Ann Thorac Surg 1995;60:1219-1225
© 1995 The Society of Thoracic Surgeons
Original Articles: Cardiovascular
Treatment of Dilated Cardiomyopathy With Dynamic Cardiomyoplasty: The Heidelberg Experience
Rüdiger Lange, MD,
Falk-Udo Sack, MD,
Bernhard Voss, MD,
Raffaele De Simone, MD,
Matthias Thielmann,
Angélique Nair, MD,
Johannes Brachmann, MD,
Rainer Haussmann, MD,
Franz Fleischer, MD,
Siegfried Hagl, MD
Abt Herzchirurgie, Abt Innere Medizin III, and Klinik für Anaesthesiologie, Universitätsklinik, Heidelberg, Germany
Accepted for publication May 31, 1995.
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Abstract
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Background. Data concerning the efficacy of dynamic cardiomyoplasty are still inconsistent, especially in terms of improvement of left ventricular function.
Methods. Between August 1990 and February 1994, eight isolated cardiomyoplasty procedures were performed in patients with cardiomyopathy (ejection fraction, 0.14 to 0.32; New York Heart Association class III) and contraindications to heart transplantation.
Results. Follow-up was 41.1 ± 14.1 months. One patient died 2 months and another 3 years after operation. Considerable symptomatic improvement was found in 6 of 7 patients, 3 of whom went back to work. One patient with severe pulmonary hypertension exhibited no improvement. Mean New York Heart Association-class decreased from 3.0 to 1.9 (p < 0.001). Echocardiography showed an increase in fractional shortening and in peak aortic flow velocity in all patients. Left ventricular ejection fraction increased from 0.21 ± 0.05 to 0.38 ± 0.16 (n = 7, p < 0.015) at 1 year, to 0.37 ± 0.18 (n = 6, p < 0.05) at 2 years, and to 0.36 ± 0.19 (n = 5, not significant) at 3 years. Pulmonary artery pressure tended to decrease over time. No significant change in exercise level or maximal oxygen consumption during treadmill testing was observed.
Conclusions. Our preliminary results show that patients may exhibit an impressive clinical improvement after cardiomyoplasty, with only moderate changes in objective hemodynamic indices. We do not consider cardiomyoplasty an alternative to heart transplantation, but reserve it for patients with contraindications to heart transplantation.
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Introduction
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See also page 1225.
The method of dynamic cardiomyoplasty was developed on the basis of the intriguing concept of supporting the failing heart with the synchronous contraction of an autologous skeletal muscle. Although first applied clinically 9 years ago, cardiomyoplasty still lacks general acceptance as a routine surgical procedure. On the one hand, a time span of 9 years for the introduction of a new technique may not be long compared with that of other new concepts in cardiac surgery, such as the routine use of the internal mammary artery as the first choice of bypass graft or the preference of mitral valve reconstruction over replacement. On the other hand, regarding cardiomyoplasty, other factors might contribute to the surgeon's hesitation: To date, only a few controlled clinical trials can show the efficacy of this procedure in terms of improvement in hemodynamic indices or in exercise capacity [1–3]. However, general agreement exists about the improvement of the patients' clinical condition as shown by a decrease in the New York Heart Association (NYHA) classification, so that the term ``surgical placebo'' arose among cardiologists and surgeons [4]. In addition, a high mortality rate in the beginning of the surgical experience may have deterred surgeons from performing cardiomyoplasty.
The present study reports our initial experience with cardiomyoplasty in a homogeneous group of patients with ischemic or dilated cardiomyopathy. We excluded combined procedures such as left ventricular (LV) aneurysmectomy, valve replacement, or myocardial revascularization because these procedures may exhibit a hemodynamic benefit that cannot be differentiated from the possible hemodynamic effect attributed to the latissimus dorsi contraction. For ethical reasons, all patients were required to have contraindications to heart transplantation.
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Material and Methods
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Between August 1990 and February 1994, 8 patients presenting with end-stage cardiomyopathy underwent operation. All patients were in NYHA class III before the operation and had suffered from one or more episodes of cardiac decompensation. The time between the onset of NYHA class III symptoms and the operation was more than 1 year in all patients; all were unstable or deteriorating on maximal medical therapy. The diagnosis was dilated cardiomyopathy in 4, ischemic cardiomyopathy in 3, and alcoholic cardiomyopathy in 1 patient. All patients had contraindications to heart transplantation (Table 1
) such as chronic infections, severe sequelae of diabetes mellitus, or alcohol abuse. Patients in NYHA classes II and IV were not accepted. Patients with serum creatinine level greater than 2.5 mg/dL, resting lung function less than 50% of predicted, a history of ventricular tachycardia and ventricular fibrillation, a previous cardiac operation, angina pectoris, or associated cardiac defects were likewise excluded from the study.
Before the operation, the following examinations were performed: (1) pulmonary function tests (forced vital capacity [L/min], forced expiratory volume in 1 second [L/s], forced expiratory volume in 1 second to forced vital capacity, and airway resistance [L/kPa•s]); (2) treadmill exercise test with a modified Naughton protocol [5] (maximum exercise capacity [W], maximum oxygen consumption [mL•min-1•kg-1); (3) transthoracic Doppler echocardiography (fractional shortening, peak aortic flow [m/s], isovolumetric relaxation time [time in milliseconds between the end of the outflow curve and the onset of the inflow curve]); (4) M-mode echocardiography (end-diastolic [EDD, mm] and end-systolic [ESD, mm] ventricular diameter), with fractional shortening of the LV (FS) calculated with the following formula: FS% = [(EDD - ESD)/EDD]; (5) right heart catheterization with supine bicycle exercise (cardiac index by thermodilution, pulmonary artery pressure); and (6) left heart catheterization, with the ejection fraction (EF) determined using the RAO projection.
Applying the operative technique described by Carpentier and Chachques [6], we performed a posterior cardiocostal wrapping procedure [7] in all cases without the use of cardiopulmonary bypass. The latissimus dorsi muscle was dissected through a lateral oblique incision and transferred into the thorax through a small lateral thoracotomy, resecting a segment of the second rip. The chest was then opened through a midline sternotomy. As a minor modification of this technique, we used four to five single, pledged 3-0 Prolene (Ethicon; Somerville, NJ) sutures to fix the spinal rim of the latissimus dorsi muscle to the posterior wall of the left ventricle, which required repeated lifting of the heart. A remaining part of the right anterior wall, which could not be covered by muscle tissue in some cases, was bridged with a pericardial flap in continuity with the pericardial sac. The Cardiomyostimulator (Medtronic SP 1005/1005A/4710; Medtronic, Minneapolis, MN) was implanted under the left rectus abdominis muscle. The postoperative stimulation protocol followed the guidelines of Chachques and associates [8]. Three months after the operation, the latissimus dorsi was stimulated in all patients with a 185-millisecond, 30–33-Hz burst impulse in a one-to-one mode. The delay was set according to the closure of the mitral valve determined echocardiographically at 50 milliseconds. This interval applied to all 8 patients.
Every 6 months, the following examinations were repeated: lung function test, exercise test, right heart catheterization, left heart catheterization, and echocardiography.
The study was approved by the human research committee of the University of Heidelberg, December 21, 1990.
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Results
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The operative time (skin to skin) decreased according to a surgical learning curve and is now approximately 5 hours for the entire procedure. The time in the intensive care unit and the time required for ventilatory support varied from 3 to 17 days and from 10 to 143 hours, respectively (Table 2). Hospital stay varied from 16 to 57 days. One patient exhibited ventricular fibrillation early after the operation; this was successfully converted by electrical defibrillation and intravenous Amiodarone. The same patient had been on mexiletin before the operation. Two patients with ventricular ectopies were temporarily treated with intravenous xylocaine. All patients received inotropic support with dobutamine. In 2 patients, low-dose norepinephrine was temporarily added. None of the patients exhibited a significant increase in the creatine kinase level.
Seven patients had a mean follow-up of 41.1 ± 14.1 months. One patient died 57 days after the operation. Before the initiation of skeletal muscle stimulation, all patients were fully mobilized and had recovered from the operation. Twelve to 56 months after the operation, 2 of the 6 patients were in NYHA class I and 4 were in NYHA class II. One patient did not improve after the operation and remained in NYHA class III. Three patients went back to work, whereas 3 had already retired before the operation but would have been able to work; only 1 patient remained disabled. The mean NYHA class decreased from 3.0 to 1.9 (p < 0.001). One patient who had been in NYHA class I after the operation and was fully active died 34 months after the operation during a vacation. No symptoms of myocardial failure preceded his death; the patient died while sleeping in the sun. Sudden ventricular arrhythmia is suspected as the cause of his death.
The patient who died 57 days after operation exhibited a severe alcohol withdrawal syndrome and bilateral pneumonia, which resulted in prolonged ventilatory support. He was transferred from the intensive care unit to the ward after 17 days. On the 29th day, the patient presented with acute abdominal pain and a paralytic ileus. Intraoperatively, a small-bowel perforation was found and treated by resection and end to end anastomosis. The patient recovered initially from this operation. However, signs of protracted liver failure and pancreatitis with ascites, icterus, and enzyme elevation developed and the patient was retransferred to the intensive care unit, where he died. Autopsy findings included advanced liver disease and acute pancreatitis. The skeletal muscle wrap showed no signs of infection, displacement, or necrosis.
All patients could be stimulated according to the protocol. An increase of the burst amplitude was necessary in all patients during the first months after the operation. In addition, the sensitivity of the Cardiomyostimulator had to be adjusted in some patients when the postoperative electrocardiogram showed either that ectopic beats were incorrectly followed by a burst or that burst impulses occurred without a triggering QRS complex. Beyond 3 months after the operation, all patients were stimulated in a 1:1 mode, with a burst frequency of 30 or 33 Hz (according to six impulses in the burst). The amplitude ranged from 3.5 to 7.0 V. The battery of the Medtronic SP 1005 Cardiomyostimulator lasted for 19.8 ± 8.2 months before it had to be replaced. A second replacement was required 27 months after the first replacement in one of these patients, who then received the new Medtronic 4710.
One patient who showed no functional improvement after the operation exhibited an episode of cardiac decompensation at 23 months, which required temporary admission to the hospital. All other patients showed no signs of cardiac decompensation and were hospitalized only for routine evaluation or change of device. When battery failure occurred, patients first noted a deterioration in the level of physical activity, which usually occurred several days after the muscle stimulation had stopped. No patients noted an immediate cessation of the palpable contractions of the proximal pedicle of the latissimus dorsi upon battery failure. All patients were receiving angiotensin-converting enzyme-inhibitors before and after the operation.
Pulmonary Function and Exercise Test
In 1 patient, pulmonary function at rest showed a decrease of forced vital capacity from 4.5 L/min before the operation to 3.5 L/min after the operation. In another patient, there was an increase in forced expiratory volume in 1 second from 1.4 to 2.6 L/s and a decrease in airway resistance from 0.4 to 0.2 L/kPa•s, respectively. In all other patients, forced vital capacity, forced expiratory volume in 1 second, forced expiratory volume in 1 second to forced vital capacity, and airway resistance did not change. Upon ergospirometry, the maximal exercise level (W) increased in 5 of 7 patients when preoperative values were compared with the postoperative values (Fig 1). Before the operation, maximal oxygen-consumption was severely reduced to about 10 mL•min-1•kg-1 in 2 patients, to less than 15 mL•min-1•kg-1 in 3 patients, and to less than 20 mL•min-1•kg-1 in 1 patient. Mean changes for the maximal exercise level and for the maximal oxygen-consumption were not significant (Fig 2).
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Fig 1. . Ergospirometry showed an increase of the maximal exercise level (W) in 5 of 7 patients when preoperative values were compared with the postoperative values.
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Fig 2. . Before the operation, maximal oxygen-consumption was severely reduced to about 10 mL•min-1•kg-1 in 2 patients, to less than 15 mL•min-1•kg-1 in 4 patients, and to less than 20 mL•min-1•kg-1 in 1 patient. In contrast to the maximal exercise capacity, the maximal oxygen-consumption increased in only 5 of the 7 patients.
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Right Heart Catheterization
Right heart catheterization revealed no consistent change of cardiac index either at rest or during exercise when the preoperative values were compared with the postoperative values. Before the operation, the mean (± standard deviation) cardiac index at rest was 2.3 ± 0.6 L/min; 1 year after the operation, it was 2.6 ± 0.6 L/min (n = 7, not significant). The values after the operation represent the mean calculated from all 6-month interval determinations. Resting systolic pulmonary artery pressure tended to decrease after the operation (Fig 3). However, the mean did not decrease significantly, from 43.5 ± 25.2 to 37.3 ± 22.4 mm Hg. The increase in pulmonary artery pressure during exercise remained pathologic after the operation, but peak values were lower than before the operation.
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Fig 3. . Right heart catheterization revealed no consistent change of cardiac index. In contrast, resting systolic pulmonary artery pressure tended to decrease after the operation in some patients.
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Left Heart Catheterization
Left ventricular EF increased considerably in 1 of the 7 patients from a preoperative value of 0.30 to a postoperative value of 0.69 (last determination). However, all patients but 1 exhibited a moderate increase in LV EF (Fig 4). Left ventricular EF increased from 0.21 ± 0.05 to 0.38 ± 0.16 (n = 7, p < 0.015) at 1 year, to 0.37 ± 0.18 (n = 6, p < 0.05) at 2 years, and to 0.36 ± 0.19 (n = 5, not significant) at 3 years.
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Fig 4. . Left ventricular (LV) ejection fraction (EF) increased considerably in 1 of 7 patients from a preoperative value of 0.30 to a postoperative value of 0.69 (last determination). However, all but 1 patient exhibited a moderate increase in LV EF. Mean LV EF increased from 0.21 ± 0.05 to 0.38 ± 0.16 (n = 7, p < 0.015) at 1 year, to 0.37 ± 0.18 (n = 6, p < 0.05) at 2 years, and to 0.36 ± 0.19 (n = 5, not significant) at 3 years.
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A typical example of a postoperative angiogram with the stimulator turned off and on is shown in Figure 5. In this example, ventricular wall motion is enhanced by skeletal muscle contraction primarily in the anterobasal and posterobasal areas, as well as in the diaphragmatic wall of the left ventricle. The contribution to the anterolateral and apical wall motion is only minimal. In this example, EF increases from 0.13 to 0.39.
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Fig 5. . Example of a postoperative angiogram with the stimulator turned off (A) and on (B). Ventricular wall motion is enhanced by skeletal muscle contraction primarily at the anterobasal and posterobasal areas, as well as at the diaphragmatic level of the left ventricle. The contribution to the anterolateral and apical wall motion is only small. In this example, ejection fraction (EF) increased from 0.13 to 0.39. (EDV = end-diastolic volume; ESV = end-systolic volume; SV = stroke volume.)
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Echocardiography
The end-diastolic diameter showed no change when values before the operation and after 1 year were compared (Table 3). However, end-systolic diameter decreased in all patients and fractional shortening increased. The isovolemic relaxation time did not change.
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Comment
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The results of the present study are in agreement with others, in that cardiomyoplasty may markedly improve functional status with only moderate changes in objective hemodynamic indices. The objective hemodynamic improvement in 6 patients in our study is only moderate when compared with the notable decrease in NYHA class. However, it is well known that patients may be functionally well compensated as long as the LV EF is approximately 0.30 and that their condition may deteriorate rapidly when the LV EF reaches values of about 0.20 or less [9, 10]. Conceivably, the moderate increase in EF in our series, from 0.21 ± 0.05 to 0.38 ± 0.16 at 1 year, could account for the improvement in NYHA class and maximal exercise capacity. A similar increase in EF from 0.24 ± 0.06 to 0.31 ± 0.05 (p < 0.05) was reported by Chachques and associates [11] in a larger population of 44 patients after cardiomyoplasty, with a mean follow-up of 21 months. Their patients also exhibited a marked decrease in the mean NYHA class from 3.3 to 1.6. The group in Sâo Paulo, Brazil, also showed an increase in LV EF from 0.20 ± 0.03 to 0.23 ± 0.07 (p < 0.05) and in LV stroke work index from 17.5 ± 5.2 to 25.6 ± 9.4 g•m•m-2 (p < 0.05) in 22 patients 1 year after the operation [12]. In this series, the mean NYHA class decreased from 3.2 ± 0.4 to 1.7 ± 0.7 (p < 0.01).
By April 1994, a total of 360 patients, including those from a recently completed Food and Drug Administration study, were enrolled in the Medtronic Dynamic Cardiomyoplasty Clinical Study [1]. This study showed a significant increase in LV EF from 0.21 ± 0.07 to 0.24 ± 0.10 (p < 0.02) and in stroke work index from 29.3 ± 8.2 to 32.3 ± 10.6 mL•beat•m-2 (p < 0.03). Again, 79% of these patients showed an improvement in their postoperative NYHA class, the mean change being 1.4 NYHA classes. In our study, we also observed a trend for the systolic pulmonary artery pressure to fall after cardiomyoplasty. In a recent report by Moreira and co-workers [12], a significant fall in pulmonary capillary wedge pressure from 24.7 ± 6.3 to 18.2 ± 5.8 mm Hg (p < 0.05) was shown in 22 patients 12 months after cardiomyoplasty. Using the right latissimus dorsi, Magovern and associates [13] failed to demonstrate a significant increase of LV EF in 9 surviving patients 6 months after cardiomyoplasty, despite a decrease in the mean NYHA class from 3.0 ± 0.2 to 1.8 ± 0.2. Yet a significant decrease was observed in left ventricular end-diastolic volume, from 316 ± 23 to 261 ± 22 mL (p < 0.05).
Although hemodynamic results from different investigating centers are inconsistent, they are compatible with the theory that the heart/skeletal muscle complex may work at a reduced volume load after cardiomyoplasty while maintaining cardiac output, suggesting improved ``contractility.'' Recently, Carpentier and colleagues [14] referred to this improvement of contractility as ``active reinforcement,'' ie, active improvement of LV wall motion by the muscle graft. The power of transformed skeletal muscle has been calculated to be identical to the power developed by cardiac muscle during systole [15]. Unfortunately, in cardiomyoplasty only the less efficient distal part of the muscle can be used for ventricular assist. Furthermore, according to LaPlace's law, the load for the muscle is very high in severely enlarged ventricles. This may explain why the improvement in LV EF is only small and why larger improvements in LV function have been observed in experimental animals with smaller hearts [16, 17]. The concept of active reinforcement is strongly supported by a recent beat-to-beat analysis of the LV pressure–volume relation in 9 patients 6 to 24 months after cardiomyoplasty. Using the conductance catheter technique, a significant increase was shown in the peak ejection rate of LV volume by 28% ± 23%, in stroke volume by 20% ± 15%, in systolic aortic pressure by 7 mm Hg, and in peak aortic ejection rate by 68% ± 24% [18].
However, passive mechanisms also have been proposed for cardiomyoplasty. Experimental data suggest that an unstimulated muscle wrap around the heart does slow progressive ventricular dilation in dogs in a rapid pacing model [19]. The intrinsic tension of the muscle may hence prevent progressive dilation of the ventricles in patients after cardiomyoplasty. This was evidenced clinically by a stable cardiothoracic ratio up to 3 years after cardiomyoplasty [14]. As another conceivable mechanism of action, Chiu and co-workers [20] suggested a ``myocardial sparing effect'': Assuming that the skeletal muscle wrap contributes to myocardial wall thickness, dynamic cardiomyoplasty results in ``functional ventricular hypertrophy,'' thus lowering myocardial oxygen demand. This could lead to recovery of intrinsic myocardial function.
Although the hemodynamic data are not always in agreement, the improvement in functional status has been shown consistently in all studies [1, 2, 11, 13]. The improvement of functional status, ie, the lessening of the impact of the disease on daily function, is an important therapeutic goal in the treatment of congestive heart failure. In this respect, the lack of correlation between functional status, exercise capacity, and EF in patients with severe congestive heart failure is well known [21, 22]. Upon retrospective questioning, 6 of the 7 patients in our study exhibited a marked decrease in their ``sickness-related dysfunction'' [21], estimated as changes in physical, psychologic, and social behavior. The group in Sâo Paulo, Brazil, explicitly addressed the issue of quality of life in a study of 14 patients, 13 ± 9 months after cardiomyoplasty. They found an important decrease in limitations of physical activity, sleep pattern, social activity, and perceptions and expectations about the treatment, suggesting improved quality of life [23]. This is confirmed by the data from the Medtronic Worldwide Cardiomyoplasty Study [1]. Prospective investigation by questionnaires before, and at least 6 months after cardiomyoplasty revealed an improvement in activities of daily living in 86.5%, in social activities in 74%, in quality of interaction in 78%, and in mental health in 69% of the patients.
Although initially high, the operative mortality rate for the cardiomyoplasty procedure currently is between 0% and 18% [1, 2, 4, 11, 24, 25]. Death has been attributed to myocardial failure, hemorrhage, sepsis, pulmonary infection, multiorgan failure, or arrhythmia [1, 11]. The strongest determinant for the postoperative mortality rate is proper patient selection [25]. For example, in the present series, 1 patient with alcoholic cardiomyopathy died 57 days after cardiomyoplasty, presumably because the preoperative liver dysfunction and the severity of the alcohol disease were underestimated. Intermediate-term mortality was low in our study population (1 of 7 surviving patients died after 34 months) and may be related to the hemodynamic benefits provided by cardiomyoplasty. Chachques and associates [11] reported that long-term survival of 44 patients was 79% after a mean follow-up of 21 months (3 months to 6.5 years). The importance of patient selection was highlighted by the results of the Medtronic Worldwide Multicenter Study. These results revealed a marked difference in intermediate-term mortality between 272 patients in NYHA class III preoperatively and 45 patients in NYHA class IV. Patients in preoperative NYHA class III had a 1-, 2-, and 3-year survival of 71.5%, 58.1%, and 50.7%, respectively. In contrast, patients in preoperative NYHA class IV had a 1- and 2-year survival of only 41.8% and 30.0%, respectively [1]. These figures have to be weighed against the natural mortality of patients with congestive heart failure who are receiving medical treatment. Patients who had to be rejected for heart transplantation because of contraindications and who had a mean maximal oxygen consumption of less than 14 mL•min-1•kg-1, had a 1-year survival rate of 47% and a 2-year survival of 32% [10]. Presuming that these patients are comparable to our patients undergoing cardiomyoplasty, 6 of whom had a maximal oxygen-consumption less than 15 mL•min-1• kg-1, survival in our study population is improved by the procedure, compared with the patients receiving medical treatment alone.
In conclusion, cardiomyoplasty was conceived as a new surgical method to treat end-stage heart failure. In the presence of increasing donor organ shortage and continuing unsolved problems with the long-term application of mechanical assist devices, there is a place for cardiomyoplasty as an additional treatment. Cardiomyoplasty is not considered an alternative treatment to heart transplantation, but may become an option in patients with contraindications to transplantation or as a ``bridge to transplantation.'' Based on as yet limited experience, one might summarize that cardiomyoplasty improves quality of life, survival, and hemodynamic function, although the latter two factors are less pronounced than initially expected. Experienced surgeons can perform cardioplasty with low patient mortality rates. Precise definition of the indications and of the risk factors for this procedure is in progress and may help to improve the results further.
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Footnotes
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Address reprint requests to Dr Lange, Abt Herzchirurgie, Chirurgische Universitätsklinik, INF 110, 69120 Heidelberg, Germany.
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References
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- Medtronic Inc. Medtronic dynamic cardiomyoplasty study worldwide experience 1 July 1985–1 April 1994 (phase I and II cardiomyoplasty study groups). 1994.
- Jatene AD, Moreira LF, Stolf NA, et al. Left ventricular function changes after cardiomyoplasty in patients with dilated cardiomyopathy. J Thorac Cardiovasc Surg 1991;102:132–8.[Abstract]
- Carpentier A, Chachques JC. Clinical dynamic cardiomyoplasty: method and outcome. In: Loop FD, Magovern GJ, eds. Seminars in thoracic and cardiovascular surgery. Vol. 3, no 2. Philadelphia: Saunders, 1991:136–9.
- Lange R, Sack F-U, Saggau W, et al. Experience with isolated cardiomyoplasty in patients with contraindications for heart transplantation. In: Carpentier A, ed. Cardiomyoplasty, 1995 (in press).
- Naughton J. Exercise testing: physiological, biochemical and clinical principles. New York: Futura, 1988.
- Carpentier A, Chachques JC. The use of stimulated skeletal muscle to replace diseased human heart muscle. In: Chiu RC-J, ed. Biomechanical cardiac assist. Mount Kisco, NY: Futura, 1986:85–102.
- Furnary AP, Christlieb IY, Magovern JA, Magovern GJ. A standardized nomenclature for latissimus dorsi cardiomyoplasty. J Cardiac Surg 1991;6(Suppl):74–9.
- Chachques JC, Grandjean PA, Carpentier A. Latissimus dorsi dynamic cardiomyoplasty. Ann Thorac Surg 1989;47:600–4.[Abstract]
- Keogh A, Freund J, Baron D, Hickie J. Timing of cardiac transplantation in idiopathic dilated cardiomyopathy. Am J Cardiol 1988;61:418–22.[Medline]
- Mancini DM, Eisen H, Kussmaul W, Rebekah M, Edmunds HL, Wilson JR. Value of peak exercise oxygen consumption for optimal timing of cardiac transplantation in ambulatory patients with heart failure. Circulation 1991;83:778–86.[Abstract/Free Full Text]
- Chachques JC, Acar C, Portoghese M, et al. Dynamic cardiomyoplasty for long-term cardiac assist. Eur J Cardiac Surg 1992;6:642–8.
- 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.[Abstract/Free Full Text]
- Magovern JA, Park SE, Cmolik BL, Trumble DR, Christlieb IY, Magovern GJ. Early effects of right latissimus dorsi cardiomyoplasty on left ventricular function. Circulation 1993;88:298–303.
- Carpentier A, Chachques JC, Acar C, et al. Dynamic cardiomyoplasty at seven years. J Thorac Cardiovasc Surg 1993;106:42–53.[Abstract]
- Salmons S, Jarvis JC. Cardiomyoplasty: a look at the fundamentals. In: Carpentier A, Chachques J-C, Grandjean PA, eds. Cardiomyoplasty. Mount Kisco, NY: Futura, 1991:3–17.
- Lange R, Sack F-U, Saggau W, Vahl C, De Simone R, Hagl S. Performance of dynamic cardiomyoplasty related to the functional state of the heart. J Cardiac Surg 1991;6(Suppl):225–35.
- Moreira LF, Chagas AC, Camarano ACP, et al. Cardiomyoplasty benefits in experimental myocardial dysfunction. J Cardiac Surg 1989;4:164–70.[Medline]
- Schreuder J, van der Veen FH, van der Velde ET, et al. 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.[Abstract/Free Full Text]
- Capouya R, Gerber RS, Drinkwater DC, et al. Girdling effect of nonstimulated cardiomyoplasty on left ventricular function. Ann Thorac Surg 1993;56:867–71.[Abstract]
- Chiu RC-J, Odim JNK, Burgess JH. The McGill Cardiomyoplasty Group. Responses to dynamic cardiomyoplasty for idiopathic dilated cardiomyopathy. Am J Cardiol 1993;72:475–9.[Medline]
- Rector TS, Francis GS, Cohn JN. Patients selfassessment of their congestive heart failure. Patients perceived dysfunction and its poor correlation with maximal exercise test. Heart Failure 1987;3:192–6.
- Franciosa JA. Why patients with heart failure die: hemodynamic and functional determinants of survival. Circulation 1987;75(Suppl IV):IV-20–7.
- Borghetti-Maio SA, Romano BW, Bocchi EA, et al. Quality of life after cardiomyoplasty. J Heart Lung Transplant 1994;13:271–5.[Medline]
- Jegaden O, Delahaye F, Finet G, et al. Late hemodynamic results after cardiomyoplasty in congestive heart failure. Ann Thorac Surg 1994;57:1151–7.[Abstract]
- Furnary AP, Magovern JA, Christlieb IY, Orie JE, Simpson KA, Magovern GJ. Clinical cardiomyoplasty: preoperative factors associated with outcome. Ann Thorac Surg 1992;54:1139–43.[Abstract]
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Abstract
Introduction
