Dynamic cardiomyoplasty in South America

DYNAMIC MYOPLASTY

Dynamic Cardiomyoplasty in South America Luiz Felipe P. Moreira, MD, Noedir A. G. Stolf, MD, Domingo M. Braile, MD, and Adib D. Jatene, MD Instituto do Coraq~o da Universidade de Sao Paulo, S~o Paulo and Hospital da Sociedade Portuguesa de Beneficencia, S~o Jos~ do Rio Preto, Brazil

Background. Dynamic cardiomyoplasty has been proposed in the treatment of severe cardiomyopathies. However, few reports to date have shown significant numbers of patients collected on a multicenter basis. Methods. From July 1987 to June 1994, dynamic cardiomyoplasty was performed in 112 patients in South America. The indications were dilated cardiomyopathy in 96 patients, Chagas' disease cardiomyopathy in 13, and ischemic cardiomyopathy in 3. Left latissimus dorsi muscle was used in all patients. Results. The thirty-day mortality rate was 8.1%, and patients were followed up for 22.1 ± 18.6 months. Data of surviving patients show that 47.3% were in New York Heart Association functional class I, 45.6% in class II, and 7% in class IIl or IV I year after the operation. The l-year survival was 78.4%; 2-year, 59.7%; and 5-year, 41.7%. The

survival at 1 year was 86.1% for patients with dilated cardiomyopathy and 40% for those with Chagas' disease. At 5 years, these values were 49.8% and 9.5%, respectively. Long-term survival was also significantly affected by preoperative functional class and pulmonary vascular resistance. However, patients operated on in class III or intermittent class IV and without elevated pulmonary vascular resistance had survival rates of 91.5% at 1 year and 76.7% at 5 years of follow-up. Conclusions. Cardiomyoplasty improves the functional status of patients with severe cardiomyopathies. Otherwise, long-term survival after this procedure is limited in patients with Chagas' disease and by patients' condition before the operation.

ince its first clinical application in 1985, dynamic cardiomyoplasty has been performed worldwide to partially replace or reinforce the myocardium in the treatment of left ventricular tumors or aneurysm and in patients with ischemic or dilated cardiomyopathies [1-3]. Its primary objectives are to reverse congestive heart failure and to halt the progression of the underlying disease by increasing ventricular pumping performance and by reinforcing the ventricular walls. In South America, this operation has been investigated especially as an alternative to heart transplantation in the treatment of dilated cardiomyopathies. The clinical experience started in 1987 with Molteni and associates [4] in Argentina, using standard dual-chamber pulse generators for skeletal muscle flap stimulation. One year later, Moreira and colleagues [5] and Braile and co-workers [6], in Brazil, performed their first clinical cases with the use of pulse train stimulators specifically designed for this procedure. The purpose of this report is to review the clinical experience with dynamic cardiomyoplasty in South America, looking for the current benefits and limitations of this procedure in the treatment of patients with severe heart failure due to dilated cardiomyopathies.

Material and M e t h o d s

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Patient Population

Presented at The Third InternationalConferenceon CirculatorySupport Devices for Severe Cardiac Failure, Pittsburgh, PA, Oct 28-30, 1994. Address requests for reprints to Dr Moreira, Divisaode Cirurgia, lnstituto do Coraq~o,Av Dr En~as c. Aguiar,44 S~o Paulo, SP, Brazil.

The indications for dynamic cardiomyoplasty included mainly patients at a high risk of dying due to severe cardiomyopathy, which does not essentially differ from heart transplantation criteria [7]. Candidates to this procedure were screened based on factors that have been related to mortality in patients with congestive heart failure [7, 8]. These included indexes relating to cardiac pump dysfunction, such as left ventricular ejection fraction less than 0.30 and high left ventricular filling pressures, as well as the degree of functional impairment assessed by New York Heart Association functional class III or IV, or by the peak oxygen consumption during exercise testing less than 20 mL • kg -1 • min -1. On the other hand, patients submitted to cardiomyoplasty need to be stable enough on medical therapy to withstand a waiting period of 2 to 3 months before effective skeletal muscle flap adaptation. Therefore, patients receiving intravenous inotropic drugs were not candidates for this procedure. In addition, the operation was contraindicated in patients with important or severe valvular dysfunction, with arrhythmias not controlled by medical therapy, or with pulmonary or multiple organ diseases. From July 1987 to June 1994, dynamic cardiomyoplasty was performed in 112 patients at 12 different institutions in Brazil (71.5%), Argentina (26.7%), and Venezuela (1.8%). Of these patients, 78.5% were male and 21.4% were female. Most patients (65.5%) were between 40 and

© 1996 by The Society of Thoracic Surgeons Published by Elsevier Science Inc

0003-4975/96/$15.00 SSDI 0003-4975(95)00998-1

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CIRCULATORY SUPPORT MOREIRA ET AL CARDIOMYOPLASTY 1N SOUTH AMERICA

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Fig 1. Indications for cardiomyop|asty in South American experience. (CARDIOM. = cardiomyopathy.)

60 years of age, and small percentages were less than 40 years of age (26.1%) and more than 60 years of age (8.3%). Figure 1 displays the indications for the procedure and shows that the vast majority of patients had the diagnosis of dilated cardiomyopathy (85.7%). Twenty-five patients (22.3%) were hospitalized in New York Heart Association functional class IV immediately before cardiomyoplasty and some of them received intravenotm inotropic support in the month preceding the operation. The other 87 patients (77.6%) were in functional class HI or intermittent class W with maximal medical therapy with digitalis, diuretics, and angiotensin-converting enzyme inhibitors. Technical Considerations SURGICALPROCEDURE.Dynamic cardiomyoplasty was norreally performed without cardiopulmonary bypass, and the left latissimus dorsi muscle was used in all patients in this series. Most patients (85.1%) had this operation done by means of two separate incisions, a lateral approach for muscle flap dissection and a subsequent median sternotomy for cardiac access [6, 9-11]. A single lateral thoracic incision was used only by one in~;titution [4, 12]. Dissection and transposition of skeletal muscle flap followed the technique described by Carpenfier and associates [13]. The left latissimus dorsi muscle was wrapped around the ventricular surfaces with its edges normally fixed directly to the myocardium by separated sutures, providing a left posterior cardiocostal wrap in the vast majority of patients (83.9%) [6, 9-11]. Cardiomyoplasty was associated with other procedures only in 3 patients (2.7%): saphenous vein aortocoronary bypass grafting was performed in 2 patients and mitral valvuloplasty in the other. Pulse train generators specifically designed for this operation (cardiomyostimulators) were implanted in 95 patients (84.8%) [5, 9, 10] and standard dual-chamber pulse generators in 17 patients (15.2%) [11, 12]. STIMULATION PROTOCOL. Skeletal muscle flap stimulation normally started 2 weeks after the operation. The 17 patients with standard dual-chamber pulse generators had the skeletal muscle flap stimulated with single pulses synchronized to every cardiac beat during the complete follow-up period. Thirteen of these patients accomplished a muscle flap training period for 9 weeks MUSCLE

409

before cardiomyoplasty, using a single-chamber pulse train generator [12]. In the 95 patients receiving the cardiomyostimulators, the progressive muscle conditioning protocol described by Carpentier and associates [13] was followed. In the late postoperative period, pulse train stimulation was used with a burst frequency of 30 Hz. The muscle flap was paced synchronized with the heart rate in 1:1 or 1:2 modes. The delay between the ventricular sensed event and the muscle burst was adjusted under echocardiographic monitoring. Exact synchronization between the muscle flap contraction and ventricular systole was achieved, with the muscle stimulation starting immediately after mitral valve closure [9] or aortic valve opening [6].

Results Immediate Surgical Results The 30 day mortality rate after cardiomyoplasty in this series was 8.1%, and the global mortality rate in the muscle conditioning period was 10.7%. The causes of death during the immediate postoperative period were ventricular arrhythmia in 4 patients, cardiogenic shock in 2 patients, pulmonary thromboembolism in 1 patient, septicemia in 1 patient, and right ventricle rupture in 1 patient. Two of the 3 patients who died during the muscle conditioning period had progression of heart failure and cardiogenic shock; the other patient had pulmonary thromboembolism and infection. Late Clinical Results Patients were followed up from 2 to 66 months in this series (mean, 22.1 months). Data of the functional status of surviving patients in the cardiomyoplasty follow-up show that 47.3% were in New York Heart Association functional class 1, 45.6% were in class 11, and only 7% were class III or IV 1 year after the operation (p = 0.001 versus preoperative data). The quality of life assessment, performed in some of these patients, demonstrated a decrease in patients' limitations for physical activities, food and sleep patterns, and social activities at the late cardiomyoplasty follow-up [14]. Furthermore, improvement of the exercise capacity was documented by individual reports of different institutions [5, 11, 12, 15]. Figure 2 displays the 5-year actuarial survival curve of all patients submitted to dynamic cardiomyoplasty with the use of cardiomyostimulators. Patients in whom standard dual-chamber pulse generators were implanted were excluded from this representation. The 1-year survival was 78.4%; 2-year, 59.7%; and 5-year, 41.7%. Most of the late deaths after cardiomyoplasty were related to heart failure progression (61.9%), and sudden cardiac death occurred in 38.1% of the patients. The actuarial survival curves according to cardiomyoplasty indications are depicted in Figure 3. Two groups of patients were analyzed: patients with dilated cardiomyopathy, and patients with Chagas" disease cardiomyopathy. As seen in Figure 3, at I year the survival was 86.1% for dilated cardiomyopathy and 40% for Chagas" disease. At 5 years these values were 49.8% and 9.5%, respec-

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tively. In the Chagas' disease group, sudden cardiac death accounts for 50% of late deaths; in the dilated cardiomyopathy group, the causes of death in most patients were related to heart failure progression (64.7%). Figure 4 illustrates that patients with dilated cardiomyopathy hospitalized in New York Heart Association functional class IV immediately before cardiomyoplasty had lower survival rates than class III or intermittent class IV patients in the long-term follow-up. For patients operated on in class IV, survival was 66.6% at 1 year, 41.6% at 2 years, and 13.8% at 3 years. For patients undergoing cardiomyoplasty in class III or intermittent class IV, current data showed a 1-year survival of 87.8%, a 2-year survival of 77.2%, and a 5-year survival of 60.1%. In Figure 5, actuarial survival curves of patients with dilated cardiomyopathy are plotted according to preoperative pulmonary vascular resistance. Two groups were analyzed: patients with pulmonary vascular resistance of more than 4 Wood units and those with less than that value. The survival at 1 year was 63.6% for patients with

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Individual reports of institutions performing cardiomyoplasty in South America documented the significant improvement of left ventricular function after this procedure. An increase in left ventricular ejection fraction from 0.20 +- 0.03 to 0.24 - 0.06 (p < 0.001) was documented in 23 patients by radioisotopic angiography at 6 months of follow-up [10]. More important changes of this parameter and of left ventricular segmental wall shortening were also shown by echocardiography [6, 9, 12, 16]. These data also were obtained in patients submitted to single-pulse

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Ann ThoracSurg 1996;61:408-12

stimulation of the skeletal muscle flap [11,12]. Finally, left ventricular cineangiographic study, performed in 10 patients at 16 + 4 months of follow-up, documented that left ventricular ejection fraction improved in patients who survived long-term after cardiomyoplasty from 0.15 + 0.08 to 0.31 + 0.08 (p < 0.01) [17]. This improvement resulted from similar modifications of anterobasal, anterolateral, apical, diaphragmatic, and posterobasal left ventricular regional wall motions. Also important is the fact that this study and other reports showed a decrease in left ventricular ejection fraction when the cardiomyostimulator was turned off [5, 9, 17], which ruled out the possibility of a placebo effect. Significant changes in the hemodynamic parameters were also documented in some patients in this experience. Right heart catheterization showed that stroke index increased from 20.2 _+ 3 to 24.9 + 7.2 mL/m 2 at 6 months of follow-up (p < 0.01), despite the maintenance of cardiac index at values similar to preoperative data [9, 10]. Significant improvement of left ventricular stroke work was also documented after cardiomyoplasty, and it was associated with a significant decrease in pulmonary pressures [9, 10]. Besides these hemodynamic benefits, cardiomyoplasty may also Influence left ventricular mechanical properties. That was documented by pressure--volume loops obtained on simultaneous echocardiographic and hemodynamic studies performed in 8 patients at 16 + 4 months of follow-up, with the cardiomyostimulator on and turned off for 24 hours [18]. Significant reduction of left ventricular end-systolic stress from 175 + 12 to 149 + 10 g/cm 2 (p < 0.05) and of left ventricular end-diastolic stress from 69 + 8 to 37 _ 5 g/cm 2 (p < 0.01) were shown with the cardiomyostimulator turned on. A significant decrease in left ventricular chamber stillness and significant improvement of left ventricular maximal elastance were also observed during skeletal muscle flap stimulation. The long-term influence of cardiomyoplasty on left ventricular function was also studied by means of Doppler echocardiography, radioisotopic angiography, and right-sided heart catheterization [19]. These studies showed that the long-term course of patients with dilated cardiomyopathy submitted to cardiomyoplasty was characterized by the maintenance of the hemodynamic improvement documented early after the operation. This fact occurred despite the tendency of left ventricular ejection fraction to decrease to preoperative levels at 5 years of follow-up. Comment The clinical experience with dynamic cardiomyoplasty in South America shows that this procedure improves left ventricular function, ameliorates congestive heart failure, and seems to improve long-term survival of patients with dilated cardiomyopathy. In spite of controversial results regarding cardiomyoplasty influence on left ventricular function and hemodynamic profile [1-3], selection of patients including especially those with dilated cardiomyopathy in the present experience was advantageous for documenting the beneficial effects of this procedure.

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Improvements of left ventricular ejection fraction and stroke volume were demonstrated after cardiomyoplasty by several individual reports from centers participating in this study [5, 6, 9-12]. Moreover, this procedure's impact on circulatory function could be better evaluated by its reported influence on left ventricular stroke work and pulmonary pressures [9, 10]. In addition, cardiomyoplasty also influenced the mechanical properties of the failing heart. Reductions of left ventricular wall stress and left ventricular chamber stiffness Were documented under skeletal muscle flap stimulation [18], indicating that cardiomyoplasty may also decrease myocardial oxygen consumption [20]. Therefore, in a dilated, failing left ventricle, the primary pathophysiologic abnormalities were partially corrected and slow progression of the underlying cardiomyopathy could result from this mechanism [21]. That this may have occurred is suggested by the maintenance of left ventricular function improvement for up to 5 years after cardiomyoplasty [6, 19]. Improvement in functional class was also shown after cardiomyoplasty in this series, which agrees with the overall clinical experience with this procedure [1-3]. Furthermore, cardiomyoplasty could be performed in these patients with low 30-day mortality. Nevertheless, despite the functional and left ventricular function improvement documented in this experience, late mortality after cardiomyoplasty was elevated. Progression of heart failure occurred in patients with more important preoperative compromise and who presented complications of the underlying disease [6, 10, 11] or evidence of skeletal muscle flap ischemia in the immediate postoperative period [10, 22]. Cardiac sudden death was also observed, but its incidence was less than that described in the literature of approximately 20% to 30% per year in patients with chronic heart failure [23]. Otherwise, this complication is probably not a~ected by cardiomyoplasty and still needs an effective means of treatment. It is important to emphasize, on the other hand, that the current indications for cardiomyopiasty included mainly patients at a high risk of dying within 1 year, as they did not essentially differ from heart transplantation criteria [7]. In this regard, a previous report showed that the survival after this operation was much more favorable than the survival of a comparable, but not randomized, group of patients maintained on medical therapy [15]. In that study, patients submitted to cardiomyoplasty had a survival rate of 65% at 2 years of follow-up, whereas the 2-year survival was only 27% in the medically treated group. Furthermore, this series included patients with Chagas' disease cardiomyopathy who had poor long-term survival after the operation. In this regard, Chagas' disease is responsible for a high incidence of atrial and ventricular arrhythmias, and for the existence of chronic active myocarditis [6, 24]. These findings are not affected by cardiomyoplasty and indicate that this disease may represent a contraindication to the procedure. Also of interest is the fact that the mortality after cardiomyoplasty in this series was significantly greater in patients with dilated cardiomyoplasty operated on in functional class IV or with elevated pulmonary vascular

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CIRCULATORY SUPPORT MOREIRA ET AL CARDIOMYOPLASTY IN SOUTH AMERICA

resistance, suggesting that the degree of cardiac functional i m p a i r m e n t before the o p e r a t i o n plays an i m p o r tant role in the l o n g - t e r m outcome, O n the other hand, patients o p e r a t e d on in functional class III or intermittent class IV a n d with p u l m o n a r y vascular resistance less t h a n 4 W o o d units had survival rates of 82.6% at 2 years and 76.7% at 5 years of follow-up, which were shnilar to those reported after cardiac transplantation [25]. These values also positively contrast with the recent reports of heart failure treatment using angiotensin-conveffing enzyme inhibitors or vasodilators, which showed a survival probability of only 40% at 5 years for ~ lII patients [8, 26, 27]. In conclusion, d y n a m i c c a r d i o m y o p l a s t y is a p r o m i s i n g surgical alternative to the t r e a t m e n t of a d v a n c e d h e a r t failure d u e to dilated c a r d i o m y o p a t h y in patients in functional class III or reversible class IV w h o also p r e s e n t mild or m o d e r a t e p u l m o n a r y hypertension. In this regard, the surgical mortality in this series e n s u r e s a low-risk p r o c e d u r e a n d c a r d i o m y o p l a s t y does not preclude future h e a r t transplantation. Furthermore, the shortage of donors a n d the increasing n u m b e r of u r g e n t c a n d i d a t e s has d e c r e a s e d the n u m b e r of h e a r t transplants for o u t p a t i e n t candidates, justifying the necessity of alternative surgical options for patients with m o d e r a t e or severe c a r d i o m y o p a t h i e s who cannot achieve a reasonable quality of life and prognosis on medical therapy [28]. Further studies are needed, however, to improve technical aspects related to skeletal muscle flap preservation at the cardiomyoplasty procedure and to the long-term muscle stimulation protocol, as well as to better evaluate the late beneficial effects of this operation.

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11. Trainini JC, Barisani JL, Varini SD, et al. Cardiomioplastia, su perspectiva en el tratamiento de la insuficiencia cardiaca avanzada. Rev Arg Cardiol 1994;62:399-405. 12. Almada H, Molteni L, Ferreira R, Ortega D. Clinical experience with dynamic cardiomyoplasty. J Cardiac Surg 1990;5:193-8. 13. Carpentier A, Chachques JC, Grandjean PA, eds. Cardiomyoplasty. Mount Kisco, New York: Futura, 1991. 14. Borghetti-Maio SA, Romano BW, Bocchi EA, et al. Quality of life after cardiomyoplasty. J Heart Lung Transplant 1994;13: 271-5. 15. Moreira LFP, Seferian P Jr, Bocchi EA, et al. Survival improvement with dynamic cardiomyoplasty in patients with dilated cardiomyopathy. Circulation 1991;84(Suppl 3):296302. 16. Almada I-I, Molteni L, Ferreira R, et al. The value of the echo-Doppler in cardiomyoplasty procedures. J Cardiac Sufg 1991;6(Suppl):113-8. 17. Bocchi EA, Moreira LFP, Moraes AV, et al. Effects of dynamic cardiomyoplasty on regional wall motion, ejection fraction and geometry of left ventricle. Circulation 1992;86(Suppl 2):231-5. 18. Bellotti G, Moraes AV, Bocchi EA, et al. Late effects of cardiomyoplasty on left ventricular mechanics and diastolic filling. Circulation 1993;88(Suppl 2):304-8. 19. Moreira LFP, Stolf NAG, Bocchi EA, et al. Clinical and left ventricular function outcomes up to five years after dynamic cardiomyoplasty. J Thorac Cardiovasc Surg 1995;109:353-63. 20. Kawaguchi O, Goto Y, Futaki S, Ohgoshi Y, Yaku H, Suga H. Mechanical enhancement and myocardial oxygen saving by synchronized dynamic left ventricular compression. J Thorac Cardiovasc Surg 1992;103:573-81. 21. Packer M. Pathophysiology of chronic heart failure. Lancet 1992",340:88-93. 22. Bocchi EAr Bellotti G, Moreira LFP, et al. Prognostic indicators of one-year outcome after cardiomyoplasty for idiopathic dilated cardiomyopathy. Am J Cardiol 1994;73:604-8. 23. Larsen L, Markham J, Haffajee C1. Sudden death in idiopathic dilated cardiomyopathy: role of ventricular arrhythrnias. PACE 1993;16:1031-9. 24. Rossi M, Bralle DM, Souza DRS, et aL Dynamic cardiomyoplasty in chronic Chagas" heart disease: clinicopathological data. Ann Thorac Surg 1991;51:649-51. 25. The registry of the International Society of Heart and Lung Transplantation: ninth official report--1992. J Heart Lung Transplant 1992;11:599-606. 26. The SOLVD Investigators. Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure. N Engl J Med 1991;325:293-302. 27. Cohn JN, Johnson G, Ziesche S, et al. A comparison of enalapril with hydralazine-isosorbide dinitrate in the treatment of chronic congestive heart failure. N Engl J Med 1991;325:303-10. 28. Stevenson LW, Warner SL, Steimie AE, et al. The impending crisis awaiting cardiac transplantation. Modeling a solution based on selection. Circulation 1994;89:450-7. Appendix 1 The following institutions participated in the clinical experience with dynamic cardiomyoplasty in South America: Instituto do Cora~o da Universidade de S~o Paulo, S~o Paulo, Brazil; Hospital da Sociedade Portuguesa de Benefic~ncia, S~o Jos~ do Rio Preto, Brazil; Hospital Frances, Buenos Aires, Argentina; [nstituto Ant~rtida, Buenos Aires, Argentina; Instituto de Cardiologia, Porto Aiegre, Brazil; Santa Casa de Miseric6rdia, Ribeirio Preto, Brazil; Clinica Cardiotor~cica, Ribeir~o Preto, Brazil; Hospital da Universidade Cat61ica, Curitiba, Brazil; Santa Casa de Miseric6rdia, Londrina, Brazil; Santa Casa de Miseric6rdia, Presidente Prudente, Brazil; Hospital Italiano, Buenos Aires, Argentina; Fundacion Favaloro, Buenos Aires, Argentina; and Clinica E1 Avila, Caracas, Venezuela.