Surgical Treatment of Papillary Muscle Rupture

Transcription

1 Surgical Treatment of Papillary Muscle Rupture Duncan A. Killen, M.D., William A. Reed, M.D., Suchint Wathanacharoen, M.D., Gary Beauchamp, M.D., and Barry Rutherford, M.D. ABSTRACT Between 1971 and 1979, 16 patients underwent mitral valve replacement for papillary muscle rupture after infarction. Nine of these patients were operated on within 3 days of papillary muscle rupture. Eight patients had low cardiac output syndrome prior to operation. Six patients had concomitant coronary artery bypass, and 1 patient had resection of an associated left ventricular aneurysm. There were 3 operative deaths (19% mortality). Surviving patients have been followed for a total of 49 patientyears. There have been 2 late deaths, each a result of coronary artery disease. Six of the 11 surviving patients are asymptomatic; the others are in New York Heart Association Functional 1 or 111. The actuarial 5year survival was 75%. These data support the concept that an aggressive attitude should be taken toward early diagnosis and surgical treatment of postinfarction papillary muscle rupture. Approximately 1 to 2% of deaths due to acute myocardial infarction result from rupture of a left ventricular papillary muscle [l41. The majority of patients with papillary muscle rupture die within a few days, and only about 15% of patients will live longer than 1 or 2 months with medical treatment alone [5]. Austen and colleagues [6], in 1965, were among the first to report successful replacement of the mitral valve for postinfarction papillary muscle rupture. The current report details our experience with surgical therapy for postinfarction papillary muscle rupture at the MidAmerica Heart Institute. Material and Methods During the 9year period ending December, 1979, the diagnosis of rupture of a left ventricular papillary muscle following infarction was From the MidAmerica Heart Institute of the Saint Luke s Hospital, Kansas City, MO. Accepted for publication Feb 18, Address reprint requests to Dr. Killen, Midwest Cardiovascular Consultants, Inc, 51 Medical Plaza Bldg, 432 Wornall Rd, Kansas City, MO documented in 16 patients. Thirteen of the patients were men. The mean age was 64.3 years (range, 54 to 78 years). Five of the 16 patients sustained the muscle rupture while hospitalized for an acute myocardial infarction at the Saint Luke s Hospital. The other 11 patients were transferred to this hospital after sustaining the papillary muscle rupture. Papillary muscle disruption was confirmed at operation in each of the 16 patients. Patients with papillary muscle necrosis without disruption, other variants of papillary muscle dysfunction, or ruptured chordae tendineae were excluded. Review of the hospital records, catheterization data, operative findings, and clinical course was performed for each patient. Patients were characterized as exhibiting low cardiac output syndrome if hypotension, inadequate peripheral perfusion, and oliguria resistant to volume loading developed, or if continuous infusions of inotropic drugs were required or if both these conditions were met. Patients were characterized as exhibiting congestive heart failure if signs of pulmonary congestion, tachycardia, and fluid retention without the signs of shock just mentioned developed. The number of coronary arteries with angiographically important obstruction was determined as previously described [7]. Operation was performed under mild hypothermia using a disposable bubble oxygenator and a standardized plan of cardiopulmonary bypass. Intermittent ischemic cardiac arrest was used except for the last 2 patients in the series in whom hyperkalemic cold cardioplegia was employed. The mitral valve replacement was performed using routine operative techniques. Detailed analysis was made of the postoperative complications and late course. Late followup was accomplished by repeat hospitalization, office visits, communication with the referring physician, or telephone contact with the patient. Survival was calculated using the lifetable method. 243

2 244 The Annals of Thoracic Surgery Vol 35 No 3 March 1983 Results The acute infarction causing the papillary muscle rupture was transmural by electrocardiographic criteria in 11 patients (Table 1). In 9 of these 11 patients, the infarct involved the inferior left ventricular wall. Five patients had clinical or electrocardiographic evidence or both of a subendocardial myocardial infarction. Catheterization of the right heart was performed in 11 patients, left ventriculography in 15, and coronary angiography in 15. Preoperative monitoring of the pulmonary artery with a SwanGanz catheter was utilized in 6 patients. The systolic pulmonary artery pressures, pulmonary artery wedge V waves, and left ventricular ejection fractions are depicted in the Figure. Radiographic or hemodynamic evidence of severe mitral regurgitation was demonstrated in each patient. A prolapsing or flail mitral valve leaflet was evident in most instances, and in 1 patient the attached papillary muscle tip could be identified as a hypermobile left ventricular filling defect. There was akinesia or hypokinesia of the area of myocardial infarction on left ventriculography. There was singlevessel coronary artery disease in 7 patients (right coronary artery, 6 patients; circumflex coronary artery, 1 patient). Seven patients had doublevessel disease (right coronary artery combined with circumflex coronary artery in 4 patients, and right coronary artery combined with anterior descending coronary artery in 3), and 1 patient had occlusive lesions of all three coronary arteries. It is evident that 14 of these 15 patients had significant lesions of the right coronary artery. Eight patients exhibited a rapidly deteriorating course and then had low cardiac output syndrome (Table 2). Seven of these 8 patients were operated on within the first 3 days following papillary muscle rupture. In addition to preoperative infusions of inotropic drugs for the low cardiac output syndrome, 2 of these patients had been placed on mechanical ventilators and 1, on intraaortic balloon pump support. Four patients had experienced successful cardiorespiratory resuscitation, 1 patient had required cardiac pacing, and 1 had undergone multiple transfusions for an acute gastrointestinal bleed preoperatively. In 8 patients, signs and symptoms of only congestive heart failure evolved. Four of these patients were operated on within the first 6 days after papillary muscle rupture, and the other 4 underwent operation late (15 days to 4 months) after rupture. There was rupture of the posteromedial papillary muscle in 12 patients and of the anterolateral papillary muscle in 4 patients. The portion of the papillary muscle disrupted was recorded at operation to be total in 2 patients and partial in 8. This information was not recorded for the remaining 6 patients. The mitral valve was replaced with a StarrEdwards compositeseat prosthesis in 3 patients and a Bjork Shiley prosthesis in the remaining 13 patients. Concomitant coronary artery bypass was performed in 6 patients (single bypass in 4 and double in 2). Resection of an associated left ventricular aneurysm was performed in 1 patient; closure of a patent foramen ovale was carried out in another patient; in 1 patient an indwelling intraaortic balloon was removed, and the femoral artery was reconstructed by femoral endarterectomy and a patch arterioplasty at the site of balloon introduction. Major postoperative complications were experienced by 11 of the 16 patients (see Table 2). The most frequent complication was low cardiac output syndrome, which was observed in 1 patients. It was associated with respiratory insufficiency requiring prolonged ventilatory support in 5 patients and with renal insufficiency (creatinine greater than 5 mg per 1 ml) in 3 patients, one of whom required hemodialysis. Low cardiac output resulted in 1 death in the operating room (Patient 6, Table 2). In 1 patient, low cardiac output syndrome precipitated a sequence of complications including respiratory insufficiency and renal shutdown, culminating in death on the seventeenth postoperative day (Patient 9, Table 2). Brain damage consisting of severe diffuse central nervous system depression was present in 1 patient; there was marked improvement, but mild, permanent residua have persisted. Also, 1 patient who awoke with hemiplegia has permanent hemiparesis. Mental cloudiness and confusion were present in 3 other patients, but there was complete recovery prior to discharge from the hospital. One patient, seemingly doing well,

3 245 Killen et al: Papillary Muscle Rupture Table 1. Pathological Anatomy Relative to Location of lnfarct No. of Type of Infarct Arteries Obstructed" Muscle Ruptured Location of Subendo Postero Antero Infarct Transmural cardial One Two Three medial lateral Inferior Lateral Anterior "Arteriogram not performed in 1 patient. died suddenly eleven hours postoperatively (Patient 14, Table 2). Emergency thoracotomy revealed rupture of the left ventricle at the site of the myocardial infarction. Other major complications were recurrent ventricular tachycardia, pneumonia, and pericardial tamponade (see Table 2). Thirteen patients (81%) were discharged from the hospital 1 to 51 days (mean, 24 days) following mitral valve replacement. These patients have been followed for a total of 49 patientyears. Six patients are in New York Heart Association Functional 1 or I11 with symptoms of congestive heart failure, and 7 patients have been without evidence of congestive heart failure during the late postoperative period. One patient has experienced postoperative angina (Class 11), and all other patients have been an Preoperative hemodynumic data included systolic pulmomy artery pressure (SYS PAP), pulmonary artery wedge V wave (WEDGE"V"), and left ventricular ejection fiac gina free. Late nonfatal comp~ications have tion (LVEF). The means (2 one standard dmiation) of these measurements were 53.9 * 13.1 mm Hg, 43. * been thrombotic occlusion of the mitral valve 17.2 mm Hg, and 54.9 * 15.3%, respectively. prosthesis 9 months postoperatively, which NUMERICAL SCALE SYS PAP IrnmHgl WEDGE V lmmhgl W UTEF (%I W W W 1

4 246 The Annals of Thoracic Surgery Vol 35 No 3 March 1983 Table 2. Clinical Course Patient No., Clinical Time of Operative Age (yr), Sex Presentation Operation" Complications Followupb 1. 64, M 2. 55, M 3. 61, M 4. 6, M 5. 78, F 6. 66, F 7. 72, M 8. 67, F 9.54, M 1. 57, M , M , M , M , M , M , M?15 d 11 d 2d 23 d 2d?5 wk 6d 3d 2d 3d 4 mo 5d ; respiratory insufficiency; recurrent ventricular tachycardia ; respiratory insufficiency; renal failure; pneumonia; sepsis; CNS injury ; pericardial tamponade; confusion ; hemiparesis and death ; confusion ; respiratory insufficiency; renal failure; and death ; respiratory insufficiency; renal failure ; respiratory insufficiency; confusion Left ventricular rupture and death Acute MI and death 1 ' Sudden death Class l (7 yr 6 mo) (5 yr 7 mo) (5 yr 4 mo) (5 yr 3 mo) (4 yr 6 mo) (4 yr 1 mo) (5 wk) (3 yr 5 mo) (3 yr 2 mo) (3 Yr) (2 yr 1 mo) (2 yr 2 mo) (2 yr 1 mo) "Time after papillary muscle rupture. bcurrent symptomatic status (New York Heart Association Functional Class) or causes of late deaths. 'Cerebrovascular accident 3 years postoperatively. dpatient required replacement of thrombosed mitral valve prosthesis 9 months postoperatively. = congestive heart failure; = low cardiac output syndrome; CNS = central nervous system; MI = myocardial infarction. necessitated repeat mitral valve replacement, and a cerebral vascular accident with resultant hemiparesis, which occurred 3 years postoperatively (see Table 2). There have been 2 late deaths. One patient discharged from the hospital on the thirteenth postoperative day suddenly and unexpectedly died five weeks postoperatively. The other late death resulted from an acute myocardial infarction experienced 7 years 6 months following mitral valve replacement. The actuarial 5year survival was 75%. Comment Papillary muscle rupture occurring after infarction was described by Merat in 183 [4, 51. Davidson [4] in 1949 was among the first to provide an antemortem diagnosis, and Austen and colleagues [6] were among the first to publish the results of successful surgical therapy. Rupture of a left ventricular papillary muscle after infarction occurs infrequently and is found in approximately 1 to 2% of patients dying of myocardial infarction [l41. Survival, once papillary muscle rupture occurs, is very poor if medical therapy alone is utilized; approximately 3% of the patients will survive twentyfour hours, and approximately 1% will survive 2 months [5]. The papillary muscles have a blood supply similar to that of all other endocardia1 muscles of the left ventricular wall, and therefore are

5 247 Killen et al: Papillary Muscle Rupture very susceptible to ischemia [8]. The posteromedial papillary muscle more frequently becomes ischemic when coronary blood flow is jeopardized [9]. This vulnerability has been related to the fact that its blood supply usually is dependent entirely on the one coronary artery that supplies the crux of the heart, whereas the anterolateral papillary muscle is often in a watershed area between two major coronary branches and is supplied by both arteries [351. The posteromedial papillary muscle ruptures much more frequently than the anterolateral papillary muscle as a consequence of its tenuous collateral arterial pattern [351. The typical patient has rupture of the posteromedial papillary muscle as a result of an inferior transmural myocardial infarction associated with either singlevessel or multivessel coronary artery disease; however, the anterolateral papillary muscle, ruptured in a substantial number of patients, is associated with a lateral or anterior myocardial infarction or both and more often with multivessel coronary artery disease (see Table 1). In our operative experience, basilar or total papillary muscle rupture has been much less prevalent than that observed in postmortem studies [9, lo]. It is likely that patients with disruption of only a portion of the papillary muscle survive to be considered for surgical intervention, while those patients with rupture of the total muscle are less apt to survive long enough to come under consideration for surgical therapy [4, 9, 11. Papillary muscle rupture is usually accompanied by abrupt hemodynamic deterioration with the appearance of pulmonary congestion or shock or both [4, 51. The detection of a new systolic murmur may help suggest the correct diagnosis, although the murmur is often not impressive and is sometimes absent. The papillary muscle dysfunction syndrome may present a clinical picture similar to that of papillary muscle rupture; however, the correct diagnosis can often be suspected from the clinical findings [4, 51. Papillary muscle dysfunction is usually accompanied by signs of mitral insufficiency, which vary in severity, and there is no abrupt onset as is seen in papillary muscle rupture. On the other hand, papillary muscle rupture usu ally results in a sudden, severe, and unrelenting picture of cardiac decompensation. The twodimensional echocardiogram may be a helpful means of noninvasively differentiating between papillary muscle rupture and papillary muscle dysfunction [ 111. Left ventriculography is also helpful in differentiating between papillary muscle disruption and papillary muscle dysfunction. However, there are instances when the differentiation is made with certainty only at operation or postmortem examination. Ruptured chordae tendineae occur rarely in the setting of an acute myocardial infarction, but this syndrome can mimic that of the ruptured papillary muscle precisely and may be difficult to distinguish from it. Rupture of the interventricular septum after infarction results in a catastrophic syndrome clinically similar to that caused by papillary muscle rupture, and sometimes the differentiation cannot be made on clinical grounds [5, 6, 91. The use of a balloon flotation catheter in the pulmonary artery for analysis of oxygen saturation and pulmonary artery wedge pressure may help in bedside differentiation between these two entities. Left ventriculography will distinguish definitively between these two complications of acute myocardial infarction. When papillary muscle rupture is suspected and low cardiac output syndrome develops, we believe that the patient should undergo emergency cardiac catheterization and coronary angiography. This permits not only documentation of severe mitral insufficiency and definition of left ventricular function but also demonstration of the pathological anatomy of the coronary artery. Some [2, 91 have advocated use of the intraaortic balloon pump for support of such patients preliminary to performing cardiac catheterization. This procedure was done only once in our patients; the balloon support had been initiated in another hospital before the patient was transferred to our institution. We think that patients who have papillary muscle rupture and low cardiac output syndrome should undergo emergency operation. Mitral valve replacement should be done, and concomitant coronary artery bypass should be performed in instances where obstructed arteries

6 248 The Annals of Thoracic Surgery Vol 35 No 3 March 1983 are supplying areas of noninfarcted myocardium. When rupture of the papillary muscle occurs and symptoms of congestive heart failure, without those of shock, develop, the patient is best managed medically over the initial period if there is continuing improvement, and should have definitive cardiac catheterization whenever elective surgical intervention is contemplated [3]. Also, patients who are seen late after papillary muscle rupture may have a clinical course less suggestive of the diagnosis. Under these circumstances, elective catheterization and mitral valve replacement are indicated if the mitral regurgitation is clinically severe. Since the successful mitral valve replacement for postinfarction papillary muscle rupture in 1965, there have been reports from many medical centers of surgical therapy for this entity [4, 1, 121. There has been a progressive increase in the salvage of such patients, and operative survivals comparable to the 81% observed in the present series have been obtained [lo, 12, 131. In the present group of patients, it is striking that single and doublevessel coronary artery disease predominated. This is at odds with the experience reported by Gerbode and associates [4]. However, it is not clear from their report whether or not patients with papillary muscle dysfunction (without rupture) were included. Also, it is evident that most of the patients in the present series had retention of relatively good left ventricular function (see Figure); the potential for adequate cardiac reserve and prolonged survival are real in many of these patients [lo]. The two late nonfatal complications in the present series were related to the valve prosthesis, whereas the 2 late deaths were cardiac in nature but were most likely due to the intrinsic coronary artery disease. Although this experience is limited, the late survival of 75% at 5 years appears to justify an aggressive attitude toward early diagnosis and surgical treatment of papillary muscle rupture. References 1. Roberts WC: Morphologic features of certain myocardial complications of acute myocardial infarction. In Moran JM, Michaels LL (eds): Surgery for the Complications of Myocardial Infarction. New York, Grune & Stratton, 198, p 1 2. Tommaso CL, Lesch M: Current diagnostic methods and medical approaches to the complicated infarction. In Moran JM, Michaels LL (eds): Surgery for the Complications of Myocardial Infarction. New York, Gmne & Stratton, 198, P Morrow AG, Cohen LS, Roberts WC, et al: Severe mitral regurgitation following acute myocardial infarction and ruptured papillary muscle. Circulation 37,38:Suppl 2:124, Gerbode F, Hetzer R, Krebber HJ: Surgical management of papillary muscle rupture due to myocardial infarction. World J Surg 2:791, Sanders RJ, Neubuerger KT, Ravin A: Rupture of papillary muscles: occurrence of rupture of the posterior muscle in posterior myocardial infarction. Dis Chest 31:316, Austen WG, Sanders CA, Averill JH, Friedlich AL: Ruptured papillary muscle. Circulation 32:597, Killen DA, Reed WA, Wathanacharoen S, et al: Reversion to "normal" survival following coronary artery bypass. South Med J 75:96, Brazier JR, Maloney JV, Buckberg GD: Papillary muscle ischemia with patent coronary arteries. Surgery 78:43, Vlodaver Z, Edwards JE: Rupture of ventricular septum or papillary muscle complicating myocardial infarction. Circulation 55:815, Wei JY, Hutchins GM, Bulkley BH: Papillary muscle rupture in fatal acute myocardial infarction. Ann Intern Med 9:149, Mintz GS, Victor MF, Kotler MN, et al: Twodimensional echocardiographic identification of surgically correctable complications of acute myocardial infarction. Circulation 64:91, Austen WG, Sokol DM, DeSanctis RW, Sanders CA: Surgical treatment of papillary muscle rupture complicating myocardial infarction. N Engl J Med 278:1137, Najafi H, Javid H, Hunter JA, et al: Mitral regurgitation secondary to ischemic heart disease. In Moran JM, Michaels LL (eds): Surgery for the Complications of Myocardial Infarction. New York, Gmne & Stratton, 198, p 157