such patients present with acute, florid left ventricular failure secondary to the severe mechanical burden imposed on the newly infarcted heart. The resulting valvular incompetence must be corrected by urgent mitral valve replacement if survival is to be lengthened. Patients with partial or apical head ruptures have a lesser degree of regurgitation and symptoms are largely dependent on intrinsic ventricular function. Both of our patients with partial muscle rupture presented with severe heart failure 2 to 4 months later, and both did well postoperatively. We believe that prompt operation without prolonged attempts at medical stabilization is the key to decreasing operative mortality, especially in instances of complete muscle rupture. Since ischemic heart disease remains the leading cause of death in such patients, coronary artery bypass surgery should be performed in conjunction with valve replacement. References 1. Fox AC, Glassman I, lsom OW. Surgically remediable complications of myocardial infarction. Prog Cardiovasc Dis 1979;21:461-84. 2. Sanders RJ, Neubuerger KT, Ravin A. Rupture of papillary muscle: occurrence of rupture of the posterior muscle in posterior myocardial infarction. Dis Chest 1957;31:31623. 3. Wei JY, Hutchins GM, Bulkley BH. Papillary muscle rupture in fatal acute myocardiil infarction-a potentially treatable form of cardiogenic shock. Ann Intern Med 1979;90:149-53. 4. Morrow AG, Cohen LS, Roberts WC, Braunwald NS, Braunwald E. Severe mitral regurgitation following acute myocardial infarction and ruptured papillary muscle-hemodynamic findings and results of operative treatment in four patients. Circulation 1968;37(suppl II): 124-32. 5. Heikkila J. Mitral incompetence complicating acute myocardial infarction. Br Heart J 1967:29:162-9. 6. Cohn PF. Problems in diagnosing acute mitral regurgitation due to coronary artery disease. Chest 1980;78:416-7. 7. Buckley MJ, Mundth ED, Daggett WM. Gold HK, Leinbach RC, Austen WG. Surgical management of ventricular septal defects and mitral regurgitation complicating acute myocardial infarction. Ann Thorac Surg 1973;16:598-609. 8. Gula G, Yacoub MH. Surgical correction of complete rupture of the anterior papillary muscle. Ann Thorac Surg 1981;32: 88-91. 9. Radford MJ, Johnson RA, Buckley MJ. Daggett WM. Leinbach RC, Gold HK. Survival followina mitral valve reolacement for mitral regurgitation due to coro&ry artery disease. Circulation 1979;6O(suppl 1):39-47.