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Ann Thorac Surg 1999;68:750-755
© 1999 The Society of Thoracic Surgeons

Alternatives To Transplantation

Dynamic cardiomyoplasty: at the crossroads

Michael A. Acker, MDa

a Division of Cardiothoracic Surgery, University of Pennsylvania School of Medicine, Philadelphia, Pennsylvania, USA

Address reprint requests to Dr Acker, Division of Cardiothoracic Surgery, University of Pennsylvania Medical Center, 3400 Spruce St, 4 Silverstein Pavilion, Philadelphia, PA 19104
e-mail: macker{at}mail.med.upenn.edu

Presented at the Fourth International Conference on Circulatory Support Devices for Severe Cardiac Failure, Houston, TX, Oct 3–5, 1997.

Abstract

Background. Dynamic cardiomyoplasty remains a promising, but still unproven surgical treatment for patients with end-stage heart failure. Lack of a clear survival advantage and ongoing misunderstanding of its mechanism of action have hindered its acceptance as a treatment alternative for patients with end-stage heart failure. This review seeks to update current clinical results and practice of dynamic cardiomyoplasty and to present its likely mechanism of action.

Methods. The method involved a literature review.

Results. More than 600 patients have undergone dynamic cardioplasty since 1985. Improvement in average New York Heart Association class was noted in 80% to 85% of hospital survivors. Operative mortality has decreased from 31% in Phase I to less than 3% in the ongoing Phase III trial. Clinical work as well as recent animal work supports the hypothesis that through a combination of long-term elastic constraint and active dynamic assist, dynamic cardiomyoplasty decreases myocardial wall stress associated with the remodeling process of progressive heart failure.

Conclusions. Though dynamic cardiomyoplasty can be shown to limit the remodeling process of heart failure in animal studies and some patients, its ultimate role in the treatment of heart failure will depend on the outcome of randomized, controlled studies.

Dynamic cardiomyoplasty (DCMP) remains a promising but still unproven surgical treatment for patients with end-stage heart failure. The procedure, first reported by Carpentier and Chachques [1] in 1985, involves mobilization of the latissimus dorsi muscle, which is then wrapped circumferentially around the heart. After a period of training, the muscle wrap is stimulated to contract in synchrony with cardiac systole. Long-term repetitive stimulation induces biochemical and physiologic transformations of the muscle, altering its characteristics toward cardiac muscle. These changes include fatigue resistance, increased aerobic capacity, prolonged contraction duration, diminution in size, and reduced maximal power [2–5].

Over the last 14 years, more than 600 patients have had DCMP worldwide. The vast majority have demonstrated significant improvement in New York Heart Association (NYHA) functional class and overall quality of life [6–8]. Despite this dramatic improvement, objective hemodynamic beneficial effects have not consistently been demonstrated, nor has a survival advantage been proved over medical therapy alone [9]. Further clouding the picture are evolving indications, uncertainty over risk stratification, relatively high operative mortality in the past, limitations of a first-generation cardiomyostimulator, concomitant operations, and a mechanism of action that remains unclear. Lack of a clear survival advantage and ongoing misunderstanding of its mechanism of action have hindered its acceptance to date as a treatment alternative for patients with end-stage heart failure. The purpose of this review is to update current clinical results and practice of DCMP and to present its likely mechanism of action.

Results of trials

Overall
In more than 600 patients implanted with Medtronic cardiomyostimulators, consistent clinical improvement has been noted in 80% to 85% of hospital survivors. On the average, the NYHA class improves 1.2 classes. The improvement begins within the first 6 months after operation and has been sustained for years. Quality-of-life measures assessing daily activity, social activity, quality of interaction, and mental health all improve significantly (Medtronic DCMP clinical database, 1996). In addition, the number of hospitalizations for heart failure has been seen to decrease [10].

Similar clinical improvement has been demonstrated in the recently completed Phase II Food and Drug Administration trial of DCMP [9]. This was a multicenter prospective trial carried out to evaluate the safety of the device in 68 patients. Outcomes were compared with those of a reference group of medically treated patients with matched demographic, etiologic, clinical, and hemodynamic variables. In both groups, almost all patients were in NYHA class III heart failure, had either ischemic or idiopathic cardiomyopathy, and were on a regimen of optimized medical therapy. The operative mortality rate was 12%. Eighty percent of patients were functionally improved at 6 and 12 months (3 ± 0.1 to 1.7 ± 0.1 NYHA class), which was significantly better than the reference group.

Hemodynamics
Despite the overwhelming evidence of clinical improvement, consistent evidence of clinically significant hemodynamic benefit is lacking. The Medtronic DCMP clinical database (1966) demonstrates a small but significant increase in left ventricular ejection fraction from 0.213 ± 0.068 to 0.242 ± 0.095 (p < 0.02). This small increase remains significant out to 2 years. In the Phase II trial [9], left ventricular ejection fraction increased from 0.227 ± 0.01 to 0.255 ± 0.019, and left ventricular stroke work index increased from 26 ± 1 to 30 ± 2 g-m · m-2 · beat-1. Both changes were significant. No change, however, was seen in cardiac index, pulmonary capillary wedge pressure, right ventricular ejection fraction, and maximal oxygen consumption. Recent reports [10–15] continue to demonstrate a small but significant improvement in left ventricular ejection fraction.

Survival
The Medtronic DCMP clinical data base reveals that the operative mortality associated with cardiomyoplasty has progressively decreased over the last decade (Medtronic DCMP, 1996). During an FDA Phase I feasibility study (1988–1991), 31% of patients did not survive hospitalization. Many of these patients were in NYHA class IV. During the FDA Phase II study [9] in which almost all patients were in class III, hospital mortality decreased to 12%. During the last 2 years, in 38 class III patients who have undergone cardiomyoplasty under the ongoing Phase III trial, the hospital mortality rate is less than 3% (Medtronic DCMP clinical database, 1996). Three quarters of hospital deaths are related to progressive heart failure and the remaining deaths, to sepsis or multisystem organ failure. Deaths that occur after initial hospital discharge are 79% cardiac in origin, with 38% of them sudden and 41% not sudden. Among the approximately 20% of deaths that are not cardiac related, about half are due to pneumonia and sepsis, and the rest are due to unknown noncardiac causes (Medtronic DCMP clinical database, 1996).

During the initial experience with cardiomyoplasty, survival for class IV patients was clearly shown to be much worse than that for class III patients. Today, most patients in NYHA class IV are not considered candidates for DCMP. The actuarial survival of FDA Phase II patients and a concurrent matched reference group is presented in Figure 1 [9]. Recently, actuarial survival appears to be showing further improvement (1 year, 78%; 2 years, 70%) for class III patients (n = 103) at experienced centers (Medtronic DCMP clinical database, 1996).



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  		Fig 1. Actuarial survival in Phase II multicenter clinical trial for dynamic cardiomyoplasty (DCMP): Comparison between patients having DCMP and matched reference group.

 
Furnary and associates [15] performed a multivariate analysis of risk factors for poor overall survival in 127 patients from three major centers who underwent DCMP. Predictors of poor results were atrial fibrillation, NYHA class IV, high pulmonary capillary wedge pressure, and need of intraaortic balloon pump. When peak O2 consumption was analyzed, pulmonary capillary wedge pressure and NYHA class were eliminated from the model. Analysis of 117 patients from the Phase II DCMP study group demonstrated that peak O2 consumption and left ventricular ejection fraction provided independent prognostic information for procedure-related death according to logistic regression analysis [16]. Rector and coworkers [17] updated the earlier multicenter analysis (n = 166) and found that in addition to peak O2 consumption and left ventricular ejection fraction, center experience and major coronary artery disease (coronary arteries with stenosis lesions > 70%) were predictors of cardiac mortality within 2 months after cardiomyoplasty. Moreira and colleagues [18] in 1995 reported 5-year follow-up of 31 patients who had DCMP. Multivariate analysis of factors influencing outcome showed that long-term survival was significantly affected by preoperative functional class and pulmonary vascular resistance.

Mechanism of action

Cardiomyoplasty was originally conceived as a method to mechanically assist the heart during ejection by "squeezing," thereby increasing beat-to-beat ejection fraction, stroke volume, and cardiac output. Though a few investigators [19, 20] have demonstrated the direct active synchronous assistance of the wrap on the failing heart, convincing hemodynamic evidence of clinically important beat-to-beat systolic assist is at best modest and often not seen at all despite significant improvement in functional status [21]. Others [11, 21, 22] have suggested that the primary action is a girdling effect whereby the muscle wrap acts to prevent further ventricular remodeling.

There continues to be substantial evidence supporting active systolic assistance in both clinical and animal studies. One year after DCMP in 13 patients, Jatene and coworkers [19] found that left ventricular ejection fraction increased with the stimulator "on" versus "off." Cho [23], Aklog [24], and their associates have shown augmentation of end-systolic elastance for assisted beats in normal hearts. My colleagues and I [25] reported that in chronically cardiomyopathic canine hearts, active cardiomyoplasty assist will result in a beat-to-beat increase in load-independent indices of contractility. In at least some patients, Schreuder and coauthors [20] showed quite convincingly that 1 year after DCMP, optimization of stimulation variables results in significant beat-to-beat improvement in cardiac function. Though most patients demonstrated no significant change, in about 50% of patients, Hagege and associates [11] saw a decrease in left ventricular ejection fraction and rate of rise of left ventricular pressure when the stimulator was turned off for 24 hours, suggesting a heterogeneous response of muscle wrap contraction. This may be related to the individual degree of latissimus dorsi muscle damage.

Passive girdling effects have been proposed as an additional mechanism of benefit. Carpentier and co-workers [6] demonstrated a stable cardiothoracic ratio for up to 3 years after DCMP; progressive dilatation would otherwise be anticipated in such patients. Capouya and colleagues [22] reported that placement of an unstimulated wrap around a normal heart followed by rapid ventricular pacing attenuated left ventricular enlargement. In our laboratory, my associates and I [25] have demonstrated that in a canine model of chronic cardiomyopathy, DCMP limits the remodeling process of ongoing heart failure, and this effect can also be achieved without long-term systolic assistance [26]. Kass and co-workers [21] found a leftward shift in the end-systolic pressure–volume relationship and stabilization of the end-diastolic pressure–volume relationship at 6 and 12 months after DCMP in 3 patients, findings suggesting a reversal of the remodeling process (Fig 2). Though no active systolic beat-to-beat assistance could be demonstrated, objective measures of systolic function improved dramatically. Evidence of reverse remodeling has also been presented by Lorusso and associates [10], who recently reported a significant reduction in left ventricular end-diastolic diameter up to 3 years after DCMP in 22 patients.



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  		Fig 2. Long-term effects of cardiomyoplasty on cardiac function as seen in pressure–volume relationship. Ventricular pressure–volume loops and relations are shown for each patient at baseline (before cardiomyoplasty) and 1 year after operation. All patients demonstrated a reduction in chamber volume. Vertical arrows show initial end-diastolic volume. (DPVR = diastolic pressure–volume relationship; ESPVR = end-systolic pressure–volume relationship.) (Reproduced from Kass and associates [21] by permission of the American Heart Association.)

 
Further evidence that active beat-to-beat assistance is not necessary for overall benefit from DCMP is provided by Hagege and coauthors [11]. In their study of 13 patients, who had all had DCMP more than 1 year before, there was no change in overall indices of left ventricular systolic or diastolic function after muscle wrap stimulation was stopped for 24 hours, though all patients showed clinical improvement and overall left ventricular ejection fraction was better compared with the preoperative value. Similar results were reported by Jondeau and coworkers [13]. Finally, there are anecdotal reports of clinical deterioration when the stimulator was found to be dysfunctional for more than 1 week to 2 weeks. This speaks more to the importance of synchronous stimulation long term than its active beat-to-beat assistance.

Kawaguchi and associates [27, 28] showed that mechanical artificial external synchronous systolic compression that mimics DCMP will decrease wall stress and myocardial oxygen consumption. In acute experiments using unconditioned muscle and normal hearts, Lee and coworkers [29] and Aklog and associates [24, 30] demonstrated decreased wall stress with active muscle wrap assistance. Recently in our laboratory, my coworkers and I [31] demonstrated in a canine model of chronic cardiomyopathy that DCMP results long term in an improvement in preload-recruitable stroke work and myocardial efficiency compared with control animals with heart failure and that muscle wrap stimulation further increased preload-recruitable stroke work and myocardial efficiency while potential energy decreased. This was seen without a change in stroke volume or cardiac output. Oh and colleagues [32] postulated that the muscle wrap of DCMP decreases wall stress according to Laplace’s law (increase thickness). For this to occur, the muscle wrap must develop and share tension with the myocardium even if there is no change acutely in overall left ventricular function [32]. These findings possibly explain why significant improvement in left ventricular ejection fraction and other standard measurements of left ventricular function are not necessarily found in patients who improve clinically.

In some patients with ischemic cardiomyopathy, DCMP can induce increased collateral blood flow to ischemic areas of the ventricle. Mannion and associates [33] demonstrated evidence of this in an ischemic animal model, and collaterals between the myocardium and the muscle wrap have been found in autopsy studies [34]. Finally, the possibility that stimulation of the latissimus dorsi nerve may affect the neurohormonal milieu by way of a central pathway must be investigated. In the future, staged mobilization procedures and new intermittent stimulation protocols may limit muscle damage and produce a stronger, yet still fatigue-resistant muscle with more potential for powerful cardiac assistance [35, 36].

Phase III randomized clinical trial

The Phase III randomized clinical trial, also known as C-SMART (Cardiomyoplasty–Skeletal Muscle Assist Randomized Trial), commenced in June 1995 (Fig 3). Its purpose is to determine the safety and efficacy of DCMP as treatment of heart failure caused by dilated cardiomyopathy or ischemic heart disease. It consists of two arms—the treatment or surgical arm and the control or medical management arm. All patients meet the same prerandomization criteria and are randomized to a specific group for 1 year. After that year, treatment patients are automatically enrolled in the follow-on phase for an additional 12 months for safety monitoring. At the end of 1 year, control patients can opt to either discontinue study participation or, if they still meet eligibility criteria, choose to receive DCMP. Safety and efficacy will be analyzed at 1 year with additional safety data on DCMP during the follow-on phase. Four hundred patients (200 with DCMP and 200 with standard medical therapy) will be recruited. The study uses the new Transform cardiomyostimulator (Medtronic). This is a second-generation system that has added features to prevent impairment of diastolic fill time and to limit excessive muscle stimulation during fast heart rates. Patient end points include hospitalizations, objective measures of exercise, quality-of-life scores, NYHA class, and survival.



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  		Fig 3. Design of Phase III randomized clinical trial, also known as C-SMART (Cardiomyoplasty–Skeletal Muscle Assist Randomized Trial).

 
Inclusion criteria include the following: adult patients with dilated cardiomyopathy or ischemic heart disease; advanced heart failure but not bedridden (NYHA class III); optimized medical therapy for heart failure; adequate pulmonary, renal, hepatic, and neurologic functions; left ventricular ejection fraction lower than 0.40; left ventricular end-diastolic pressure of less than 35 mm Hg; peak oxygen consumption of 10 to 22 mL · kg-1 · min-1; and intact latissimus dorsi muscle. Major exclusion criteria are as follows: current dependence on intravenous inotropic agents; diastolic blood pressure greater than 95 mm Hg with medication; myocardial infarction, cardiac arrest, or angioplasty within preceding 3 months; previous cardiac surgical procedure; anticipated concomitant cardiac procedure; participation in concurrent cardiac drug study; and symptomatic cardiac arrhythmia requiring an implantable cardiac defibrillator (separate study to begin assessing compatibility of cardiomyostimulator with an implantable cardiac defibrillator for patients with risk of ventricular arrhythmia who otherwise would be candidates for DCMP).

The phase III study should provide a clearer picture of the role of DCMP as a treatment alternative for patients with end-stage heart failure. Legitimate doubts about the efficacy of DCMP remain. Though patients are improved functionally, no significant hemodynamic or survival benefit has been demonstrated. Many cardiologists and cardiac surgeons agree with Leier [37], who wrote in a recent editorial, "In short those who need it, don’t survive it and those who survive it, don’t need it." Although many class III heart failure patients can be managed effectively with medication alone, there are clearly many patients on a regimen of maximal medical therapy whose quality of life and exercise capacity have worsened, but they are not sick enough to consider transplantation. Comparison of Minnesota Living with Heart Failure scores of recent DCMP patients with those of the class II and III patients in the Study On Left Ventricular Dysfunction (SOLVD) treatment arm demonstrates that the cardiomyoplasty patients perceive substantially greater limitations of daily living [10], which motivates them to seek surgical treatment of the heart failure in lieu of medication alone. It is clear that a more potent treatment alternative for these patients is necessary.

Conclusions

Chronic dilatation and remodeling are initially valuable adaptations that allow weakened hearts to achieve nearly normal systolic pressure and flows at increased, but still tolerable, diastolic pressures. Although initially adaptive, this ongoing process is maladaptive and represents a major risk factor for mortality [21]. The remodeled ventricle has a larger chamber with an increased radius of curvature, increased wall stress, increased myocardial oxygen consumption, impaired subendocardial blood flow, impaired myocardial energetics, and increased risk of arrhythmias [38]. It is likely that DCMP, through a combination of long-term elastic constraint and active dynamic assistance, decreases myocardial wall stress and attenuates the ventricular dilatation and remodeling associated with progressive heart failure (Fig 4).



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  		Fig 4. Dynamic cardiomyoplasty probably acts by at least two mechanisms to ultimately limit the remodeling process of progressive heart failure.

 
It is well accepted that the small, but important survival benefit attributed to angiotensin-converting enzyme inhibitors in patients with heart failure is secondary to an attenuation of progressive cardiac enlargement. This important but subtle effect was not realized until completion of large prospective randomized studies (SOLVD) [38]. What is now abundantly clear is that although DCMP has been shown in animal studies and in some patients to limit the remodeling process of heart failure, its ultimate role in the treatment of heart failure will depend on the outcome of properly designed randomized control studies such as C-SMART. The recent decline in the associated operative mortality of DCMP, a better understanding of its mechanism of action, the patient risk stratification, and the improved cardiomyostimulator may result in a demonstrable survival benefit. The results of C-SMART potentially will go a long way in determining whether DCMP will become a legitimate treatment alternative for patients with severe heart failure or be relegated to an interesting idea whose clinical niche is too small to be of larger clinical importance.

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