A clinical comparison of mitral valve repair versus valve replacement in ischemic mitral regurgitation

A clinical comparison of mitral valve repair versus valve replacement in ischemic mitral regurgitation

J THORAC CARDIOV ASC SURG 1988;95: 165- 77 Original Communications A clinical comparison of mitral valve repair versus valve replacement in ischem...

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J THORAC

CARDIOV ASC SURG

1988;95: 165- 77

Original Communications

A clinical comparison of mitral valve repair versus valve replacement in ischemic mitral regurgitation Severe mitral regurgitation caused by acute myocardial infarction bas been a particularly difficult management problem with disappointing clinical results. Over a 75-month period, ending March 31, 1987, 611 patients underwent mitral valveoperations at Duke University Medical Center. Within this group, 55 patients had clearly defined ischemic mitral regurgitation, and 37 of these required emergency operations. Thirty-one of the 55 patients had isolated posterior papillary muscle dysfunction, nine had papillary m~le rupture, and 15 had severe ventricular dysfunction and generalized annular dilatation. Thirty-two patients were treated with primary mitral valve replacement, and 23 had mitral valve repair. In 18, repair was accomplished by a transventricular approach, combining the techniques of commissural annuloplasty, papillary muscle shortening or reimplantation, and infarct exclusion. Transventricular mitral valve repair proved to be safe, expeditious, and effective in restoring valve competence. Although the repair and replacement groups were similar with respect to aU relevant baseline characteristics, improved operative sunival was observed after valve repair, as compared to replacement, both for the overall group (p = 0.03) and for acute papillary muscle dysfunction (p = 0.05). These data suggest that a policy of predominant mitral valve repair, when appropriately applied in patients with ischemic mitral regurgitation, offers the potential for improving therapeutic results.

1. Scott Rankin, MD (by invitation), Michael P. Feneley, MD (by invitation), Mark SU. Hickey, MB, BCh (by invitation), Lawrence H. Muhlbaier, PhD (by invitation), Andrew S. Wechsler, MD, Richard D. Floyd, MD (by invitation), 1. G. Reves, MD (by invitation), Thomas N. Skelton, MD (by invitation), Robert M. Califf, MD (by invitation), James E. Lowe, MD, and David C. Sabiston, Jr., MD, Durham. N.C

herapeutic results of conventional valve replacement and coronary grafting in ischemic mitral regurgitation have been disappointing; in the recent studies that

From the Departments of Surgery, Medicine, and Anesthesiology, Duke University Medical Center, Durham, N.C. Supported by National Institutes of Health Grant Nos. HL09315, HL29536, and HLl7670. Read at the Sixty-seventh Annual Meeting of The American Association for Thoracic Surgery, Chicago, Ill., April 6-8, 1987. Address for reprints: J. Scott Rankin, MD, Department of Surgery, Box 3851, Duke University Medical Center, Durham, NC 27710.

defined patients requmng acute valve replacement, hospital mortality ranged from 48% to 85%.1.5 Outcome was somewhat better (hospital mortality 7% to 29%), although perhaps still suboptimal, in patients managed in the subacute phase, and long-term prognosis after valve replacement for ischemic mitral regurgitation has been especially unfavorable.r? Possible explanations for these findings include (I) the acute nature of clinical presentation, (2) longer global myocardial ischemic times for coronary-valve procedures, (3) difficulty in mitral valve exposure in patients with a small left atrium, (4) detrimental effects of mitral apparatus destruction on left ventricular function, (5) difficulty in 165

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Fig. 2. Initial steps of transventricular mitral valve (MVj reconstruction. The apex of the heart is lifted superiorly, and the ventriculotomy is performed to the left of the posterior descending coronary artery (PDA) through the posterior infarct. The posterior annuloplasty suture is illustrated, as are the posterior (PPM) and anterior (APM) papillary muscles. The ventriculotomy is shown larger for illustrative purposes. See text for details.

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Fig. 1. Categorization into three types was performed objectively on the basis of the right anterior oblique (RAQ) left ventriculogram. A modified center-line regional wall motion analysis was used.!':" wherein the circumference of the right anterior oblique projection was divided into 100 equidistant chords constructed perpendicular to a center line drawn midway between the end-diastolic and end-systolic contours. The shortening fraction for each chord was normalized by defining the average shortening observed for each chord in a normal group of 50 patients as 100% wall motion, and akinesis at 0%. Average chordal shortening was computed for the anterior wall (chords II to 40), the apical region (chords 41 to 60), and the posterior wall (chords 61 to 90). Chords I to 10 and 91 to 100 were omitted from the analysis because of greater variability in defining normal wall motion in the para valvular regions. Type I, Papillary muscle dysfunction. Type II, Papillary muscle rupture. Type III, Severe left ventricular dysfunction. constructing the mitral suture line because of thin normal annular tissue, and (6) significant long-term complications of prosthetic valves. Thus investigation of new therapeutic approaches would seem appropriate. Recent authors have suggested that mitral valve repair in patients with ischemic mitral regurgitation

might circumvent many of these problems. 10. 11 However, no carefully documented data are available comparing mitral valve reconstruction and replacement, and significant differences in patient selection and baseline characteristics may exist for repair operations in many centers. This study compares clinical results obtained with mitral valve repair with those observed after mitral valve replacement in the entire spectrum of patients with ischemic mitral regurgitation.

Methods Patient population. In this study, ischemic mitral regurgitation was defined as incompetence of the mitral valveat 3+ or 4+ ventriculographic levels associated with significant V waves on the pulmonary wedge pressure recording or congestive heart failure, or both; the regurgitation had to begin during an acute myocardial infarction, to result from angiographically definable myocardial dysfunction in a region perfused by a coronary artery obstructed more than 75%, and to be associated with essentially normal leaflet and chordal morphologic or histologic characteristics. A total of 611 isolated mitral valve operations were performed at Duke University Medical Center between Jan. I, 1981, and March 31, 1987. Fifty-fivepatients met these criteria and werejudged by the operating surgeon to require a mitral valve procedure. Lesser degrees of incompetence may have prognostic significance"" but were not considered in this analysis. Of the 55

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patients, 32 had primary mitral valve replacement and 23 had mitral valve reconstruction. Patient data were acquired by direct physician review of all 611 hospital records and relevant cineangiograms, and 100% follow-up information was obtained. Patient classification. Ischemic mitral regurgitation was divided into three distinct etiologic subgroups: posterior papillary muscle dysfunction, papillary muscle rupture, and extensive left ventricular infarction or anterior aneurysm with generalized annular dilatation. The subgroups were defined objectively by quantitative left ventriculograms (Fig. I) and a modified centerline regional wall motion analysis.'>" The patients were further categorized into those requiring an acute operation while hospitalized for the precipitating infarct and those undergoing a more elective procedure. Thirty-one of the 55 patients were in the posterior papillary muscle dysfunction subgroup and had inferior infarcts manifested on the ventriculograms as posterior wall motion defects with no evidence of papillary muscle rupture. Seventeen of them required an acute operation and 14, an elective procedure. Average posterior wall shortening was less than 25% of normal in 24 of these 31 patients, and the remaining seven had either intermittent postinfarction ischemia or circumflex infarcts that were manifested incompletely on the right anterior oblique projection. In these 31 patients, anterior and apical wall motion was preserved at greater than 25% of normal values. In the second subgroup, comprising nine patients, papillary muscle rupture was uniformly definable as a negative ventriculographic contrast defect in the inflow region or a highly mobile echocardiographic target in the area of the mitral apparatus. All nine required an acute operation. Ventricular function was well preserved in seven of these patients, with greater than 25% of normal shortening in all three regions. The third subgroup of patients had generalized annular dilatation associated with diffuse ventricular dysfunction and less than 25% of normal wall motion in two of the three regions. Fifteen patients were in this group, II requiring an acute operation and four, an elective procedure. The degree of mitral regurgitation was evaluated in all patients from the contrast left ventriculogram and estimated as 0 to 4+ by standard criteria." Left ventricular ejection fraction was calculated from the right anterior oblique projection by the area-length method. Surgical technique. Throughout the 75-month period, all operative procedures were performed by the same six surgeons using cardiopulmonary bypass and systemic hypothermia. Myocardial protection was accomplished with cold potassium crystalloid cardioplegia during a single period of aortic clamping." After 1983,90% of patients received at least one internal mammary artery graft, and five of them had reoperation. Thirty-three patients ultimately underwent prosthetic valve replacement (32 primary and one after a failed repair). Thirty-one valve replacements were performed transatrially, and two were accomplished through left ventriculotomies. Of the 33 prosthetic valves, 28 were bioprostheses and five were mechanical valves, reflecting individual preferences among surgeons. Twenty-three patients underwent mitral valve repair. Two had transatrial Carpentier ring annuloplasty"" and five had various modifications of the Kay procedure, I I involving bilat-

Ischemic mitral regurgitation

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Fig. 3. The annuloplasty suture has been tied, and pledgetsupported mattress sutures have been placed for posterior papillary muscle shortening RV, Right ventricle. LV, Left ventricle. LA, Left atrium. eral commissural annuloplasty (three transatrial and two through anterior left ventriculotomies during aneurysm resections). In the final 16 patients, mitral valve repair was accomplished transventricularly, through the area of infarction, by combining multiple technical principles.7.11.16.18.2o,21 In most situations, transventricular repairs were performed with single venous cannulation and aortic venting, techniques that are routine for coronary revascularization in this center. After completion of the distal coronary anastomoses, the left ventricle was opened through the infarcted region (Fig. 2), which was in the distribution of the posterior descending or right coronary artery in 12, in the posterolateral circumflex distribution in three, and in the anterolateral distribution of a first circumflex marginal in one patient with anterior papillary muscle rupture. Fifteen of the patients had thinned-out transmural infarcts, scars, or aneurysms, and the mural incision was performed initially toward the atrioventricular groove to avoid the bases of the papillary muscles. Once the papillary muscles were identified, the incision was extended toward the apex so that it avoided the papillary insertions. In most cases, a 5 ern vertical incision, placed to within I cm of the base, provided excellent exposure; however, larger incisions were used occasionally to resect posterior wall aneurysms. The mitral valve leaflets and the subvalvular structures then were inspected. A detailed knowledge of mitral valve anatomy was essential and has been reviewed elsewhere. 16,22 In all patients, the anterior papillary muscle was single, was considerably longer than its posterior counterpart, and had a firm consistency. In contrast, the posterior papillary apparatus consisted of two or three short muscles arising discretely from the posterior ventricular walL Depending on the region of the infarct, the ventriculotomy was positioned to the right of the posterior papillary muscle heads (Figs. 2 and 3), between them (Figs. 4 and 5), or to the left with circumflex infarcts.

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1 6 8 Rankin et al.

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Fig. 4. A Carpentier chordal shortening procedure, as performed transventricularly for elongated anterior chordae to the central posterior leaflet (A), and a transventricular bilateral commissural annuloplasty (B).

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Fig. 5. Reimplantation of a ruptured lateral head of the posterior papillary muscle complex. Abbreviations are the same as for Fig. 2. See text for details.

For isolated posterior papillary muscle dysfunction, a posterior commissural annuloplasty was performed (Fig. 2), as modified from the technique of Johnson, Pedraza, and Kayser." A pledget-supported horizontal mattress suture of 3-0 polypropylene was placed deep to the valve anulus at the posterior commissure and tied firmly. It was important to obtain substantial bites of ventricular and atrial tissue with this suture, since the only failed valve repair occurred when a superficially placed suture separated the valve anulus from the ventricular wall. In most cases, the infarcted posterior papillary heads appeared elongated, which resulted in the posterior chordae to both leaflets being slack. Suturing the papillary muscles to the ventricular wall at a slightly more apical level compensated for the elongation and prevented leaflet prolapse beyond the

annular plane (Fig. 3). When pledget-supported horizontal mattress sutures were placed into a papillary muscle, the fibrous tip was used for at least one of the two arms. The ventriculotomy then was closed with four or five large horizontal mattress sutures of No. I braided polyester buttressed with Teflon felt strips and oversewn with a running No. I polypropylene suture for hemostasis. The initial row of horizontal mattress sutures was placed at the margins of the infarct to exclude the dysfunctional segment. In many patients, inspection of the valve disclosed a prominent posterior commissural "cleft" (Fig. 6), representing either a developmental abnormality or an exaggerated commissure. Deficient posterior leaflet tissue may have predisposed patients with papillary muscle dysfunction to valve incompetence after inferior wall infarctions. With this type of anatomy, either the posterior valve leaflets were closed with pledget-supported mattress sutures (Fig. 7, A) or the cleft was sutured directly (Fig. 7, B). The orifice area was reduced insignificantly by this procedure, and direct leaflet closure seemed to prevent minor residual incompetence. Other coincidental valve abnormalities could be corrected during repair. If chordae to the anterior papillary muscle were elongated (Fig. 4, A), a precise chordal shortening was performed by the Carpentier" technique. For anterior papillary muscle or chordal elongation, the anterior papillary muscle was never sutured to the ventricular wall, because of concern over shortening the chordal apparatus too much. In aU patients with severe left ventricular dysfunction and a few with posterior papillary muscle dysfunction necessitating elective repair, some component of anterior annular dilatation also was evident. In this situation, an anterior commissural annuloplasty was performed, with care taken to avoid the aortic valve by placing the cephalad sutures into the left fibrous trigone (Fig. 4, B). Two patients were noted to have coexistent rupture of minor primary chordae, which were repaired by suture transfer to adjacent secondary chordae." One subacute patient with severe left ventricular dysfunction and sustained ventricular tachycardia had electrophysiologic mapping and subendocardial resection of a posterior ventricular aneurysm in addition to mitral valve repair. When a ruptured papillary muscle was expected in the

Volume 95 Number 2 February 1988

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Fig. 6. Postmortem specimen of the mitral valve in a patient who died of renal sepsis after transventricular mitral valve repair. A prominent posterior commissural "cleft" extends to within 2 mm of the anulus, whereas a continuous "skirt" of valve tissue is present at the anterior commissure. This was a common finding in patients with papillary muscle dysfunction.

Fig. 7. Repair techniques for posterior leaflet closure when inadequate commissural leaflet tissue was encountered. See text for details.

repair group, the ventriculotomy was performed through the transmural infarct as described earlier. Rupture of the lateral head of the anterior papillary muscle occurred in one patient with a first circumflex marginal infarct, and because of the acute presentation, annular architecture was preserved. In this case, the muscle head was sutured to the ventricular wall with pledget-supported horizontal mattress sutures," and no annuloplasty was performed. In two other patients, ruptured posterior papillary muscles were reimplanted, and posterior commissural annuloplasties were performed. Again, at least one of the reimplantation sutures was placed into the fibrous tip of the papillary muscle, and the sutures were crossed if more than one tip was present (Fig. 5). Thus far, each ofthethree ruptured papillary muscles has been sutured back toitsoriginal base; however, if this maneuver seemed to tighten the chordae excessively in future cases, the reimplantation site could be moved more toward the atrioventricular groove.

To evaluate the efficacy of these reconstructive procedures, the first 11 survivors of transventricular mitral valve repair were subjected to late postoperative color-flow Doppler studies of mitral valve function. First-pass radionuclide determination of resting left ventricular ejection fraction also was obtained. Follow-up data were acquired through clinic interviews or telephone contact on all surviving patients during March 1987. The relationship between relevant clinical variables and hospital survival for the entire population was evaluated by a logistic regression procedure. Variables included in the analysis were age, sex, ejection fraction, number of obstructed (:0:::75%) vessels, left main disease, acute versus subacute presentation, valve repair versus replacement, and the preoperative presence of pulmonary edema or intra-aortic balloon pump requirement. To examine differences in hospital survival, late survival, symptomatic status, and all other clinical variables with repair versus replacement in both the overall group and the individual subgroups, X2 tests were used for discrete variables and

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The logistic regression procedure performed on the entire series identified only two variables as influencing hospital mortality. The need for an acute operation significantly worsened hospital mortality (p = 0.02), and management by valve repair improved mortality (p = 0.03). Hospital mortality for the overall group after treatment by valve repair was 26% ± 9% as compared with 53% ± 9% with valve replacement. Operative results appeared similar for each of the repair procedures used. For comparison, hospital mortality for all other valve operations at Duke over a similar time period was 8.6%, and 5.6% for elective isolated primary valve procedures. Corresponding results with other forms of ischemic heart disease have been published else-

where." 24

.2 Preoperative Study

Postoperative Study

Fig. 8. Preoperative and postoperative mitral valve function (top panel) and left ventricular ejection fraction (bottom panel) data in the first 11 survivors of transventricular mitral valve repair.

Wilcoxon rank sum tests for continuous variables. Individual patient characteristics are listed in Appendix A. Summary data are presented as mean ± I standard deviation.

Results Statistical comparisons: Overall group. Baseline characteristics of the valve repair group differed insignificantly (p > 0.05) from those of the replacement group with respect to age (62 ± 10 years versus 63 ± 7 years), sex (34% female versus 37% female), number of vessels diseased (83% three-vessel or left main coronary artery versus 53%), ejection fraction (0.39 ± 0.12 versus 0.42 ± 0.14), degree of regurgitation (3.7 ± 0.5+ versus 3.6 ± 0.5+), New York Heart Association (NYHA) anginal class (3.7 ± 0.9 versus 3.4 ± 0.9), NYHA heart failure class (3.7 ± 0.8 versus 3.7 ± 0.6), or other preoperative factors, including pulmonary edema, balloon pump requirement, acute presentation, and subgroup type. Several operative variables were different, however. Patients having valve repair received 3.0 ± 1.1 grafts per patient, whereas those undergoing replacement had 2.2 ± 1.2 (p = 0.01). Aortic cross-clamp time was shorter for transventricular repair (74 ± 15 minutes versus 108 ± 67 minutes for replacement; p = 0.02), despite the increased number of grafts. Valve replacement was more likely to result in postoperative low cardiac output associated with hospital death (47% ± 9% versus 17% ± 8% for repair; p = 0.02).

With 17 hospital deaths, two late deaths, and two poor symptomatic results (persistent NYHA class III heart failure), the replacement group had a worse symptom-free survival rate (34%) than the repair group (65%; six hospital deaths, one late death, and one poor result). However, because of the low late postoperative event rate and the limited follow-up (0.6 years mean for repair versus 3.2 years mean for replacement), statistical comparison is inappropriate at this time. Only 20% ± 10% (3/15) of patients in the severe left ventricular dysfunction subgroup were surviving with less than NYHA class III symptoms at follow-up, as compared with 58% ± 8% of the remaining patients (four of nine with papillary muscle rupture; 19 of 31 with papillary muscle dysfunction; p = 0.01). Operative results. Papillary muscle dysfunction. Hospital mortality for valve replacement was significantly higher in acute than in elective operations (p = 0.02). Five of the seven acute patients died after valve replacement, and another died late. The uniform cause of death in this group was cardiac pump failure. In contrast, only one of nine patients died early after elective valve replacement. One died late of prosthetic endocarditis, another died late of noncardiac causes, and six continue to do well. Valve repair was associated with a better hospital survival than valve replacement (p = 0.05) in patients requiring acute operations. Only two of the 10 acute patients died in hospital, and all seven patients surviving transventricular repair are well at a mean follow-up of almost 1 year. One acute patient with a transatrial Kay annuloplasty died late of a presumed ventricular arrhythmia. All four patients undergoing elective transventricular valve repair survived hospitalization and are well. One patient electively undergoing a Carpentier ring annuloplasty died early postoperatively. Hospital deaths after repair were due to diffuse coronary disease

Volume 95 Number 2 February 1988

that precluded adequate bypass grafting in two patients and to renal sepsis in another. All valve repairs functioned well early postoperatively as assessed by the absence of significant left atrial V waves. Eleven patients having transventricular repair were studied late by color-flow Doppler echocardiograrns. Mitral regurgitation was graded as a to 1+ in nine and 2+ in two (Fig. 8, A). Left ventricular ejection fraction improved in most (Fig. 8, B), although precise comparisons were difficult because of differing analytic techniques. The patient exhibiting the 14-point fall in ejection fraction postoperatively had a relatively minor preoperative posterior wall motion defect (93% of normal), and transventricular repair of a posterior papillary muscle rupture was performed through potentially viable myocardium. Papillary muscle rupture. Four of the six patients requiring acute mitral valve replacement died, but the two survivors are well at follow-up. Cardiac pump failure accounted for three of the deaths, and postoperative posterior wall rupture occurred in one. Of the three patients undergoing urgent valve repair, one required valve replacement. In this patient, the annuloplasty suture separated the valve leaflets from the ventricular wall 4 hours postoperatively and necessitated return to theoperating room and successful transventricular valve replacement. The single death in the group having acute valve repair occurred because of worsening of preoperative pneumonia and renal failure, despite normal postoperative valve function. Severe left ventricular dysfunction. Results were suboptimal in most of these patients, with only six surviving hospitalization. Cardiac power failure was a prominent factor in most hospital deaths in both the repair and replacement groups, whereas valve competence appeared good by left atrial pressure measurements in all 5 patients having repair. A trend did exist, however, toward improved results after repair, with three of five (60% ± 22%) patients surviving repair and only three of 10 (30% ± 15%) surviving replacement (p = 0.18). Three of the patients with severe left ventricular dysfunction are experiencing intractable NYHA class III heart failure late postoperatively, so that only one with valve replacement and two with valve repair have done well over the long term. Discussion Posterior papillary muscle dysfunction is the most common variety of ischemic mitral regurgitation necessitating a valve operation, accounting for 56% of patients in this series. Characteristically, the onset of congestive heart failure in papillary muscle dysfunction is coinci-

Ischemic mitral regurgitation 1 7 1

dent with an extensive posterior wall infarct involving the right or circumflex coronary arteries. The pathophysiologic combination of posterior annular dilatation, papillary muscle elongation, and loss of papillary muscle shortening produces valvular incompetence by diminishing the surface area of leaflet coaptation.v" Deficient leaflet tissue, such as prominent commissural "clefts" (Fig. 6) or scalloping around persistent fetal commissural leaflets, also may be important. Patient subgroups with papillary muscle rupture or severe left ventricular dysfunction are less common, comprising 16% and 27% of this series, respectively. The majority of patients with papillary muscle rupture have relatively small infarcts; congestive heart failure, together with a new but often subtle murmur, develops at an interval of 2 to 7 days. Most ruptures involve a posterior papillary head in the distal right or circumflex coronary distribution. Patients with severe left ventricular dysfunction usually have a history of multiple myocardial infarctions, left ventricular dilatation, and severely reduced ejection fraction. Although components of papillary muscle dysfunction may exist in this group, generalized annular dilatation is a major anatomic feature. Moreover, congestive heart failure in some may be caused more by insufficient myocardium than by valvular dysfunction, since this distinction is difficult to make clinically. In this report as well as others, acute mitral valve replacement for ischemic mitral regurgitation was associated with the highest hospital mortality observed for any form of ischemic or valvular heart disease. Several authors have suggested that valve repair could improve these results,'? 11 and objective analysis of this series confirmed that survival was better after valve reconstruction (p = 0.03). This result occurred despite baseline similarities in replacement and repair groups and also seemed independent of the type of repair used. Explanations for this finding may relate to shortened operative time, technical simplification, preservation of the mitral apparatus.P?" and reduction in complications associated with prosthetic valves. Since more coronary grafts were performed in the repair group, it is also possible that the shorter time required for valve reconstruction allowed more complete revascularization. Normal leaflet and chordal structure in this setting facilitates reconstruction, and resection of infarcted segments during repair may contribute to preservation of left ventricular ejection fraction." The major improvement in hospital mortality with valve reconstruction occurred in the subgroup undergoing acute operation for papillary muscle dysfunction and was related to a lower incidence of ventricular failure

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postoperatively. Physiologic repair of myocardial abnormalities in these patients appeared effective in restoring valve competence, and left ventricular function was well maintained (Fig. 8). With a preserved ejection fraction and elimination of the regurgitant volume, ventricular pumping efficiency and associated hemodynamic variables, such as forward cardiac output and mean left atrial pressure, should have improved significantly." Consistent with previous reports.r': 10 results in patients having elective operations for papillary muscle dysfunction were good with either approach, so that valverepair produced less of a clinical difference. However, physiologic reconstruction with autologous tissue still seems preferable and may reduce late prosthetic complications. Potentially, elective valve repair for papillary muscle dysfunction might establish long-term survival patterns similar to those observed for isolated coronary bypass.23,24 Although sample size limitations precluded specific conclusions in patients with papillary muscle rupture or severeleft ventricular dysfunction,trends also existed in these subgroups toward improved results with valve repair. Several important concepts related to mitral valve reconstruction for ischemic incompetence need to be discussed. First, patients with papillary muscle rupture usually have well-preserved ventricular function, and ventriculotomy may be disadvantageous by damaging viable myocardium. For this reason, patients with good wall motion, including the majority with papillary muscle rupture, should probably undergo transatrial procedures; transventricular mitral repair should be reserved for patients with large transmural infarcts or aneurysms. Ventriculotomy also could be complicated by uncontrollable bleedingor late false aneurysm formation, but with proper technique these problems should be rare. As with all repair procedures, a small incidence of acute valve failure should be expected. This complication produces a difficult clinical situation necessitating reoperation for valve replacement. The combination of satisfactory patient selection, adequate technical performance, and increasing operative experience should minimize failure rates. Finally, the findings of this study must be considered preliminary, and larger numbers of patients together with longer clinical follow-up will be necessary to fully establish this approach. Mitral regurgitation associated with a large anterior ventricular aneurysm was managed variously in this series with transventricular or transatrial valve repair or replacement as described elsewhere." However, all of the patients with an anterior aneurysm died postoperatively of low cardiac output (Appendix A), results that

parallel the findings of Najafi and associates.' This observation suggests that the pathophysiology of mitral annular dilatation associated with anterior aneurysm is unique and that direct valve procedures may be unsuccessful because of inadequate residual myocardium. In fact, long-term results in the severe left ventricular dysfunctionsubgroup treated by either repair or replacement were disappointing, as in previous reports.v " This finding raises questions about the propriety of valvecoronary procedures in these patients and suggests that cardiac transplantation may be preferred. This study does not address the preoperative management and selection of patients for valve operations, and the following protocol is given to clarify our general institutional policy. Most patients with severe mitral regurgitation associated with acute infarction (ie, within 6 to 10 hours of infarct onset) undergo attempted pharmacologic thrombolysis or coronary angioplasty, in the absence of contraindications. Initial experience with this approach has been quite favorable." If mitral incompetence resolves by serial Doppler examination, elective coronary bypass or percutaneous angioplasty can be performed as appropriate. Even without reperfusion, regurgitation in acute papillary muscle dysfunction can resolve spontaneously, so that these patients are usually followed with Doppler studies for at least 24 hours in the coronary care unit before operative intervention. An intra-aortic balloon pump can be placed before or during cardiac catheterization in unstable patients and assists with clinical stabilization during this period. If regurgitation resolves, only a coronary revascularization is performed; if incompetencepersists at 3+ to 4+ levels, mitral valve repair is incorporated into the operative plan. Selection of patients with moderate ventriculographic incompetence (2+ to 3+) for valve procedures can be difficult. 10, 12 Ventriculograms do not permit clear distinctions about hemodynamic significance, and regurgitation can be extremely volume dependent, becoming evident only when left atrial pressure exceeds moderate levels. An 8% to 20% operative mortality has been observed when patients with moderate to severe ischemic mitral incompetence were treated only with coronary revascularization,10, 12 and a significant perioperative and late morbidity has been attributable to residual valve dysfunction with this approach. This problem is currently addressed by intraoperative testing of valves with any degree of ventriculographic incompetence by left atrial pressure and transesophageal Doppler velocity measurements after aortic cannulation, Volume loading is performed via the aortic cannula to a

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mean left atrial pressure of 12 to 15 mm Hg, and if hemodynamics remain stable, a conventional coronary revascularization is undertaken. If prominent V waves (greater than 5 mm Hg higher than the A waves) develop and are accompanied by Doppler evidence of severe regurgitation, the mitral valve is repaired. In the presence of a significant wall motion defect and a transmural infarct or scar, the repair is accomplished transventricularly. Otherwise, a transatrial Kay annuloplasty is performed when the structural characteristics of the valve are normal. When significant leaflet or chordal abnormalities are encountered, a Carpentier repair can be used. If the remaining aortic clamp time is judged inadequate for a Carpentier procedure, a St. Jude Medical prosthesis is inserted in the intravalvular position," thus avoiding destruction of the mitral apparatus associated with conventional valve replacement. Recent experience suggests than this individualized approach will be safe and effective, and expanded application of valve repair for moderate to severe ischemic mitral regurgitation may significantly improve the outlook of these critically ill patients. In summary, ischemic mitral regurgitation can be separated into three distinct clinical subgroups that have physiologic and prognostic significance. Preliminary data suggest that mitral valve repair, as compared to valve replacement, reduces operative mortality, especially in patients with acute posterior papillary muscle dysfunction. Transventricular reconstruction of valve competence is a simple and effective alternative, when properly applied to patients with large transmural infarcts or aneurysms. Finally, improved operative techniques and patient management protocols offer the potential for enhancing the care of future patients with ischemic mitral regurgitation.

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REFERENCES I. Gerbode FLA, Hetzer R, Krebber HJ. Surgical manage-

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ment of papillary muscle rupture due to myocardial infarction. World J Surg 1978;2:791. DiSesa VJ, Cohn LH, Collins JJ Jr, Koster JK, VanDevanter S. Determinants of operative survival following combined mitral valve replacement and coronary revascularization. Ann Thorac Surg 1982;34:484. Pinson CW, Cobanoglu A, Metzdorff MT, Grunkemeier GL, Kay PH, Starr A. Late surgical results for ischemic mitral regurgitation. J THORAC CARDlOVASC SURG 1984; 88:663. Geha AS, Francis CK, Hammond GL, Laks H, KopfGS, Hashim SW. Combined valve replacement and myocardial revascularization. J Vase Surg 1984;1:27. Tepe NA, Edmunds LH Jr. Operation for acute postin-

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farction mitral insufficiency and cardiogenic shock. J THORAC CARDIOVASC SURG 1985;89:525. Salomon NW, Stinson EB, Griepp RB, Shumway NE. Patient-related risk factors as predictors of results following isolated mitral valve replacement. Ann Thorac Surg 1977;24:519. Najafi H, Javid H, Hunter JA, Goldin MD, Serry C, Dye WS. Mitral insufficiency secondary to coronary heart disease. Ann Thorac Surg 1975;20:529. Merin G, Giuliani ER, Pluth JR, Wallace RB, Danielson GK. Surgery for mitral valve incompetence after myocardial infarction. Am J Cardiol 1973;32:322. Czer LSC, Matloff J, Chaux A, DeRobertis M, Yogananthan A, Gray RJ. A 6 year experience with the St. Jude Medical valve: hemodynamic performance, surgical results, biocompatibility and follow-up. J Am Coli Cardiol 1985;6:904. Connolly MW, Gelbfish JS, Jacobowitz IJ, et al. Surgical results for mitral regurgitation from coronary artery disease. J THORAC CARDlOVASC SURG 1986;91:379. Kay GL, Kay JH, Zubiate P, Yokoyama T, Mendez M. Mitral valve repair for mitral regurgitation secondary to coronary artery disease. Circulation 1986;74(Pt 2):188. Hickey MSJ, Smith LR, Muhlbaier LH, et al. Current prognosis of ischemic mitral regurgitation: implications for future management. Circulation (in press). Rankin JS, Newman GE, Muhlbaier LH, Behar VS, Fedor JM, Sabiston DC Jr. The effects of coronary revascularization on left ventricular function in ischemic heart disease. J THORAC CARDIOVASC SURG 1985; 90:818. Sheehan FH, Stewart OK, Dodge HT, Mitten S, Bolson EL, Brown BG. Variability in the measurement of regional left ventricular wall motion from contrast angiograms. Circulation 1983;68:550. Sheehan FH, Dodge HT, Bolson EL, Hok-Wai W, Caputo GR, Stewart OK. Value of partial ejection fraction, volume increment, and regional wall motion in identifying patients with clinically significant coronary artery disease. Circulation 1983;68:756. Rankin JS. Mitral and tricuspid valve disease. In: Sabiston DC, Jr, ed. A textbock of surgery, 13th ed. Philadelphia: W.B. Saunders Company, 1986:2344. Carpentier A, Deloche A, Dauptain J, et al. A new reconstructive operation for correction of mitral and tricuspid insufficiency. J Thorac Cardiovasc Surg 1971; 61:1. Carpentier A: Cardiac valve surgery-the "French correction." J THORAC CARDlOVASC SURG 1983;86:323. Cosgrove OM, Chaves AM, Lytle BW, et al. Results of mitral valve reconstruction. Circulation 1986;74(Pt 2): 182. Johnson WD, Pedraza PM, Kayser KL. Preservation and restoration of the mitral mechanism during inferior wall

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aneurysmectomy. In: Duran CMG, Angell WW, Johnson AD, Oury JH, eds. Recent progress in mitral valve disease. London: Butterworth & Co, 1984. Gula G, Yacoub MH. Surgical correction of complete rupture of the anterior papillary muscle. Ann Thorac Surg 1981;32:88. Perloff JK, Roberts we. The mitral apparatus: functional anatomy of mitral regurgitation. Circulation 1972; 46:227. Pryor DB, Harrell FE, Rankin JS, et al. The changing survival benefits of coronary revascularization over time. Circulation 1987;76(Pt 5):V 13. Califf RM, Harrell FE, Lee KL, et al. The evolution of medical and surgical therapy for coronary artery disease: a 15-year perspective. Circulation 1987;76(Pt 4): IV1394. Mittal AK, Langston J Jr, Cohn KE, Selzer A, Kerth WJ. Combined papillary muscle and left ventricular wall dysfunction as a cause of mitral regurgitation: an experimental study. Circulation 1971;44:174. Godley RW, Wann LS, Rogers EW, Feigenbaum H, Weyman AE. Incomplete mitral leaflet closure in patients with papillary muscle dysfunction. Circulation 1981; 63:565. Tei C, Sakamaki T, Shah PM, et al. Mitral valve prolapse in short-term experimental coronary occlusion: a possible mechanism of ischemic mitral regurgitation. Circulation 1983;68:183. David TE, Ho We: The effect of preservation of chordae tendineae on mitral valve replacement for postinfarction mitral regurgitation. Circulation 1986;74(Pt 2):1116. Bonchek LI, Olinger GN, Siegel R, Tresch DD, Keelan MH Jr. Left ventricular performance after mitral reconstruction for mitral regurgitation. J THORAC CARDIOVASC SURG 1984;88:122. Hansen DE, Cahill PD, Derby GC, Miller De. Relative contributions of the anterior and posterior mitral chordae tendineae to canine global left ventricular systolic function. J THORAC CARDIOVASC SURG 1987;93:45. Spratt JA, Olsen CO, Tyson GS Jr, et al. Experimental mitral regurgitation: physiological effects of correction of left ventricular dynamics. J THORAC CARDIOVASC SURG 1983;86:479. Gold FL, Sharma B, Hodges M, Helseth HK. Combined left ventricular aneurysmectomy, mitral valve replacement and aortocoronary bypass grafting: results of surgery. Circulation 1980;62(Pt 2):1147. Radford MJ, Johnson RA, Buckley MJ, Daggett WM, Leinbach RC, Gold HK. Survival following mitral valve replacement for mitral regurgitation due to coronary artery disease. Circulation 1979;60(Pt 2):139. Cooley DA, Ingram MT. Intravalvular implantation of mitral valve prostheses. Texas Heart Inst J 1987; 14:188.

Discussion Dr. L. Henry Edmunds, Jr. (Philadelphia, Pa.). Dr. Rankin stratified the 55 patients into three groups on the basis of their varying anatomy, and he further divided each group into those with an acute and those with a subacute presentation. Although the anatomic considerations are very important in how the repair is conducted, I do not think this is the most important thing from the patient's point of view. I believe the functional impairment bears more on the patient's chances of survival than the specific anatomic disease involved. The important thing is to separate the patients with an acute myocardial infarction, significant mitral insufficiency, and cardiogenic shock-s-who therefore have an immediate lifethreatening situation-s-from the larger group who are not in such critical condition. Among our patients we found only 12 with acute mitral insufficiency and cardiogenic shock who had to have an operation within I month of the infarct or less. The mortality we had was 50%. Among other things, we found that the survival depended on the amount of left ventricle that remained viable, that early operation was mandatory, and that the ejection fraction does not assess the function of the residual ventricle in the presence of mitral insufficiency. In Dr. Rankin's report I found 20 patients who had had an operation in the same month that they had an acute myocardial infarction. All 20 of these patients were in pulmonary edema and most of them were intubated before operation. Fifteen of the 20 had preoperative insertion of the intra-aortic balloon. Of the 12 patients who had mitral valve replacement, eight died in the hospital. Of the eight patients who had transventricular repair, only three died in the hospital; this difference is significant by X' analysis. Thus Dr. Rankin and his colleagues at Duke have clearly shown us that transventricular repair for acute mitral insufficiency after acute myocardial infarction is a safer operation than mitral valve replacement. Dr. Alain F. Carpentier (Paris, France). It was not clear to me how many of the patients in this series were operated on in the acute phase of myocardial infarction, that is, within the first 10 days. In this particular group of patients. we have not had the courage to approach the mitral valve through the ventricle, being afraid of the fragility of the necrotic ventricular wall and of a reduced ventricular compliance if one resects the infarcted area at this early stage. I would like to ask the authors how many patients with an acute myocardial infarction were operated on in the first week. and I would appreciate further details on the technique and tricks used to repair these very fragile ventricles. I noticed with great interest that they could successfully perform the various techniques of valve repair. including papillary muscle reimplantation and chordal transposition, through this ventricular approach, but it is hard for me to imagine how they could ascertain the results through this approach without opening the left atrium. Dr. Rankin (Closing). Dr. Edmunds clearly emphasized the importance of acute presentation. and that was one of the most important factors determining hospital survival in our study. I believe that a relationship also exists between residual myocardium and survival, in that patients with very poor ventricular function had a worse hospital mortality and also a

Volume 95 Number 2 February 1988

worse intermediate-term survival quality. Of the IS patients with poor ventricular function, only one treated with valve replacement and two with valve repair are surviving with class I or II symptoms at late follow-up. Thus, from our experience, such patients seem to be a particularly difficult group, and perhaps alternative therapy such as cardiac transplantation should be considered in many of these patients. Dr. Edmunds also emphasized earlier operation, which is important. We believe that the transventricular approach is easier and quicker. As compared to valve replacement, transventricular repair took 30 minutes' less clamp time on average, and that may have been one major factor in improving the operative mortality. With regard to Dr. Carpentier's remarks, 37 of the 55 patients were operated on in the acute phase of the infarct, defined as requiring operation directly out of the coronary care unit. The technique of ventriculotomy is very simple. Depending on the location of the infarct or aneurysm, a vertical incision is made in the left ventricle close to the base,

Ischemic mitral regurgitation

17 5

and exposure of the mitral valve is excellent. I believe that valve repair for ischemic incompetence is easier through that exposure than through the atrium. The ventriculotomy is closed directly over Teflon felt strips, as is done for posterior aneurysm or ventricular septal defect repair. We currently perform valve testing with transesophageal Doppler echocardiography as bypass is discontinued. Valve reconstruction has failed in only one of the patients. This occurred 4 hours postoperatively and necessitated return to the operating room for successful transventricular mitral valve replacement. Thus, in our early experience, it appears that transventricular mitral valve repair in most patients with papillary muscle dysfunction and some with papillary muscle rupture will simplify the operative approach and improve results in this acutely ill and difficult subset of mitral valve disease. For Appendix A see page /76.

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Appendix A. Individual patient profiles Catheterization variables

Demographic variables 2

I 2 3 4 5 6 7 8 9 10 II 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27

28 29 30 31 32 I 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23

3

I1IB

7

8

9

55

2/85 7/81 9/81 11/86 4/83 1/87 3/87 8/83 2/84 11/76 6/78 10/82 4/74 5/83 7/76 8/85 9/85 12/81 12/82 8/81 4/83 11/82 2/81 2/87 7/86 10/82 6/81 10/84 11/86 6/78 9/80 12/85

7/85 10/81 10/81 11/86 7/83 1/87 3/87 2/85 7/84 2/83 8/81 1/83 11/83 11/83 5/82 10/85 9/85 12/81 12/82 8/81 4/83 11/82 4/81 2/87 8/86 3/83 6/81 10/84 12/86 1/81 4/81 1/86

59 61 73 54 75 56 74 64 48 63 58 68 70 63 69 71 62 59 35 74 48 74 59

F F M M F M M M F M M F F F F M M M M M M M M

8/86 9/85 10/85 9/86 9/85 9/86 11/86 11/85 9/85 11/86 6/78 11/86 2/80 1/87

8/86 11/85 10/85 10/86 9/85 10/86 11/86 2/86 2/87 12/86 8/83 12/86 7/86 3/87 3/87 11/85 7/86 7/86 8/85 12/86 5/86 10/85 3/87

Mitral valve repair patients 4 2 9/86 4 12/85 3 4 11/85 3 4 3 10/86 HD 4 3 4 3 10/86 HD 4 3 4 3 3/86 4 2 2/87 4 12/86 3 4 3 HD 4 12/86 3 4 3 7/86 4 2 3/87 4/87 4 2 4 12/85 3 4 3 7/86 HD 3 2 4 9/85 3 1,2,3,4 HD 1,2,3 1,2,4 1,3 8/86 1,2,3 HD 1,2,3,4 4 3 4/87

I1IB I1IB

IB IIA IIA IIA IlIA IlIA IlIA IlIA

6

M M M F F F F F M F M M M M M M F M M F M F M F M F M M M M F M

59 59 59 80 66 65 59 68 48

IB

5

Mitral valve replacement patients HD 4 2 4 3 HD HD 4 3 4 2 12/86 4 2 7/83 HD 4 3 4 3 HD 4 3 2/85 4 3 7/84 4 2 3/83 4 2 8/81 HD 4 3 4 12/83 2 4 3 11/83 4 3 5/82 4 3 1/86 4 3 HD 1,3 2 12/81 1,3 2 1/83 4 3 HD 4 3 HD 4 3 HD I I 5/81 4 3 HD HD 4 2 I I HD HD 1,3 I 10/84 4 3 HD 1,3 I HD I I HD I I 1,2 I 2/86

IA IA IA IA IA IA IA IB IB IB IB IB IB IB IB IB IIA IIA IIA IIA IIA IIA IlIA IlIA IlIA IlIA IlIA IlIA IlIA IIIB

IA IA IA IA IA IA IA IA IA IA IB IB IB

4

62 55 65 61 71 55 55 62 64 67 65 59 66 70 55 68 69 61 66 58 73

72

?

10/85 7/86 6/86 8/85 11/86 5/86 10/85 2/87

Operative variables

10

11

12

3 3,4 2 2 3 2 3 2 3,4 I 3 3 2 3 2 3 2 3 2 3 3 3 3 I I 3,4 2 2 3 2 I 3

43 37 63 50 63 35 57 58 42 42 53 22 48 40 52 57 59 69 57 41 38 24 32 40 42 21 30 23 23 51 29

3 3 3 4 4 4 4 4 4 4 4 4 3 3 4 3 4 4 4 4 4 3 3 4 3 4 4 3 4 3 3 4

2 4 2 2 3 2 3 I 4 2 2 2,9 2 3 I 4 2 2 2 3 4 2 3,9 I 0 2 9 2 4 1,9 1,9 0

7 6 6 6 6 4 4 6 6 5 7 5 6 6 6 6 5 6 6 7 6 6 6 6 6 6 6 2 4 6V 5 6

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

3 3 3,4 3 3 3 3,4 3 3 3 2 2 3,4 3 3 2 3,4 3 3 3 3 3,4 2

53 40 47 24 48 28 62 38 29 37 50 48 25 45 30 51 48 55 26 25 32 21 38

4 4 4 4 3 4 3 3 4 3 3 3 3 4 4 4 4 4 4 4 3 4 4

3 4 4 2 4 3 3 4 2 3 2,12 2,12 4,12 2 2 2 5 3 3 2 5 4 I

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 4V' 0 0 0 0 0 0 0

6A 5V,3 5V,7 5V 5V 5V 5V 5V 7,SV 5V 4A 4A 6A 5V SV 8,5V 8,SV 8V 5V 6V,9 6A 6V,9 5V

27

13

14

15

Legend: Codes for variables: I = patient number; 2 = subgroup type (I = papillary muscle dysfunction. II = papillary muscle rupture. III = severe left ventricular dysfunction, A = operation during period of acute infarction. B = elective operation); 3 = age in years, 4 = sex; 5 = date of infarct (monthfyear), 6 = date of operation: 7 = date of hospital discharge (HD = hospital death); 8 = location of infarct (1 = anterior, 2 = septal, 3 = lateral, 4 = posterior); 9 = vessel infarcted (I = left anterior descending, 2 = circumflex, 3 = right coronary artery, 4 = left main); 10 = number of vessels diseased (4 = left main); II = ejection fraction; 12 = degree of mitral regurgitation (3+ to 4+); 13 = number of bypass grafts (9 = ventricular aneurysm resection); 14 = prosthetic valve (2 = Bjork-Shiley, 4 = SI. Jude Medical, 5 = Hancock, 6 = Carpentier-Edwards, 7 = Ionescu-Shiley, V = transventricular, others are transatrial); 15 = valve repair (3 = De Vega tricuspid annuloplasty, 4 = Carpentier ring annuloplasty, 5 = posterior commissural annuloplasty plus posterior papillary muscle shortening, 6 = modified Kay annuloplasty, 7 = chordal transfer, 8 = papillary muscle reimplantation, 9 = anterior aneurysm resection, A = transatrial, V = transventricular). 'Valve replacement performed after acute failure of valve repair. tVentriculogram not available and classification based on clinical criteria,

Volume 95 Number 2 February 1988

Ischemic mitral regurgitation

Preoperative risk factors

Postoperative complications

Follow-up data

16

17

18

19

20

21

22

23

24

25

26

27

0 0 0

0 1 1 1 1 1

0 0 0

0 1 0 0 0 1 1 0 0 0 0 0 0 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 1 I 0 0 1 0 0 0

4 4 4 4 4 4 4 2 2 2 3 3 3 3 1 4 4 4 4 4 4 4 2 4 4 4 4 4 4 2 3 3

3 4 4 4 4 4 4 4 3 3 3 4 3 1 4 4 4 4 4 4 4 4 4 4 4 4 4 4 4 3 3 4

0 1 0 0 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 1 1 0 1 0 1 0 0 0

0 0

1 1 0 0 0 1 0 0 0 0 0

0 0

1 0 0 0 0 0 1 0 0 0 0 0

0 1 1 0 0 0 0 0 0 0 0 0 0 0 0 0 0 I

4 4 4 4 4 4 4

4 4 4 4 4 4 4 4 3 4 2 3 4 1 4 4 4 4 4 4 4 4 3

0 1 0 0 1 0 0 0 0 0

0

1 0

1 0 0 0 0

0 0 1 0 0 0 1 0 0 0 I

0 0 0 1 0

0 1 0 1 0 I I

1

0 1 0 0 1 1 0 1 0 1 1 1 I I 1 1 1 1 1 1 1 I 0 1 0

0

1 1 1 1 1 1

I

1

0 0 0 1 0 1 0 0 0

0 I 0 1 1 0 0 I

I

1

0

1 1 1 1 1 0

0

0 0

0

0 0 0 0

1

0

0 0 1 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 1

1 0 0 0 1 0 0 0 0 I 0 1 0 0 0 0 0 0 0 0 0 0 0 0 0 1

1

1 0 1 1

0 0 1 0 1 I 1 I 0 0 0 1 1 1

1 0 1 1

0 0 0 0 0 0 0 0 0 1 1

1

I

I

1

0 1 0 0

1 0 0 0

1 I 0

1 4 4 4 4 4 2 4 4 4 4 4 4 4 4 4

1

0 0 0 0 0 0 1 0 1 1 1 1

1 0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 1 1 0 0 0

1

0

0 0 0 0 1 0 0 0 0 1 1 1 0 0 1 0 1 1 1 0

0 0 0 0 0 0 0 0 0 0 0 0 1 0 0 0 0 0 0 0 0 1 0 1 0 1 0 0 0

0 0 0 1 0 0 0 0 1 0 0 0 1 0 0 0 1 0 0

0 0 0 0 I 0 1 0 0 0 1 0 0 0 0 0 0 1 0 1 0 1 0

0 0 0 0 1 0 0 0 0 0 1 0 1 0 0 0 0 0 0 1 1 1 0

0 0 0 1 0 0 1 0 0 0 1 0 0 0 0 1 0 1 1 1 0 0 0

0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 0

1

0 1

1

28

29

30

Wall motion

31

32

33

118 48

50 70

-13 28

111 109 97 94 85 93 112 47 63 69 70 106 117

80 82 26 112 96 51 101 41 53 59 64 105 56

19 66 25 23 25 25 -5 7 62 13 2 36 7

76 87 76 89

75 80 58 50 59 -2 17 16 8 -40 -44 9 -2 -51 21

161 108

79 80 51 28 100 34 126 74 69 100 73 58 44

52 16 17 17 10 18 41 -1 29 8 -21 24 3 22 22 -8 93 119 4 38 23 43 14

t

0 0 1 1 1 2

2 2 1 2

0 0 0 0

1 3 1

4/85 0 12/86 0

2 1

0 0

0

t

77

0

3

0

10 74 90 -20 41 43 7 22

2

3

0

1 1 2

9/86 0 0 0 0 0 0 0

2

1 1 1 1 1

0 0 0 0 0 0 0

2

0

3

0

17 7

23 6 49 128 104 78 133 52 151 85 116 116 115 102 87 71 123 116 96 74 77

3 51 -29 158

t

t

27

40 84 132 64 -26 2 -45 25 3

t

t

27

41 6 48 24 5 78 14 7 76 80 78 54

Legend cont'd: 16 = diabetes; 17 = preoperative pulmonary edema; 18 = preoperative endotracheal intubation; 19 = preoperative intra-aortic balloon pump; 20 = serum creatinine> 2.0; 21 = preoperative angina class (NYHA); 22 = preoperative congestive heart failure (NYHA); 23 = postoperative mechanical ventilation >48 hours; 24 = postoperative renal dialysis; 25 = either new postoperative requirement for intra-aortic balloon pump or postoperative requirement >48 hours; 26 = major postoperative infection; 27 = death intraoperatively; 28 = late postoperative angina class (NYHA); 29 = late postoperative congestive heart failure class (NYHA); 30 =date of late death; 31 = average anterior wall motion (% normal); 32 = average apical wall motion (% normal); 33 = average posterior wall motion ('k normal). 'Valve replacement performed after acute failure of valve repair. tVentriculogram not available and classification based on clinical criteria.