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Ann Thorac Surg 1996;61:413-419
© 1996 The Society of Thoracic Surgeons
Division of Thoracic Surgery, Department of Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania
Abstract
Background. Clinical trials of dynamic cardiomyoplasty were pioneered at Allegheny General Hospital beginning in September 1985. Data from 9 years of experience with the procedure at this institution and more recent data from newer cardiomyoplasty centers have been analyzed for outcome analysis and future trends.
Methods. Each patient underwent a cardiomyoplasty procedure using the left or right latissimus dorsi muscle. Thirty-four patients were studied at Allegheny: 5 patients implanted with dual chamber pacemakers as single stimulus myostimulators, 11 patients composing the phase I Food and Drug Administration trial of the Medtronic burst myostimulator, and 18 patients entered in the phase II Medtronic trial. Patients from seven additional centers entered the phase II trial in 1991. Fifty-seven patients completed follow-up studies to 1 year after operation in this trial.
Results. Operative mortality was 5/57 (11%) in the American phase II group and 5/34 (15%) in the Allegheny group (1/18, 6% for Allegheny phase II). Nineteen patients (19/57, 33%) from the combined phase II population died in the first year, and 10/34 (29%) in the Allegheny study. The predominant cause of postdischarge death was arrhythmia (12/19, 63% American; 7/10, 70% Allegheny). In all groups significant improvement was seen in quality of life and functional class. Phase II patients demonstrated significant increases in ejection fraction and stroke work.
Conclusions. Failure to sustain improvement and arrhythmia-related death are complex challenges for this procedure; however, realistic solutions have been proposed and are under investigation.
The first clinical cardiomyoplasty in North America (and the second in the world) was performed at Allegheny General Hospital (AGH) on September 11, 1985 [1]. Nine years later it is apparent that we are experimenting not only with an innovative surgical procedure, but with an entirely new approach to the treatment of heart failure. These early studies have revealed the complexity, and promise, involved in harnessing skeletal muscle power for cardiac assist. A critical review of the clinical experience with cardiomyoplasty defines the challenges for ongoing research and suggests directions for future experimental studies.
Material and Methods
Cardiomyoplasty Procedure
Details of the procedure have been extensively described elsewhere [2, 3]. Briefly, the latissimus dorsi muscle (LDM) is resected from its tendinous origin and insertion while the intact neurovascular bundle is preserved. Electrodes for muscle stimulation are implanted. The second or third rib is resected and the LDM and distal pedicle are placed in the pleural cavity. Via a midsternotomy or thoracotomy incision, the muscle is wrapped around the ventricles in one of several orientations based on the regional pathology and geometric configuration of the heart. The sensing lead implanted on the right ventricle and the LDM electrodes are tunneled to a pocket in the abdominal wall and connected to a pacemaker or cardiomyostimulator, which will control muscle contraction in synchrony with the heart. Beginning 2 weeks after the wrap operation, the LDM is trained for 8 weeks with gradually increasing electrical stimuli. The use of electrically transformed and stimulated skeletal muscle to reinforce and augment damaged myocardium is termed ``dynamic cardiomyoplasty.''
Allegheny General Patient Population
Thirty-four patients (23 men) underwent cardiomyoplasty at AGH between September 1985 and April 1993. Indication for operation was ischemic cardiomyopathy in 22 patients and idiopathic cardiomyopathy in 12. Mean age at operation was 57 years (range, 33 to 71 years).
Concomitant operation performed in 10 patients consisted of left ventricular aneurysm repair or resection in 3 patients and coronary artery bypass grafting in 7 patients. Our institution has a multiple option approach to operation for congestive heart failure [4], which offers heart transplantation, coronary bypass, or cardiomyoplasty to appropriate patients. Bypass grafting in conjunction with cardiomyoplasty was performed in an effort to protect the myocardium during the perioperative period. These patients were not predicted to have significant hemodynamic benefit from the bypass procedure based on stress thallium testing; however, such benefits cannot be definitively ruled out in these patients. Coronary bypass was performed with cardiomyoplasty using either the right or left LDM; no wrap configuration compromised flow through a graft.
I. PATIENTS 1 THROUGH 5 (SEPTEMBER 1985 TO SEPTEMBER 1988).
The first patients studied were 3 women and 2 men, all with ischemic cardiomyopathy. Cardiomyoplasty was performed using the left LDM in the anterior cardiocostal configuration [5]. Stimulation of the LDM was accomplished in each patient with a standard dual-chamber pacemaker. The LDM was implanted with a perineural lead, which was affixed directly over the trunk of the thoracodorsal nerve. Mobilization of the LDM was performed in a separate surgical procedure before cardiomyoplasty in 1 patient (two-stage cardiomyoplasty). Three patients had concurrent aneurysectomy or aneurysm repair; 2 additional patients had coronary bypass procedures.
II. PATIENTS 6 THROUGH 15 (DECEMBER 1988 TO JANUARY 1991).
The second group of patients comprised 3 women and 7 men. The cause of cardiomyopathy was ischemic in 6 and idiopathic in 4 patients. This group was studied under the guidelines of a United States Food and Drug Administration protocol evaluating the Medtronic SP1005 burst cardiomyostimulator. Food and Drug Administration criteria required study patients to be in an advanced stage of heart failure for inclusion in the protocol. One patient had a one-stage procedure; the other 9 had two stage procedures. The left LDM was used in the posterior cardiocostal orientation in 5 patients, the anterior cardiocostal orientation in 3 patients, and the posterior cardiosubcutaneous orientation in 2 patients [5]. The LDM leads were implanted intramuscularly, interwoven between but not in contact with the branches of the thoracodorsal nerve. Two patients had coronary bypass operation concurrent with the myoplasty procedure.
III. PATIENTS 16 THROUGH 34 (MARCH 1991 TO APRIL 1993).
The final group of patients was made up of 5 female and 14 male patients. Eleven patients had ischemic and 8 idiopathic cardiomyopathy. These patients were studied under the phase II Food and Drug Administration protocol for further evaluation of the Medtronic burst stimulator. (One patient in this group entered study as a phase I patient but met phase II entry criteria and had follow-up evaluation completed under phase II guidelines.) Protocol inclusion criteria were adjusted in phase II to permit patients with slightly more cardiac reserve to enter the study. One patient (patient 16) had a two-stage procedure; in all others cardiomyoplasty was performed immediately after LDM mobilization. Sixteen patients had an anterior cardiocostal wrap using the right LDM. Three additional patients had posterior cardiocostal wraps with the left LDM. All LDM leads were placed intramuscularly, as described above. Two patients had coronary bypass grafting concurrent with the myoplasty procedure.
United States Combined Phase II Patient Population (March 1991 to June 1993)
The phase II protocol for evaluation of the Medtronic burst stimulator included expansion of the study to 7 North and South American sites in addition to AGH [6]:
Fifty-seven patients were studied between September 1985 and January 1994. Mean age was 58.7 ± 10.6 years and 44 were male (77%). Fifty-three patients (93%) were in New York Heart Association (NYHA) class III preoperatively, 31 (5%) were in NYHA class II, and 1 was in NYHA class IV. Cause of cardiomyopathy was idiopathic in 37 patients (65%), ischemic in 19 (33%), and Chagas' disease in 1 patient (2%). Cardiomyoplasty was performed using the left or right (AGH group only) LDM in the anterior cardiocostal (13 patients), the posterior cardiocostal (21 patients), or the posterior cardiosubcutaneous (23 patients) orientation. Concurrent operation was performed in 4 patients.
Results
Group I
An updated report on the results in these first United States cardiomyoplasty patients has recently been published [7].
Preoperatively, 4 patients were in NYHA class IV and 1 was in NYHA class III. Mean left ventricular ejection fraction (LVEF) was 0.29. One patient died of a ventricular arrhythmia 2 months postoperatively; all others were long-term survivors (greater than 6 months survival). Two patients had sudden death (presumed arrhythmia) at 28 months postoperatively. The remaining 2 patients are still alive more than 8 years after cardiomyoplasty.
All long-term survivors reported improvement in functional capacity (NYHA class I in 3, class II in 1). This subjective measure was not consistently matched to changes in hemodynamic parameters; however, serial exercise studies in 2 of the 4 survivors demonstrated consistent improvement in LVEF with paced as compared with unpaced LDM (Fig 1
). Similar studies could not be done in the remaining patients due to severe pulmonary vascular disease in 1 patient and early removal of the LDM pacer because of infection in the other.
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Preliminary risk analysis studies [8] in the 15 patients from groups I and II revealed that biventricular failure, pulmonary hypertension, and elevated pulmonary vascular resistance were associated with operative or early death. The 40% operative mortality clearly demonstrated that the procedure was inappropriate for patients lacking the reserve to survive a major cardiac operation and the 8-week period necessary for LDM training.
Long-term survivors had a significant increase in LVEF from 0.22 before operation to 31% after operation (p < 0.05). The salient observation in these patients, however, was the failure of early positive results to be sustained beyond 12 months after operation. Figure 1
presents left ventricular end-diastolic volume (LVEDV) data for 3 long-term survivors. These changes appeared to be correlated with patient reports of increased cardiac symptomology.
Group III
Eighteen patients in group III were in NYHA class III before cardiomyoplasty. Patient 25, accepted for study as a NYHA class III candidate, had sudden onset of congestive heart failure while awaiting operation outside the hospital. She was admitted and treated medically with excellent results, but is designated as in NYHA class IV because she was not discharged preoperatively. Mean preoperative LVEF for group III patients was 0.26.
There was one operative death in this group, secondary to perioperative myocardial infarction. All other patients survived to discharge. Three early deaths occurred, all due to sudden death (presumed arrhythmia). Fifteen patients became long-term survivors. Seven long-term survivors have died: 4 of presumed arrhythmia and 3 of heart failure.
Eight patients are currently alive at a mean of 29 months (range, 18 to 40 months) postoperatively. All survivors have reported increased ability to perform their preferred normal activities including recreational activities outside the home. Mean NYHA class for long-term survivors is 1.7.
Sixteen patients had cardiomyoplasty using the right LDM instead of the left LDM. Early results with the right LDM subset demonstrated impressive increases in LVEF and reductions in LVEDV. Results are presented in Figure 2. At 6 weeks postoperatively, LVEF by multigated acquisition scan had increased from a mean of 0.26 preoperatively to a mean of 0.33 (p < 0.03). The LVEDV was reduced at 6 weeks, but the decrease did not become significant until 6 months after operation. Preoperative mean LVEDV of 305 mL had fallen to a mean of 249 mL at that time (p < 0.01). Later in the follow-up period, LVEF and LVEDV tended to move toward baseline levels. Figure 3 presents summary data for the five 24-month survivors to illustrate this pattern of response. Left ventricular stroke work index rose in 10 of 12 patients studied at 6 months after operation, although the increase did not reach statistical significance. For most of these patients the increases were not sustained beyond 1 year.
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At the midpoint of the phase II enrollment period data from patients 1 through 32 were combined with matching data from 13 patients at a second American center (St. Vincent, Portland, OR) for analysis of risk factors for mortality [9]. Univariate analysis revealed a significant association between mortality and preoperative atrial fibrillation, low right ventricular ejection fraction, and elevated pulmonary artery pressures. Atrial fibrillation and low right ventricular ejection fraction had significant predictive power by multivariate analysis.
United States Combined Phase II Patient Population
Preliminary analysis of the results from the 57-patient phase II protocol has recently been completed [6]. The preoperative hemodynamic profile of this group was similar to the AGH phase II subset (Table 1). Mean preoperative LVEF was 0.22. Center differences in methodology for determining right ventricular ejection fraction prevented direct comparison of numeric results. Comparison of right heart function was therefore determined by investigator evaluation. Allegheny General Hospital enrolled significantly fewer patients with evidence of right heart dysfunction when compared with the other largest participating centers (p < 0.001).
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There were 7 operative deaths (12%), and 19 deaths (33%) occurred from 1 to 21 months after hospital discharge. Arrhythmia was the predominant cause of postdischarge death (12/19 deaths, 63%). Two patients died of ventricular failure and 5 patients died of noncardiac causes (sepsis, gastrointestinal, respiratory).
Analysis of mortality data demonstrated that preoperative arrhythmia, as a correlate for heart failure severity, is predictive of all mortality, not just sudden death. Of note, regression analysis of determinants of sudden death in the worldwide phase II study have failed to suggest additional screening criteria to reduce the risk of sudden death.
Six-week LVEF data were not collected for the combined study group; however, a significant increase in LVEF was seen in the 20 patients surviving at least 12 months (0.25 to 0.30; p < 0.05). Left ventricular stroke work index was also increased in these patients from a preoperative value of 26.1 g•m-1•beat-1 to 34.3 g• m-1•beat-1 at 12 months (p < 0.05).
Peak O2 consumption by metabolic exercise testing was unchanged at 6 and 12 months after cardiomyoplasty; however, patient perception of quality of life, as measured by a validated questionnaire [10], was significantly improved. As seen with AGH group III patients this shift centered on the ability to perform accustomed daily tasks and recreational activities without limitations imposed by cardiac symptomology. This observation is reflected in the significant improvement seen in NYHA class in 6 month survivors (Fig 4). Improvement in NYHA class was sustained in 12-month survivors.
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In heart failure, medical therapy is directed toward ameliorating the symptoms of inadequate cardiac output without altering the underlying cause. Substitution of a new human or mechanical pump for the failing native heart is obviously not the answer for more than a small percentage of patients. The failing ventricle needs to be stabilized, supported, and supplied with the power to circulate blood. Dynamic cardiomyoplasty is conceptually attractive as a method for accomplishing these tasks. Pioneering research in muscle plasticity has provided the means for producing the essential tool: a strong, malleable, nonfatigable contractile tissue. The initial results with cardiomyoplasty in the clinic have delineated complex problems involved in the application of this technique, while directing us to possible solutions.
Heart failure develops from multiple causes, and patients vary in presenting symptomology and degree of compensation. Our current criteria for the ideal patient are NYHA class III, LVEF greater than 0.20, preserved right ventricular function, sinus rhythm without atrial fibrillation or uncontrolled ventricular arrhythmia, and normal or reversible pulmonary function. It should be possible to expand inclusion criteria with improvements in methodology and equipment.
Arrhythmia is the primary cause of death after hospital discharge, as expected in a population with NYHA class III or IV heart failure. Although postcardiomyoplasty implantation of an implantable cardioverter-defibrillator has been accomplished in at least one urgent situation, very little is known about the potential interaction between the cardiomyostimulator and an implantable cardioverter-defibrillator. An LDM stimulator incorporating implantable cardioverter-defibrillator functions would be the ideal solution; however, definitive studies of combination implantations with currently available devices could be expected to decrease mortality.
The LDM wrap can be accomplished in at least four different configurations and can be performed using either the right or left muscle. Our clinical experience has convinced us that the choice of wrap should be tailored to the individual patient. In the case of the large, globally dilated ventricle, the left LDM wrap appears to be best suited to support and stabilize the myocardium. Rotating the LDM to the posterior cardiosubcutaneous position is useful in providing coverage to the severely enlarged heart. Some ischemic pathologies, such as ventricular aneurysm, may require regional support and stabilization; again, the left LDM is most easily manipulated for application to the affected area. In this context it is interesting to note the work of Mannion and colleagues [11], who have demonstrated evidence of collateral formation between the LDM and the myocardium. At this time cardiomyoplasty is not indicated for patients limited by angina; this finding has potential for extending the technique to these patients. In any case, increased vascularization of the myocardium would likely be beneficial to most patients.
The right LDM wrap was developed at AGH specifically to provide systolic augmentation for the failing left ventricle. The muscle is brought across the heart anteriorly and sutured to the posterior pericardium at the level of the atrioventricular groove, forming a slinglike orientation with the direction of contraction upward and to the right. Latissimus dorsi muscle contraction should theoretically vector the blood toward the left ventricular outflow tract. Our early results with 16 right LDM patients support the supposition that this approach can lead to augmented hemodynamic function.
A recent clinical study by Acker and associates [12] has provided evidence of a hemodynamic benefit conferred by the unstimulated LDM. Patients were studied at 6 and 12 months after cardiomyoplasty with the myostimulator turned off. Improvements were noted in left ventricular end-diastolic pressure, LVEF, and right atrial pressures, as well as a leftward shift in the left ventricular systolic pressure-volume relation. Acker and associates speculate that the LDM is acting as a ``girdle'' to remodel the ventricle toward a more normal size and configuration.
Analysis of follow-up data for the combined phase II study has not been completed for the patients surviving longer than 1 year postoperatively. In both AGH groups II and III (burst stimulator groups), some patients who survived longer than 1 year exhibited deterioration in cardiac function or reversal of early hemodynamic gains to baseline levels. It is possible that the LDM cannot sustain forceful contraction at a stimulus ratio of 1:2 with the LDM training and maintenance protocol now mandated for Food and Drug Administration-sanctioned studies. Long-term stimulation with this or similar regimens has been shown to produce a muscle with predominantly type I myofibers [13]. Fatigue resistance in the muscle is produced at the expense of significant power loss [14]. It may not be possible to develop a highly oxidative muscle without some sacrifice of power, but a reasonable goal would be a fiber mix expressing a combination of these traits. Preliminary work in this area suggests that a muscle composed of fiber types IIA and IID would express these characteristics. The mode of contraction during training has been shown to determine the properties of the transformed muscle fibers. Using shortening rather than isometric contractions is thought to produce fatigue-resistant (oxidative) fibers with little power loss [15]. We are currently evaluating protocols for muscle transformation, but this will be a slow process. Large animals are not economically feasible for these studies due to the number of stimulation variables and combinations to be compared. To this end, we have recently developed a miniaturized burst stimulator [16] for use in animals as small as the rat to increase our efficiency in chronic studies.
Long-term burst stimulation has been shown to produce skeletal muscle fibrosis in both animal and human studies, and this may also contribute to a late loss of LDM efficacy. In the clinic we have experimented with daily resting periods for the LDM, and some patients appear to have benefited (no deleterious effects were observed in this small sample). We first instituted this procedure in a patient hospitalized for end-stage heart failure at 18 months after cardiomyoplasty. The myostimulator was turned off by magnet for two 2-hour intervals every day. The patient was able to be discharged home to his regular activities and had an increased LVEF at his next evaluation. The LVEF in a second patient had fallen below baseline after impressive early increases. One month after starting the rest regimen, LVEF had increased 11 points (0.33 to 0.44).
The capacity of the LDM to perform the work of dynamic cardiomyoplasty is dependent on the sustained integrity of the muscle after translocation into the thoracic cavity. Postmortem histologic analysis frequently demonstrates pronounced fibrosis in the distal third of the wrapped LDM. This portion of the LDM is perfused in situ by chest wall perforating vessels. Isolation of the LDM on its neurovascular bundle creates an immediate ischemic insult to this area, which may be exacerbated by muscle edema. The muscle can produce new vascular patterns if allowed to adapt more slowly to its new role in a two-stage cardiomyoplasty procedure based on the concept of ``vascular delay'' [17]. In stage one the LDM is dissected from the chest wall, dividing the perforators and leaving the neurovascular bundle intact. The subcutaneous surface of the muscle is not dissected at this time to retard the development of muscle edema. Mobilization, transposition, and cardiac wrap are performed during stage two about 10 days later. The LDM pacing electrodes can be implanted during either stage, and muscle conditioning can be initiated during the delay period by direct or transcutaneous stimulation. The two-stage procedure is routinely used in experimental cardiomyoplasty but is thought to carry an unacceptable risk in the clinical setting. We have performed cardiomyoplasty as a two-stage procedure in 11 patients with morbidity and mortality rates comparable with one stage. The advantages of reclaiming up to 30% of LDM function are a strong argument for instituting this procedure in our patients.
It may be possible to enhance LDM strength by pharmacologic manipulation. Cheng and associates [18] have recently reported preliminary laboratory studies in which an anabolic steroid was infused directly into the electrically stimulated LDM. Increases in contractile force were seen with no change in LDM transformation patterns. As noted by Cheng and associates, this approach may be especially beneficial in enhancing the LDM of the chronically debilitated heart failure patient.
Several of our patients with the burst cardiomyostimulator have exhibited symptoms consistent with diastolic compromise. We have hypothesized that in these patients LDM relaxation is delayed beyond the initiation of diastole. Echocardiographic studies done on 2 patients paced at 1:2 appear to show LDM contraction continuing into the subsequent (nonpaced) cardiac cycle, although the evidence is not conclusive. With current technology, stimulation is fixed at a minimum burst duration of 185 ms, which may be too long at higher heart rates. An important advance would be the ability to program the burst duration to a percentage of the R-R interval. This should be especially advantageous in increasing patient exercise tolerance.
Another approach to the problem of delayed LDM relaxation is to look again at the standard dual-chamber pacemaker as a myostimulator. Unlike the summated tetanic contraction elicited by burst stimulation, the single spike muscle twitch elicited with this type of device provides a ``quick kick'' and fast relaxation. With careful timing to coincide with mitral closure, this limited LDM contraction may be all that is necessary in certain patients where the primary function of the LDM is to stabilize the ventricle. When the goal of LDM stimulation is to maintain LDM tone for support, the dual-chamber pacemaker should be the most logical choice.
In conclusion, clinical trials with dynamic cardiomyoplasty have thus far primarily served to demonstrate the complexity involved in its application. Our view of cardiomyoplasty in 1994 is much different, and more sophisticated, than the systolic assist procedure envisioned in 1985. Many problems have been encountered, but realistic solutions have been proposed for each obstacle. Ongoing studies should soon produce a healthier, stronger muscle and a choice of myoplasty configurations to match the wide range of human cardiac pathology. Enhanced control of muscle stimulation will be provided by a new generation of rate-responsive myostimulators, and the complementary roles of single and burst stimulation will be defined. Safe and effective methods for implantable cardioverter-defibrillator use should dramatically reduce mortality due to arrhythmia-a problem cardiomyoplasty was never intended to solve.
Initial results with clinical cardiomyoplasty are not consistent enough to warrant widespread application in the heart failure population at this time. However, when we analyze results in individual patients we can see improvement or stabilization in ventricular function when the cardiomyoplasty procedure is appropriate to the mode of cardiac dysfunction.
This is a pivotal time for dynamic cardiomyoplasty. Successes and failures have furnished us with the impetus and knowledge needed to solve the riddles. The same persistence that 40 years ago produced cardiac valve replacement can achieve similar results in this exciting new field.
Footnotes
Presented at The Third International Conference on Circulatory Support Devices for Severe Cardiac Failure, Pittsburgh, PA, Oct 28-30, 1994.
Address reprint requests to Dr Magovern, Division of Thoracic Surgery, Department of Surgery, Allegheny General Hospital, 320 E North Ave, Pittsburgh, PA 15212.
References
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V. S. Chekanov and V. V. Nikolaychik Suggestions for Overcoming the Weak Points of Cardiomyoplasty Ann. Thorac. Surg., October 1, 1996; 62(4): 1245 - 1247. [Full Text]
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