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Ann Thorac Surg 1999;67:1703-1707
© 1999 The Society of Thoracic Surgeons
a Prince of Wales Hospital, Hong Kong
b Shonan Kamakura General Hospital, Kamakura, Japan
c Madras Medical Mission, Chennai, India
d P. D. Hinduja National Hospital, Bombay, India
e Sapporo Medical University, Sapporo, Japan
Accepted for publication December 23, 1998.
Address reprint requests to Dr Izzat, PO Box 33831, Damascus, Syria
e-mail: izzat{at}cyberia.net.lb
| Abstract |
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Methods. Partial left ventriculectomy was done in 48 patients (mean age, 43 years) with advanced symptomatic cardiomyopathy. The origin of cardiomyopathy was idiopathic in 30 patients, valvular in 10, ischemic in 3, peripartum in 3, sarcoidosis in 1, and viral myocarditis in 1. Procedures performed on the mitral valve were repair with Alfieri method in 8 patients, ring annuloplasty in 2, and replacement in 25.
Results. Seventy-seven percent of patients required myocardial support for weaning from cardiopulmonary bypass, and the overall in-hospital mortality rate was 27%. Mean follow up was 6.5 months (range, 1 to 18 months), and patient survival at 1, 3, and 6 months after discharge was 91%, 88%, and 84%, respectively. Sixty-five percent of survivors with idiopathic and valvular disease achieved significant and sustained improvement in ventricular contractility and symptoms, but there were no clear symptomatic benefits from partial left ventriculectomy in patients with cardiomyopathy from other causes. Most cases of late recurrence of heart failure symptoms (90%) appeared to be related to the development of progressive mitral incompetence.
Conclusions. After partial left ventriculectomy left ventricular function improved in patients with idiopathic and valve related cardiomyopathies. Late deterioration was related to the development of significant mitral valve incompetence postoperatively, hence definitive mitral valve repair or replacement at the time of the partial left ventriculectomy procedure is advised.
| Introduction |
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The Surgical Reduction of Ventricular Volume Trial (SURVIVAL) group is an international working group recently formed in the Asia-Pacific region to share experiences with PLV operations and to improve the understanding of indications, techniques, and outcome of this procedure [5, 8]. This report describes the clinical experience of members of the SURVIVAL group with PLV operations.
| Material and methods |
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Between November 1996 and July 1998, 48 patients (mean age, 43 years; range 3 to 67 years; 81% male) had PLV surgery. Preoperatively, all patients had advanced symptomatic congestive heart failure (New York Heart Association [NYHA] functional class III [n = 20] or IV [n = 28]) despite maximal tolerated medical therapy consisting of angiotensin-converting enzyme inhibitors, diuretics, digitalis, and, in 13 cases, dobutamine infusion or intraaortic balloon pump support.
The cause of cardiomyopathy was idiopathic in 30 patients, valvular in 10, ischemic in 3, peripartum in 3, sarcoidosis in 1, and viral myocarditis in 1. The left ventricle was assessed preoperatively by echocardiography. Left ventricular ejection fraction (EF), measured through the parasternal cross-sectional plane, was 23% ± 1% (mean ± standard error of the mean) and end-diastolic diameter (EDD) was 7.6 ± 0.2 cm. Ethics committee approval was obtained in all centers, and each patient gave informed consent for the operation.
Surgical technique
Standard cardiac anesthesia was used, with hemodynamic monitoring using Swan-Ganz catheters intraoperatively and postoperatively. Normothermic cardiopulmonary bypass and cardioplegic arrest with intermittent antegrade warm blood cardioplegia was used in 32 patients, and the procedure was done on a beating heart in 16 patients, as described by Batista and associates [1].
Our PLV technique is similar to that described previously [1, 2]. Briefly, the ventricular incision was started at the apex, 2 cm lateral to the left anterior descending coronary artery, and extended towards the mitral valve annulus. In the early cases (n = 23), attempts were made to preserve the papillary muscles of the mitral valve, so only the interpapillary myocardium was excised. In 8 of these patients, the midpoints of the free edges of the two mitral leaflets were approximated with a single suture (Alfieri repair) [2]. In later patients (n = 25), a larger segment of the ventricular wall was excised, and the mitral valve was replaced with a valve prosthesis. The free wall of the left ventricle (LV) was reconstituted in a linear fashion with pericardium or Teflon strips for added reinforcement. Other associated procedures were then done (eg, coronary artery bypass grafting or aortic valve replacement) before removal of the aortic cross-clamp.
Most patients were weaned from cardiopulmonary bypass with inotropic support with dobutamine or dopamine in combination with afterload reduction with nitrates infusion; however, additional intraaortic balloon pump support was necessary in 19% of patients. Once hemodynamic stability had been established, patients were extubated as soon as possible, and myocardial support was weaned as appropriate. During the following 7 to 10 days, aggressive antifailure pharmacologic therapy was reintroduced gradually using a combination of angiotensin-converting enzyme inhibitors, nitrates, and diuretics.
Procedures performed
Myocardial resection was directed purposely to the lateral wall of the LV, except in 1 patient who had a dense scar in the anterior LV wall from previous myocardial infarction; hence the resection was limited to this region. The average width of the resected area was 6.3 cm (range, 3 to 10 cm).
Procedures done on the mitral valve included repair with Alfieri method in 8 patients, annuloplasty with ring in 2, and replacement with a valve prosthesis in 25, and the mitral valve was left intact in 13 patients. Associated procedures were aortic valve replacement in 9 patients, coronary artery bypass grafting in 3, tricuspid valve repair in 17, right ventricular plication in 1, and the Maze procedure in 1.
| Results |
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Because the origin of cardiomyopathy might influence the outcome of PLV procedures, results are classified according to cardiomyopathic origin.
Idiopathic cardiomyopathy
Thirty patients with idiopathic dilated cardiomyopathy (LVEDD 7.3 ± 0.1 cm and EF 19 ± 1%) had PLV procedures. Preoperatively, 10 patients were in NYHA functional class III and 20 in functional class IV, with 9 patients dependent on inotropic agents or intraaortic balloon pump support. Twenty-five patients (83%) required the aid of inotropic drugs to be weaned from cardiopulmonary bypass, and 6 (20%) required additional intraaortic balloon pump support. One patient had cardiac arrest immediately preoperatively and failed to recover postoperatively. There were seven more in-hospital deaths resulting from low cardiac output and multiorgan failure, and 1 patient died of acute bacterial mediastinitis. Therefore, there were 21 hospital survivors (70%), and predischarge echocardiography showed a decrease in LVEDD to 5.7 ± 0.2 cm and an increase in EF to 32% ± 2% (both p < 0.01, paired Student t-test).
One patient was lost to follow-up after discharge; otherwise follow-up was complete for 20 patients, and ranged from 1 to 14 months (mean, 6 months). Seven patients had progressive heart failure after discharge, of whom 6 showed evidence of worsening mitral incompetence (3 had had Alfieri repair and 3 had no mitral valve repaired). Redo mitral valve replacement was done in 1 patient 6 weeks later, and another patient had heart transplantation at 6 months postoperatively. Of the 5 medically treated patients, 3 died at 1, 2, and 7 months postoperatively, and the other 2 remain in NYHA class III. The remaining 13 patients are in NYHA classes I (n = 5) and II (n = 8). Repeated echocardiography showed that LVEDD was maintained at 5.8 ± 0.2 cm and EF at 3% ± 2%.
Valvular cardiomyopathy
Nine patients with long-standing aortic valve incompetence and 1 patient with chronic mitral incompetence (LVEDD 8.6 ± 0.4 cm and EF 31% ± 4%) had PLV surgery. Preoperatively, 6 patients were in NYHA functional class III and 4 in functional class IV, with 2 patients dependent on inotropic agents.
All patients but one were weaned from cardiopulmonary bypass with the aid of inotropic drugs, and two required additional intraaortic balloon pump support. One patient died in-hospital of low cardiac output, and 9 survived and were discharged from hospital. Predischarge echocardiography showed a decrease in LVEDD to 7.9 ± 0.6 cm and an increase in EF to 42% ± 3% (both p < 0.01).
Follow-up was complete in all patients and ranged from 1 to 18 months (mean, 7 months). After discharge, 1 patient died of prosthetic valve thrombosis 3 months postoperatively. In 3 patients, one with Alfieri repair and two with un-repaired mitral valves, progressive mitral incompetence developed. Two of these patients died of intractable heart failure 1 and 13 months postoperatively, and the third remains in NYHA class III. The remaining 5 patients improved to NYHA class I (n = 3) and II (n = 2) at a mean follow-up period of 8 months (range, 2 to 18 months), and repeated echocardiography showed persistent LVEDD of 8.0 ± 1 cm and EF of 40% ± 4%.
Ischemic cardiomyopathy
Three patients with ischemic cardiomyopathy (all NYHA class III, LVEDD 7.1 ± 0.2 cm and EF 24% ± 3%) had PLV procedures. The lateral wall of the LV was resected in 2 patients, whereas the densely scarred anterior wall was resected in the third. All three patients had an uneventful postoperative course and were discharged from hospital within 2 weeks postoperatively. Predischarge echocardiography showed a LVEDD of 6.8 ± 0.2 cm and EF of 34% ± 2% (p < 0.01). There was no symptomatic benefit from the procedure in 2 patients, and only mild improvement in the third. Severe mitral incompetence developed in 1 patient (Alfieri repair), and redo mitral valve replacement was done 3 months later. This patient died 7 months after the second procedure of intractable heart failure. Another patient died suddenly 15 months after PLV, and the third patient remains in NYHA class II. Repeated echocardiography in this patient showed a persistent ejection fraction of 37%.
Other causes
Five other patients had PLV procedures, and the origin of heart failure was peripartum cardiomyopathy in 3, viral myocarditis in 1, and sarcoidosis in 1. All patients were in NYHA class IV preoperatively, with 2 patients dependent on inotropic support. The LVEDD was 7.4 ± 1 cm and EF was 22% ± 2%. All 3 patients with peripartum cardiomyopathy died postoperatively of low cardiac output. The remaining 2 patients were discharged from the hospital but did not seem to derive notable symptomatic benefit from the procedure. Echocardiography 6 months postoperatively did not show any increase in LV ejection fraction compared with preoperative values.
| Comment |
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Experience with PLV procedures has been predominantly in patients with idiopathic dilated cardiomyopathy, and data concerning the efficacy of the procedure in cardiomyopathy from other causes has been lacking. Although the number of patients is small, our data suggest that the PLV procedure might not be beneficial where there has been advanced structural damage to the cardiomyocytes and myocardial fibrosis (eg, in ischemic, viral, and peripartum cardiomyopathy), which agrees with a recent proposal [9]. Conversely, patients with cardiomyopathy related to valvular disease appear to benefit from PLV procedures, which is likely to be related, at least in part, to the natural tendency of the left ventricle to recover and to remodel after successful valve repair or replacement [12].
The influence of mitral valve competence on patient outcome merits particular attention. The isolated correction of severe mitral incompetence can improve LV function in dilated cardiomyopathy [12], and the beneficial effects of PLV and mitral valve repair are believed to be complimentary [11]. In the present series, most patients in whom heart failure symptoms recurred after PLV also had significant mitral incompetence. It is conceivable, therefore, that the development of progressive postoperative mitral incompetence had substantially increased LV overload and wall stress and was responsible for compromizing the remodeling process of PLV. Although this hypothesis is yet to be substantiated in a larger series, it is evident that maintenance of mitral valve competence is of paramount importance after PLV procedures.
Several factors might be involved in the development of mitral incompetence after the PLV procedure. The change in orientation of the papillary muscles could create redundant length to the chordae and leaflet prolapse [2]. Also, resection of left ventricular wall is associated with acute myocardial infarction surrounding the incision, and often involving one or both papillary muscles [4], with the attendant risk of papillary muscle fibrosis or dysfunction. It is not surprising, therefore, that when the mitral valve was unrepaired or the simple Alfieri suture was used, patients had a 55% to 60% risk of developing progressive mitral valve incompetence postoperatively. We now believe that definitive mitral valve repair [2, 10] or its replacement at the time of the PLV procedure is necessary to ensure long-term valve competence. Future experience will indicate whether this will translate into improved midterm outcome after PLV procedures, and larger series are also required before other factors responsible for late procedural failure are recognized.
Increased experience with PLV and future advances in postoperative treatment methods are likely to improve the outcome from PLV surgery [5]. In this regard, we recently reported a perioperative management strategy through which we have achieved hemodynamic stability and improved early patient outcome [13]. We believe that future development of more successful, but still widely attainable, methods for myocardial protection and pharmacological support of the chronically failed myocardium will lead to wider adoption of the PLV procedure [5]. This study has several limitations. Patients were not randomized, and there is no control group. Our group included patients with heterogeneous clinical diagnoses treated in six different medical centers, with inherent differences in care methods. The lack of back up with left ventricular assist devices or heart transplantation in our practice means that this experience does not reflect the expected outcome from the PLV procedures in centers where such facilities are available. Nevertheless, our settings are representative of a significant number of cardiac surgical centers worldwide which are currently treating many patients with advanced heart failure without access to such facilities.
In our experience, PLV improves left ventricular function in patients with idiopathic and valve related cardiomyopathies. Late postoperative deterioration appears related to the development of progressive mitral valve incompetence. Therefore, we believe that definitive mitral valve repair or replacement is necessary at the time of the PLV procedure to ensure maintenance of the critical mitral valve competence (Appendix 1).
| Appendix |
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| References |
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