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Dynamic cardiomyoplasty: long-term clinical results in patients with dilated cardiomyopathy
Dynamic Cardiomyoplasty: Long-Term Clinical Results in Patients With Dilated Cardiomyopathy Domingo M. Braile, MD, PhD, Moacir F. Godoy, PhD Gra´cia H. The`venard, MD, Rubens S. The`venard, MD, PhD, Maria C. V. B. Braile, MD, Joa˜o C.F. Leal, MD, and Max Schaldach, PhD Faculdade de Medicina de Sa˜o Jose´ do Rio Preto-Medical School FAMERP, and Hospital Beneficeˆncia Portuguesa de Sa˜o Jose´ do Rio Preto, Sa˜o Paulo, Brazil
Background. Dynamic cardiomyoplasty has been considered to be an effective method of surgical treatment of patients with end-stage heart failure, and is an alternative to heart transplantation. Methods. We critically evaluated the long-term course of 52 patients with dilated cardiomyopathy who underwent dynamic cardiomyoplasty and were followed-up for up to 110 months. Results. Dilated cardiomyopathy was due to undetermined cause in 42 patients (80.8%), Chagas disease in 8 (15.4%), viral infection in 1 (1.9%), and peripartum cardiomyopathy in 1 (1.9%). In the nonchagasic group the survival rates were 79.5% ⴞ 6.1%, 67.8% ⴞ 7.1%, 53.7% ⴞ 8.3%, 49.9% ⴞ 8.3%, 14.9% ⴞ 12.2%, and 14.9% ⴞ 12.2%,
respectively, at 12, 24, 48, 60, 80 and 110 months of follow-up. In the chagasic patients the survival rates were 37.5% ⴞ 17.1%, 12.5% ⴞ 11.7%, 12.5% ⴞ 11.7% and 0%, respectively, at 12, 24, 48, and 60 months of followup, making chagasic cardiomyopathy a possible contraindication for dynamic cardiomyoplasty. Conclusions. There was no correlation between the clinical improvement and hemodynamic data. Ventricular fibrillation was a frequent cause of immediate and late death, suggesting the need for prophylactic use of antiarrhythmic drugs or implantable cardioverter/ defibrillators. (Ann Thorac Surg 2000;69:1445–7) © 2000 by The Society of Thoracic Surgeons
M
Dilated cardiomyopathy was due to undetermined causes in 42 (80.8%), Chagas disease in 8 (15.4%), viral infection in 1 (1.9%), and peripartum cardiomyopathy in 1 (1.9%). Functional class IV patients with ejection fractions less than 30% (as measured by echocardiography) and with eventual aggravating factors at rest underwent intensive clinical treatment so that, by the time of the surgical procedure, they had better functional conditions. The surgical technique used was basically that originally reported by Carpentier and Chachques [7]. For muscle stimulation, a Myos pacemaker (Biotronik, Berlin, Germany) was used. Left ventricular function was documented by one- and two-dimensional echocardiography (Echo-Doppler SIM 7000 CFM by ESAOTE Biomedical, Florence, Italy) assessing ejection fraction, segmental shortening fraction, systolic and diastolic diameters and volumes, and cardiac output, both preoperatively and in the late postoperative period. The results were compared by analysis of variance and Tukey’s test, assuming an ␣ error of 5%. The survival actuarial rates were calculated using the Kaplan-Meier method.
ortality by dilated cardiomyopathy in the first year after diagnosis ranges from 20% to 50% [1–3]. In the Framingham study, the survival rate of the patients who developed congestive heart failure was 50% after 5 years. In hospital series, the death rate was 50% in the first year. Furthermore, the life quality of such patients was severely hindered [4]. Dynamic cardiomyoplasty has been considered to be an effective method for the surgical treatment of patients with end-stage heart failure, and is an alternative to heart transplantation. The procedure was first introduced experimentally by Kantrowitz and McKinnon in 1959 [5], and was developed for use in human subjects by Carpentier and Chachques in 1985 [6]. The present study was developed to evaluate critically the long-term course of 52 patients with dilated cardiomyopathy who underwent dynamic cardiomyoplasty from 1988 to 1995 and were followed-up for up to 110 months.
Material and Methods A total of 52 patients were selected for cardiomyoplasty who, after the diagnosis of severe myocardial disorder, were considered to be at high risk for death within a 1-year period. Of these, 21 were female and 31 male. The mean age was 47 years (range, 13 to 72 years). Accepted for publication Nov 16, 1999. Address reprint requests to Dr Braile, Av Juscelino Kubitschek 3101, 15091450, Sa˜o Jose´ do Rio Preto, Sa˜o Paulo, Brazil; e-mail: [email protected].
© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Results Immediate Postoperative Period Of the patients who underwent cardiomyoplasty, 5 (9.6%) died before the end of the first postoperative month: 3 with chagasic dilated myocardiopathy (1 had massive 0003-4975/00/$20.00 PII S0003-4975(00)01184-X
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BRAILE ET AL DYNAMIC CARDIOMYOPLASTY: LONG-TERM RESULTS
Fig 1. Kaplan-Meier estimate of the probability of survival in chagasic patients with dilated cardiomyopathy undergoing dynamic cardiomyoplasty.
pulmonary embolism and 2 had ventricular fibrillation), and 2 with idiopathic cardiomyopathy (all due to ventricular fibrillation). The remaining patients had a good course during the early postoperative period.
Late Postoperative Period All of the patients were tolerant to the chronic stimulation of latissimus dorsi muscle, and did not complain of pain or discomfort during the muscle training. The 47 patients who were discharged from the hospital were followed-up for up to 110 months, with a mean follow-up of 37.3 ⫾ 25.7 months. The comparative statistical analyses between preoperative and postoperative means for left ventricular ejection fraction, segmental shortening, systolic and diastolic diameters, systolic volume, and cardiac output, evaluated by echo-Doppler cardiography, did not show significant difference in any of the areas studied. The causes of late death in the 5 chagasic patients discharged were cardiac failure in 2, ventricular fibrillation in 2, and sudden death in 1. Of the 23 deaths in the nonchagasic group there were at least 6 documented cases of ventricular fibrillation. For the chagasic group the actuarial study showed a survival rate of 37.5% (SEM 17.1), 12.5% (SEM 11.7), 12.5% (SEM 11.7), and 0%, respectively, at 12, 24, 48, and 60 months of follow-up. For the nonchagasic patients the survival rates were 79.5% (SEM 6.1), 67.8% (SEM 7.1), 53.7% (SEM 8.3), 49.9% (SEM 8.3), 14.9% (SEM 12.2), and 14.9% (SEM 12.2), respectively, at 12, 24, 48, 60, 80 and 110 months of follow-up There was a significant difference late mortality rates between the chagasic and nonchagasic groups (Figs 1 and 2).
Ann Thorac Surg 2000;69:1445–7
status of the patients, however, Odim and colleagues [13] pointed out the fact that no significant changes were shown in the left ventricular ejection fraction and cardiac index, emphasizing the need for further anatomopathologic studies aiming to clarify the mechanism of action of cardiomyoplasty. Schreuder and colleagues [14], looking for an explanation for the discrepancy between unchanged measurements of cardiac function and clinical outcome, performed a beat-to-beat analysis of cardiac performance at rest in 9 cardiomyoplasty patients 6 to 24 months after operation using conductance and micromanometer catheters placed in the left ventricle and aorta, and concluded that the cardiomyostimulator settings seemed to be critical in obtaining an increase or decrease in stroke volume during stimulation, and that clinical improvement (according to New York Heart Association class) may have been caused by active prevention of cardiac dilation. It must be remembered, however, that measurements were made while patients were at rest. To evaluate better the mechanical consequences of cardiomyoplasty, Kass and colleagues [15] performed serial left ventricular pressure–volume analysis in 3 patients with idiopathic dilated cardiomyopathy both before and at 6 and 12 months after surgery. They speculated that the muscle wrap can provide an elastic constraining effect to the heart, which in turn can partially reverse chronic chamber remodeling of heart failure. A worrisome observation is that there are still some deaths after cardiomyoplasty as a consequence of ventricular arrhythmias, mainly ventricular fibrillation. Therefore it is clear that cardiomyoplasty does not protect the patient from severe arrhythmias, even though it helped to improve survival and quality of life when compared with medical treatment with drugs, thus raising the question as to whether prophylactic use of antiarrhythmic drugs or implantable cardioverter/defibrillators would be a valid approach. The present study is unusual in that it allows a differential analysis between the late course of chagasic and nonchagasic patients undergoing cardiomyoplasty. We verified a clear, statistically significant difference between the two groups. The reason for this could be that
Comment From studies involving long-term follow-up of patients undergoing cardiomyoplasty, it can be seen that there is a clear improvement in the life quality of most of the patients in terms of functional class [8 –12]. Despite the clinical improvement in the functional
Fig 2. Kaplan-Meier estimate of the probability of survival in nonchagasic patients with dilated cardiomyopathy undergoing dynamic cardiomyoplasty.
Ann Thorac Surg 2000;69:1445–7
chagasic patients usually exhibit a higher prevalence of complex ventricular arrhythmias and, in addition, as shown in one patient by Rossi and colleagues [16], the reactivation of the disease is a possibility. The disease may also have a faster course, which might contribute to the earlier deterioration of the patient’s condition. In conclusion, in the present study, a clear improvement was documented in the survival of patients with nonchagasic dilated cardiomyopathy who underwent dynamic cardiomyoplasty. In the 44 patients comprising this group the survival rates were 79.5% (SEM 6.1), 67.8% (SEM 7.1), 53.7% (SEM 8.3), 49.9% (SEM 8.3), 14.9% (SEM 12.2), and 14.9% (SEM 12.2), respectively, at 12, 24, 48, 60, 80, and 110 months of follow-up. In the chagasic patients the survival rates were 37.5% (SEM 17.1), 12.5% (SEM 11.7), 12.5% (SEM 11.7) and 0%, respectively at 12, 24, 48 and 60 months of follow-up. This was not statistically significantly different from the results of clinical treatment, making chagasic cardiomyopathy a contraindication to dynamic cardiomyoplasty. There was no correlation between the clinical improvement and hemodynamic data such as left ventricular ejection fraction, systolic and diastolic volumes, and cardiac output. Ventricular fibrillation is a frequent cause of both immediate and late death, suggesting the need for prophylactic use of antiarrhythmic drugs or implantable cardioverter/defibrillators.
References 1. Espinoza R. Life expectancy analysis in patients with Chagas disease: prognosis after one decade (1973–1983). Int J Cardiol 1985:8:45– 6. 2. Stevenson LW, Perloff JK. The dilated cardiomyopathies: clinical aspects. In: Perloff JK, ed. Cardiology clinics: the cardiomyopathies, 2nd edition. Philadelphia: WB Saunders, 1988:187. 3. Unverferth DV, Magorien RD, Moeschberger ML, Baker PB, Fetters JK, Leier CV. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 1984;54: 147–52.
BRAILE ET AL DYNAMIC CARDIOMYOPLASTY: LONG-TERM RESULTS
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4. McKee PA, Gastelli WP, McNamara PM, et al. The natural history of congestive heart failure: the Framingham study. N Engl J Med 1971;285:1441–5. 5. Kantrowitz A, McKinnon W. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9: 266– 8. 6. Carpentier A, Chachques JC. Myocardial substitution with a stimulated skeletal muscle: first successful clinical case [Letter]. Lancet 1985;1:1267. 7. Carpentier A, Chachques JC. The use of stimulated skeletal muscle to replace diseased human heart muscle. In: Chiu RCJ, ed. Biomechanical cardiac assist: cardiomyoplasty and muscle-powered devices. Mount Kisco, NY: Futura, 1986:85– 101. 8. Almada H, Molteni L, Ferreira R, Ortega D. Clinical experience with dynamic cardiomyoplasty. J Card Surg 1990;5: 193– 8. 9. Grandjean PA, Austin L, Chan S, Terpstra B, Bourgeois IM. Dynamic cardiomyoplasty: clinical follow-up results. J Card Surg 1991;6(Suppl 1):80– 8. 10. Chachques JC, Acar C, Tapia M, et al. Mid-term results of cardiomyoplasty. Arch Mal Coeur Vaiss 1994;87:49–56. 11. Moreira LF, Stolf NA, Bocchi EA, Bacal F, Pego-Fernandes PM, Jatene AD. Cardiomyoplasty perspectives in the treatment of heart failure. Arq Bras Cardiol 1994;63:261– 6. 12. Chiu RCJ. Cardiomyoplasty for patients with ejection fraction (EF) less than 10%. Eur J Card Pacing Electrophysiol 1994;4:261. 13. Odim JN, Burgess JH, Williams BH, Blundell PE, Rabinovitch MA, Stewart JA, Lough JO, Chiu RC. Pathophysiology of dynamic cardiomyoplasty: a clinico-pathological case study. J Card Surg 1990;5:336– 46. 14. Schreuder JJ, van de Veen FH, van der Velde ET, Delahaye F, Alfieri O, Jegaden O, Lorusso R, Jansen JRC, van Ommen V, Finet G, Wellens HJJ. Beat-to-beat analysis of left ventricular pressure-volume relation and stroke volume by conductance catheter and aortic modelflow in cardiomyoplasty patients. Circulation 1995;91:2010–7. 15. Kass DA, Baughman KL, Pak PH, Cho PW, Levin HR, Gardner TJ, Halperin HR, Tsitlik JE, Acker MA. Reverse remodeling from cardiomyoplasty in human heart failure. Circulation 1995;91:2314– 8. 16. Rossi MA, Braile DM, Souza DR, Santos JL, Thevenard RS, Pinto GH, Suzigan S, Grecco O. Dynamic cardiomyoplasty in chronic Chagas’ heart disease: clinicopathological data. Ann Thorac Surg 1991;51:649–51.
Background. Dynamic cardiomyoplasty has been considered to be an effective method of surgical treatment of patients with end-stage heart failure, and is an alternative to heart transplantation. Methods. We critically evaluated the long-term course of 52 patients with dilated cardiomyopathy who underwent dynamic cardiomyoplasty and were followed-up for up to 110 months. Results. Dilated cardiomyopathy was due to undetermined cause in 42 patients (80.8%), Chagas disease in 8 (15.4%), viral infection in 1 (1.9%), and peripartum cardiomyopathy in 1 (1.9%). In the nonchagasic group the survival rates were 79.5% ⴞ 6.1%, 67.8% ⴞ 7.1%, 53.7% ⴞ 8.3%, 49.9% ⴞ 8.3%, 14.9% ⴞ 12.2%, and 14.9% ⴞ 12.2%,
respectively, at 12, 24, 48, 60, 80 and 110 months of follow-up. In the chagasic patients the survival rates were 37.5% ⴞ 17.1%, 12.5% ⴞ 11.7%, 12.5% ⴞ 11.7% and 0%, respectively, at 12, 24, 48, and 60 months of followup, making chagasic cardiomyopathy a possible contraindication for dynamic cardiomyoplasty. Conclusions. There was no correlation between the clinical improvement and hemodynamic data. Ventricular fibrillation was a frequent cause of immediate and late death, suggesting the need for prophylactic use of antiarrhythmic drugs or implantable cardioverter/ defibrillators. (Ann Thorac Surg 2000;69:1445–7) © 2000 by The Society of Thoracic Surgeons
M
Dilated cardiomyopathy was due to undetermined causes in 42 (80.8%), Chagas disease in 8 (15.4%), viral infection in 1 (1.9%), and peripartum cardiomyopathy in 1 (1.9%). Functional class IV patients with ejection fractions less than 30% (as measured by echocardiography) and with eventual aggravating factors at rest underwent intensive clinical treatment so that, by the time of the surgical procedure, they had better functional conditions. The surgical technique used was basically that originally reported by Carpentier and Chachques [7]. For muscle stimulation, a Myos pacemaker (Biotronik, Berlin, Germany) was used. Left ventricular function was documented by one- and two-dimensional echocardiography (Echo-Doppler SIM 7000 CFM by ESAOTE Biomedical, Florence, Italy) assessing ejection fraction, segmental shortening fraction, systolic and diastolic diameters and volumes, and cardiac output, both preoperatively and in the late postoperative period. The results were compared by analysis of variance and Tukey’s test, assuming an ␣ error of 5%. The survival actuarial rates were calculated using the Kaplan-Meier method.
ortality by dilated cardiomyopathy in the first year after diagnosis ranges from 20% to 50% [1–3]. In the Framingham study, the survival rate of the patients who developed congestive heart failure was 50% after 5 years. In hospital series, the death rate was 50% in the first year. Furthermore, the life quality of such patients was severely hindered [4]. Dynamic cardiomyoplasty has been considered to be an effective method for the surgical treatment of patients with end-stage heart failure, and is an alternative to heart transplantation. The procedure was first introduced experimentally by Kantrowitz and McKinnon in 1959 [5], and was developed for use in human subjects by Carpentier and Chachques in 1985 [6]. The present study was developed to evaluate critically the long-term course of 52 patients with dilated cardiomyopathy who underwent dynamic cardiomyoplasty from 1988 to 1995 and were followed-up for up to 110 months.
Material and Methods A total of 52 patients were selected for cardiomyoplasty who, after the diagnosis of severe myocardial disorder, were considered to be at high risk for death within a 1-year period. Of these, 21 were female and 31 male. The mean age was 47 years (range, 13 to 72 years). Accepted for publication Nov 16, 1999. Address reprint requests to Dr Braile, Av Juscelino Kubitschek 3101, 15091450, Sa˜o Jose´ do Rio Preto, Sa˜o Paulo, Brazil; e-mail: [email protected].
© 2000 by The Society of Thoracic Surgeons Published by Elsevier Science Inc
Results Immediate Postoperative Period Of the patients who underwent cardiomyoplasty, 5 (9.6%) died before the end of the first postoperative month: 3 with chagasic dilated myocardiopathy (1 had massive 0003-4975/00/$20.00 PII S0003-4975(00)01184-X
1446
BRAILE ET AL DYNAMIC CARDIOMYOPLASTY: LONG-TERM RESULTS
Fig 1. Kaplan-Meier estimate of the probability of survival in chagasic patients with dilated cardiomyopathy undergoing dynamic cardiomyoplasty.
pulmonary embolism and 2 had ventricular fibrillation), and 2 with idiopathic cardiomyopathy (all due to ventricular fibrillation). The remaining patients had a good course during the early postoperative period.
Late Postoperative Period All of the patients were tolerant to the chronic stimulation of latissimus dorsi muscle, and did not complain of pain or discomfort during the muscle training. The 47 patients who were discharged from the hospital were followed-up for up to 110 months, with a mean follow-up of 37.3 ⫾ 25.7 months. The comparative statistical analyses between preoperative and postoperative means for left ventricular ejection fraction, segmental shortening, systolic and diastolic diameters, systolic volume, and cardiac output, evaluated by echo-Doppler cardiography, did not show significant difference in any of the areas studied. The causes of late death in the 5 chagasic patients discharged were cardiac failure in 2, ventricular fibrillation in 2, and sudden death in 1. Of the 23 deaths in the nonchagasic group there were at least 6 documented cases of ventricular fibrillation. For the chagasic group the actuarial study showed a survival rate of 37.5% (SEM 17.1), 12.5% (SEM 11.7), 12.5% (SEM 11.7), and 0%, respectively, at 12, 24, 48, and 60 months of follow-up. For the nonchagasic patients the survival rates were 79.5% (SEM 6.1), 67.8% (SEM 7.1), 53.7% (SEM 8.3), 49.9% (SEM 8.3), 14.9% (SEM 12.2), and 14.9% (SEM 12.2), respectively, at 12, 24, 48, 60, 80 and 110 months of follow-up There was a significant difference late mortality rates between the chagasic and nonchagasic groups (Figs 1 and 2).
Ann Thorac Surg 2000;69:1445–7
status of the patients, however, Odim and colleagues [13] pointed out the fact that no significant changes were shown in the left ventricular ejection fraction and cardiac index, emphasizing the need for further anatomopathologic studies aiming to clarify the mechanism of action of cardiomyoplasty. Schreuder and colleagues [14], looking for an explanation for the discrepancy between unchanged measurements of cardiac function and clinical outcome, performed a beat-to-beat analysis of cardiac performance at rest in 9 cardiomyoplasty patients 6 to 24 months after operation using conductance and micromanometer catheters placed in the left ventricle and aorta, and concluded that the cardiomyostimulator settings seemed to be critical in obtaining an increase or decrease in stroke volume during stimulation, and that clinical improvement (according to New York Heart Association class) may have been caused by active prevention of cardiac dilation. It must be remembered, however, that measurements were made while patients were at rest. To evaluate better the mechanical consequences of cardiomyoplasty, Kass and colleagues [15] performed serial left ventricular pressure–volume analysis in 3 patients with idiopathic dilated cardiomyopathy both before and at 6 and 12 months after surgery. They speculated that the muscle wrap can provide an elastic constraining effect to the heart, which in turn can partially reverse chronic chamber remodeling of heart failure. A worrisome observation is that there are still some deaths after cardiomyoplasty as a consequence of ventricular arrhythmias, mainly ventricular fibrillation. Therefore it is clear that cardiomyoplasty does not protect the patient from severe arrhythmias, even though it helped to improve survival and quality of life when compared with medical treatment with drugs, thus raising the question as to whether prophylactic use of antiarrhythmic drugs or implantable cardioverter/defibrillators would be a valid approach. The present study is unusual in that it allows a differential analysis between the late course of chagasic and nonchagasic patients undergoing cardiomyoplasty. We verified a clear, statistically significant difference between the two groups. The reason for this could be that
Comment From studies involving long-term follow-up of patients undergoing cardiomyoplasty, it can be seen that there is a clear improvement in the life quality of most of the patients in terms of functional class [8 –12]. Despite the clinical improvement in the functional
Fig 2. Kaplan-Meier estimate of the probability of survival in nonchagasic patients with dilated cardiomyopathy undergoing dynamic cardiomyoplasty.
Ann Thorac Surg 2000;69:1445–7
chagasic patients usually exhibit a higher prevalence of complex ventricular arrhythmias and, in addition, as shown in one patient by Rossi and colleagues [16], the reactivation of the disease is a possibility. The disease may also have a faster course, which might contribute to the earlier deterioration of the patient’s condition. In conclusion, in the present study, a clear improvement was documented in the survival of patients with nonchagasic dilated cardiomyopathy who underwent dynamic cardiomyoplasty. In the 44 patients comprising this group the survival rates were 79.5% (SEM 6.1), 67.8% (SEM 7.1), 53.7% (SEM 8.3), 49.9% (SEM 8.3), 14.9% (SEM 12.2), and 14.9% (SEM 12.2), respectively, at 12, 24, 48, 60, 80, and 110 months of follow-up. In the chagasic patients the survival rates were 37.5% (SEM 17.1), 12.5% (SEM 11.7), 12.5% (SEM 11.7) and 0%, respectively at 12, 24, 48 and 60 months of follow-up. This was not statistically significantly different from the results of clinical treatment, making chagasic cardiomyopathy a contraindication to dynamic cardiomyoplasty. There was no correlation between the clinical improvement and hemodynamic data such as left ventricular ejection fraction, systolic and diastolic volumes, and cardiac output. Ventricular fibrillation is a frequent cause of both immediate and late death, suggesting the need for prophylactic use of antiarrhythmic drugs or implantable cardioverter/defibrillators.
References 1. Espinoza R. Life expectancy analysis in patients with Chagas disease: prognosis after one decade (1973–1983). Int J Cardiol 1985:8:45– 6. 2. Stevenson LW, Perloff JK. The dilated cardiomyopathies: clinical aspects. In: Perloff JK, ed. Cardiology clinics: the cardiomyopathies, 2nd edition. Philadelphia: WB Saunders, 1988:187. 3. Unverferth DV, Magorien RD, Moeschberger ML, Baker PB, Fetters JK, Leier CV. Factors influencing the one-year mortality of dilated cardiomyopathy. Am J Cardiol 1984;54: 147–52.
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4. McKee PA, Gastelli WP, McNamara PM, et al. The natural history of congestive heart failure: the Framingham study. N Engl J Med 1971;285:1441–5. 5. Kantrowitz A, McKinnon W. The experimental use of the diaphragm as an auxiliary myocardium. Surg Forum 1959;9: 266– 8. 6. Carpentier A, Chachques JC. Myocardial substitution with a stimulated skeletal muscle: first successful clinical case [Letter]. Lancet 1985;1:1267. 7. Carpentier A, Chachques JC. The use of stimulated skeletal muscle to replace diseased human heart muscle. In: Chiu RCJ, ed. Biomechanical cardiac assist: cardiomyoplasty and muscle-powered devices. Mount Kisco, NY: Futura, 1986:85– 101. 8. Almada H, Molteni L, Ferreira R, Ortega D. Clinical experience with dynamic cardiomyoplasty. J Card Surg 1990;5: 193– 8. 9. Grandjean PA, Austin L, Chan S, Terpstra B, Bourgeois IM. Dynamic cardiomyoplasty: clinical follow-up results. J Card Surg 1991;6(Suppl 1):80– 8. 10. Chachques JC, Acar C, Tapia M, et al. Mid-term results of cardiomyoplasty. Arch Mal Coeur Vaiss 1994;87:49–56. 11. Moreira LF, Stolf NA, Bocchi EA, Bacal F, Pego-Fernandes PM, Jatene AD. Cardiomyoplasty perspectives in the treatment of heart failure. Arq Bras Cardiol 1994;63:261– 6. 12. Chiu RCJ. Cardiomyoplasty for patients with ejection fraction (EF) less than 10%. Eur J Card Pacing Electrophysiol 1994;4:261. 13. Odim JN, Burgess JH, Williams BH, Blundell PE, Rabinovitch MA, Stewart JA, Lough JO, Chiu RC. Pathophysiology of dynamic cardiomyoplasty: a clinico-pathological case study. J Card Surg 1990;5:336– 46. 14. Schreuder JJ, van de Veen FH, van der Velde ET, Delahaye F, Alfieri O, Jegaden O, Lorusso R, Jansen JRC, van Ommen V, Finet G, Wellens HJJ. Beat-to-beat analysis of left ventricular pressure-volume relation and stroke volume by conductance catheter and aortic modelflow in cardiomyoplasty patients. Circulation 1995;91:2010–7. 15. Kass DA, Baughman KL, Pak PH, Cho PW, Levin HR, Gardner TJ, Halperin HR, Tsitlik JE, Acker MA. Reverse remodeling from cardiomyoplasty in human heart failure. Circulation 1995;91:2314– 8. 16. Rossi MA, Braile DM, Souza DR, Santos JL, Thevenard RS, Pinto GH, Suzigan S, Grecco O. Dynamic cardiomyoplasty in chronic Chagas’ heart disease: clinicopathological data. Ann Thorac Surg 1991;51:649–51.