Dynamic cardiomyoplasty acutely impairs left ventricular diastolic function.

In patients with congestive heart failure, medical treatment has a high rate of mortality and morbidity, and transplantation is limited by the availability of donor hearts. Dynamic cardiomyoplasty is being investigated as surgical therapy to improve left ventricular function in these patients. To evaluate the early postoperative effects of this procedure on left ventricular diastolic function, we studied seven dogs through the use of sonomicrometry and micromanometry in a canine model of dynamic cardiomyoplasty. Left ventricular diastolic parameters were determined before wrapping the latissimus dorsi muscle (baseline), after latissimus dorsi muscle wrap but without stimulation, and with synchronous left ventricular contraction-latissimus dorsi muscle stimulation. End-diastolic pressure was increased in both conditions after latissimus dorsi muscle wrap (without stimulation, 5 +/- 1; with stimulation, 6 +/- 2 mm Hg; p < 0.05) compared with baseline (3 +/- 2 mm Hg). The peak rate of diastolic pressure decay was greater at baseline (1560 +/- 370 mm Hg/sec) than after latissimus dorsi muscle wrap, both without (1260 +/- 330 mm Hg/sec, p < 0.01) and with (1120 +/- 420 mm Hg/sec, p < 0.01) stimulation. The constant of pressure decay was prolonged both without (53 +/- 10 seconds, p < 0.05) and with (62 +/- 11 seconds, p < 0.01) latissimus dorsi muscle stimulation compared with the baseline (38 +/- 5 seconds). Compared with baseline (0.2 +/- 0.2 cm-2), the constant of passive chamber stiffness increased after the latissimus dorsi muscle was wrapped around the heart (1.6 +/- 0.7 cm-2, p < 0.05) and with stimulation (2.1 +/- 1.0 cm-2, p < 0.01). The maximal diastolic filling rate (baseline, 18.1 +/- 6.7; without stimulation, 16.6 +/- 8.9; with stimulation, 16.6 +/- 4.1 cm2/sec, not significant) and end-diastolic short-axis area (baseline, 7.3 +/- 2.3; without stimulation, 7.4 +/- 2.1; with stimulation, 7.5 +/- 2.3 cm2, not significant) were similar among the three conditions. The latissimus dorsi muscle wrap prolonged relaxation and increased left ventricular passive stiffness. Synchronous latissimus dorsi muscle stimulation with left ventricular contraction did not improve diastolic function in this model. The results suggest that in the early postoperative period, dynamic cardiomyoplasty impairs diastolic function.     

Full-thickness dynamic cardiomyoplasty of the left ventricle with free revascularized latissimus dorsi myografts. An experimental feasibility study.

Dynamic cardiomyoplasty, with use of a free latissimus dorsi myograft revascularized by the internal thoracic artery and vein, was performed in eight dogs subjected to electrical preconditioning for 8 to 12 weeks (group I) and in six unconditioned dogs (group II). The procedure was performed after the resection of the anterior wall of the left ventricle. Cardiac output and left ventricular stroke work were augmented by 23.7% +/- 9.4% and 44.1% +/- 15.9% after graft pacing with 50 Hz burst stimulation at a 1:1 synchronization ratio, while left atrial pressure ranged from 8 to 12 mm Hg. Analysis of the left ventricular function curve showed that graft pacing at rates of 1:1, 2:1, and 3:1 augmented global left ventricular function. Hemodynamic benefit by continuous pacing at a 3:1 ratio was seen for 1.97 +/- 1.90 hours (0.5 to 6.1 hours) in group I until complications unrelated to the graft terminated the study, while it lasted for only 0.19 +/- 0.09 hour in group II. During the stimulation, the ratio of the lactate output to the oxygen consumption of the graft in group I, a possible indicator of metabolic shift, was significantly less than in group II, (0.46 +/- 0.58 and 6.34 +/- 1.73; p < 0.01). We conclude that free grafts of transformed latissimus dorsi muscle can augment global left ventricular performance, with a physiologic preload by oxidative metabolism, and provide a viable option in full-thickness dynamic cardiomyoplasty.     

Effects of dynamic cardiomyoplasty on indices of left ventricular systolic and diastolic function in a canine model of chronic heart failure.

The effects of cardiomyoplasty were evaluated with multiple-gated equilibrium radionuclide angiocardiography and catheterization in a canine model of chronic heart failure. Doxorubicin was administered to 12 dogs at a dose of 1 mg/kg/wk intravenously for 10 weeks. Left ventricular ejection fraction was reduced from a mean of 53.6% +/- 3.4% to 33.5% +/- 2.3% preoperatively. Two dogs died of presumed arrhythmia during this period. Cardiomyoplasty with the left latissimus dorsi muscle was performed on 10 dogs. The muscle was wrapped around both the left and right ventricles. Five dogs died of infection or arrhythmia after the operation. Postoperatively the muscle remained unstimulated for 2 weeks to allow adhesion to the heart. After this period, the latissimus dorsi muscle was conditioned by a progressive stimulation protocol. After the muscle was conditioned, multiple-gated equilibrium radionuclide angiocardiography studies showed that left ventricular global ejection fraction was 18.4% +/- 7.2% at 0 volts (nonstimulation), 26.2% +/- 3.7% at 5-volt stimulation (p less than 0.05), and 31.0% +/- 5.4% at 10-volt stimulation (p less than 0.05). Regional ejection fractions in low lateral, apical, and low septal regions at 5 volts and 10 volts were higher than those at 0 volts (p less than 0.05). Regional wall motion (percent radial shortening) of the low lateral region was higher than that during nonstimulation (p less than 0.05). Peak emptying rate was 2.07 +/- 0.95 end-diastolic counts per second at 0-volt, 3.10 +/- 0.67 at 5-volt, and 3.34 +/- 0.89 at 10-volt stimulation (p less than 0.05). Peak filling rate was 1.81 +/- 0.52 end-diastolic counts per second at 0-volt, 2.67 +/- 1.18 at 5-volt, and 3.11 +/- 0.65 at 10-volt stimulation (p less than 0.05). Cardiac catheterization data showed a nonsignificant increase in left ventricular rate of pressure rise with increasing voltage (1302 +/- 355 mm Hg/sec at 0 volts, 1450 +/- 413 mm Hg/sec at 5 volts, and 1568 +/- 455 mm Hg/sec at 10 volts). Left ventricular systolic pressures were unchanged. End-diastolic pressures decreased (11.2 +/- 1.48 mm Hg at 0 volts, 10.4 +/- 2.30 mm Hg at 5 volts, and 9.6 +/- 1.52 at 10 volts; p less than 0.05). These data show that cardiomyoplasty can improve indices of systolic and diastolic function in a canine model of chronic heart failure.     

Cardiomyoplasty Benefits in Experimental Myocardial Dysfunction

Beneficial effects of cardiomyoplasty have been documented and the use of this technique in the treatment of dilated cardiomyopathy have been suggested. This study was undertaken to evaluate the effectiveness of stimulated preconditioned latissimus dorsi muscle flaps wrapped around the heart in order to restore ventricular contractility in six adult mongrel dogs with induced myocardial dysfunction by administration of beta blockers and volume loading. Hemodynamic and two-dimensional echocardiographic evaluation were performed 1 week after the surgical procedure and immediately after heart failure induction. With synchronous pulse train electrical stimulation, cardiac output increased from 1.46 +/- 0.13 (+/- SD) to 2.01 +/- 0.16 L/min (p less than 0.01), pulmonary wedge pressure decreased from 15.5 +/- 1.2 to 11.3 +/- 1.6 mmHg (p less than 0.01) and left ventricular end-diastolic pressure from 18.3 +/- 2.4 to 13.5 +/- 1.4 mmHg (p less than 0.04). Echo derived left ventricular ejection fraction increased from 39.3 +/- 2.4 to 59.6 +/- 2.9% (p less than 0.01) and segmental wall shortening from 15.4 +/- 1.2 to 26.3 +/- 1.7% (p less than 0.01), inclusive when the muscle flap was wrapped only around the left ventricle. In conclusion, this study suggests that cardiomyoplasty may be an alternative method of treatment for irreversible cardiomyopathy, including in patients with a great cardiac enlargement in which muscle flap may only be wrapped partially around the heart.     

Skeletal muscle ventricles in the pulmonary circulation: up to 16 weeks' experience.

Skeletal muscle ventricles (SMVs) were constructed from the right latissimus dorsi muscle of 8 mongrel dogs. After a 3-week vascular delay period, each SMV was electrically preconditioned with 2-Hz continuous stimulation of the thoracodorsal nerve for 6 weeks. A porcine-valved conduit was then anastomosed between the right ventricle and the SMV, with a second valved conduit connecting the SMV to the main pulmonary artery. The pulmonary artery was then ligated proximal to the conduit. The SMVs were stimulated to contract in 1:2 diastolic mode with a 33-Hz burst frequency. Effective right ventricular assist was achieved in all dogs. Cardiac output increased by 22.6% (1,799 +/- 97 versus 1,467 +/- 84 mL/min; p less than 0.001), systemic systolic arterial pressure by 9.3% (90.1 +/- 3.5 versus 82.4 +/- 3.9 mm Hg; p less than 0.005), and peak pulmonary artery pressure by 31.8% (27.8 +/- 2.0 versus 21.1 +/- 1.7 mm Hg; p less than 0.001) at the initiation of this study. In 6 dogs, effective right heart assist was sustained for periods of between 1 week and 12 weeks. Two dogs survived for longer than 3 months, though with evidence of deteriorating SMV function. These results demonstrate the feasibility of providing sustained right ventricular assist using this modified "Rastelli-SMV" configuration, which obviates the limitations imposed by low right atrial preload.     

Effects of dynamic cardiomyoplasty on left ventricular performance and myocardial mechanics in dilated cardiomyopathy

We tested the hypothesis that dynamic cardiomyoplasty produces beneficial changes in the functional mechanics of the dilated, failing left ventricle. Chronic dilated cardiomyopathy was induced in seven mongrel dogs by rapid ventricular pacing (260 beats/min) for 3 to 4 weeks. After completion of the induction period, dynamic cardiomyoplasty was performed with the left latissimus dorsi muscle, paced synchronously with the R waves of the electrocardiogram (Medtronic SP1005). Instruments included an aortic flow probe, a left ventricular Millar pressure catheter, and piezoelectric sonomicrometric crystals on the left ventricle for measurements of wall thickness and minor and major axis dimensions. Data were obtained with the stimulator off and on. Statistical comparisons were made with Student's t test for paired data. Dynamic cardiomyoplasty increased the cardiac output of the failing heart (966 +/- 124 versus 1166 +/- 112 ml/min; p less than 0.01). Systolic shortening of both minor and major axis dimensions increased (3.1 +/- 0.3 versus 4.7 +/- 0.3 mm, p less than 0.01, and 4.6 +/- 0.3 versus 7.3 +/- 0.9 mm, p less than 0.05, respectively). Left ventricular end-diastolic pressure decreased by 16% (18 +/- 1 versus 15 +/- 1 mm Hg, p less than 0.01). Although skeletal muscle contraction increased the pressure development in the left ventricular chamber, mean systolic wall stress was diminished by concomitant changes in left ventricular dimensions (116,144 +/- 11,530 versus 101,268 +/- 7464 dynes/cm2, p less than 0.05). At end-systole, wall thickness increased (11.8 +/- 1.1 versus 12.7 +/- 1.1 mm, p less than 0.01), minor axis dimension decreased (51.3 +/- 1.4 versus 49.2 +/- 1.8 mm, p less than 0.01), and major axis dimension also decreased (85.6 +/- 3.3 versus 79.0 +/- 2.3 mm, p less than 0.05). Our detailed evaluation of left ventricular chamber mechanics suggests that dynamic cardiomyoplasty may have a role in ameliorating the functional and mechanical derangements associated with progression of dilated cardiomyopathy both by augmenting cardiac performance and by diminishing determinants of myocardial oxygen consumption. (All values are expressed as mean +/- standard error of the mean.)     

Left ventricular full-thickness cardiomyoplasty with pericardial neoendocardium: experimental development of a surgical procedure

Cardiomyoplasty, a surgical procedure using stimulated skeletal muscle graft to replace or repair damaged myocardium, has been successfully performed in experimental animals and clinical patients. Whenever feasible, endocardium of the damaged myocardial segment is retained and partial-thickness cardiomyoplasty should be carried out. However, if this procedure were to be applied to enlarge a hypoplastic ventricle or to maintain normal dimensions of the ventricular cavity in some repairs in adults, full-thickness replacement of the ventricular wall with contractile skeletal muscle mass would be required. To develop such a technique, several canine experiments were carried out. In 7 dogs, "simple full-thickness cardiomyoplasty" was performed by using a latissimus dorsi muscle graft to repair a full-thickness left ventricular wall defect. We found it was difficult to obtain adequate hemostasis between the nonscarred myocardial tissue and the skeletal muscle graft, and excessive suturing to obtain hemostasis resulted in strangulation of the muscle grafts. The skeletal muscle-blood interface in the left ventricle was found to be highly thrombogenic. The perioperative hemorrhage and the risk of muscle graft strangulation by excessive sutures were avoided by using a pericardial patch as neoendocardium in 5 dogs that underwent similar full-thickness cardiomyoplasty procedures. Although the pericardial neoendocardium was not fully antithrombogenic in this canine model, endothelialization of the endocardium occurred within several weeks after operation. Thus, when combined with an implantable synchronized burst stimulator, this technique may in the future provide an effective "full-thickness dynamic cardiomyoplasty" to enlarge the ventricles and augment myocardial function in select patients.     

Bilateral latissimus dorsi cardiomyoplasty.

This study was undertaken to test the hypothesis that a bilateral latissimus dorsi cardiomyoplasty provides greater hemodynamic augmentation than a unilateral procedure. Two types of bilateral procedure and a left posterior cardiomyoplasty were tested in each of 8 mongrel dogs. R-wave synchronous muscle pacing was achieved with a programmable burst stimulator. Hemodynamic variables of stimulated beats were compared with those of a nonstimulated baseline using paired t tests. The effects of a double anterior muscle wrap were equal to a right anterior/left posterior configuration. Therefore, the data on the two types of bilateral procedure were combined and compared with the left wrap. Stimulation of the bilateral cardiomyoplasty resulted in significant increases in right ventricular pressure (44 +/- 3.1 versus 26 +/- 1.8), first derivative of right ventricular pressure (595 +/- 117 versus 196 +/- 14), pulmonary artery pressure (34 +/- 1.9 versus 23 +/- 1.6), left ventricular pressure (90 +/- 5.9 versus 69 +/- 5.3), first derivative of left ventricular pressure (1454 +/- 141 versus 1072 +/- 107), aortic pressure (80 +/- 5.4 versus 67 +/- 4.9), and peak aortic flow (9.4 +/- 1.1 versus 7.7 +/- 0.8) (p less than 0.05). Significant increases in all of these variables also occurred with stimulation of the left cardiomyoplasty, but the increases in right ventricular pressure, first derivative of right ventricular pressure, pulmonary artery pressure, and aortic pressure were larger for the bilateral than the left cardiomyoplasty. The bilateral and the left procedure can each augment systolic ventricular function. The bilateral procedure appears to have greater effects, especially on right ventricular function.     

Right ventricular dynamic cardiomyoplasty for the univentricular heart with pulmonary hypertension

OBJECTIVES: We conducted an acute experimental study to test the feasibility of dynamic cardiomyoplasty in a setting of modified Fontan procedure for univentricular heart with pulmonary hypertension to obtain a possible proxy for high-risk Fontan candidates. METHODS: After electrical preconditioning of the left latissimuss dorsi for 6 weeks in 8 dogs, the right ventricular cavity was totally obliterated with concomittent closure of the tricuspid valve and right pulmonary artery. Modified Fontan circulation was established with the aortic homograft anastomosed between the right atrium and pulmonary trunk, incorporated with a pericardial pouch as a compression chamber (neoright ventricle) fixed onto the epicardial surface of the ventricle. After cardiopulmonary bypass termination, a latissimus dorsi was applied to wrap the pericardial pouch and ventricle clockwise and stimulated with a trained-pulse (25 Hz) at 1:1 synchronization ratio with cardiac beats. RESULTS: Profound right heart failure was noted during Fontan circulation in increased pulmonary vascular resistance (11 +/- 3.2 Wood units), whereas graft pacing showed significant augmentation of systolic pulmonary pressure by 54 +/- 12%, the mean pulmonary flow by 68 +/- 23%, and aortic pressure by 23 +/- 5% at a physiological range of central venous pressure (13.2 +/- 0.7 mmHg). Right heart function curve analysis confirmed marked augmentation of right heart performance, restoring almost normal pulmonary circulation. These functional benefits were sustained up to 4 hours in 4 animals until experiments were terminated. CONCLUSIONS: Dynamic cardiomyoplasty in a modified Fontan procedure is a viable surgical option for univentricular heart, not a Fontan candidate.     

The Muscle-Powered Dual-Chamber Counterpulsator: Rheologically Superior Implantable Cardiac Assist Device

To enable long-term studies of a totally implantable cardiac assist device powered by transformed fatigue-resistant skeletal muscle, we developed a dual-chamber extraaortic counterpulsation system that uses hydraulic fluid for power transfer. Six dogs had our dual-chamber extraaortic counterpulsator implanted, 2 of which had undergone prior transformation of their latissimus dorsi muscle. The blood pump, with a Dacron graft at each end, was anastomosed end-to-side and parallel to the thoracic aorta, allowing continuous blood flow to minimize thrombus formation caused by stasis and turbulence. The blood pump was powered by a hydraulic bulb placed beneath the latissimus dorsi muscle. The latissimus dorsi muscle was stimulated to contract during diastole using a synchronized burst electrical stimulator. The ratio of diastolic pressure time product over systolic time tension index, which reflects the myocardial oxygen supply and demand ratio, was calculated from ascending aortic pressure tracings. A consistent increase in this ratio of 44% in 4 dogs with nontransformed latissimus dorsi muscle and of 70% in 2 dogs with transformed latissimus dorsi muscle was obtained when the device was activated. Preliminary chronic implantation studies using a Medtronic cardiomyo-stimulator (Model SP1005) as the burst stimulator for our dual-chamber extraaortic counterpulsator produced an average augmentation in aortic diastolic pressure of 34 mm Hg for up to six days.Our results indicate that, with further refinement of this device, a long-term totally implantable cardiac assist device powered by endogenous skeletal muscle will be feasible.     

Skeletal muscle ventricles as left atrial-aortic pumps: short-term studies.

In 5 dogs, skeletal muscle ventricles (SMVs) were constructed from the latissimus dorsi muscle and placed in the left hemithorax. After a 3-week vascular delay period, SMVs were electrically preconditioned with 2-Hz stimulation for 6 weeks. At a second operation, SMVs were connected between the left atrium and thoracic aorta by afferent and efferent aortic root homografts, and stimulated to contract in a 1:2 diastolic mode. At a mean left atrial pressure of 12.4 +/- 1.3 mm Hg and a burst stimulation frequency of 33 Hz, SMV stroke volume was initially 43% of that of the native left ventricle, achieving a flow equivalent to 21% of cardiac output (194 +/- 38 versus 902 +/- 85 mL/min). At 50-Hz stimulation, this figure rose to 27% (246 +/- 41 mL/min; p less than 0.05). Skeletal muscle ventricle power output (the product of stroke work and contraction rate) at 33 Hz was 0.016 +/- 0.003 W, increasing to 0.024 +/- 0.004 W at 50 Hz (p less than 0.05), corresponding to 14% and 22%, respectively, of left ventricular power output (0.11 +/- 0.012 W). After 4 hours of continuous pumping, four of the SMVs were still generating flows of more than 70% of starting values and more than 60% of initial power output. This study demonstrates that SMVs can function in the systemic circulation at physiologic left atrial preloads.     

Adynamic cardiomyoplasty: effect on cardiac efficiency and contractile reserve in dogs with adriamycin-induced cardiomyopathy

The girdling effect of the skeletal muscle wrap seems to be the primary mechanism of action of cardiomyoplasty. It is associated with a myocardial sparing effect. Myocardial sparing effect has been shown with an active muscle wrap or an active muscle wrap acutely turned "OFF". The purpose of the study was to evaluate the effect of a passive skeletal muscle wrap on cardiac energetics parameters and contractile reserve in a canine model of cardiomyopathy. Six dogs with adriamycin-induced cardiomyopathy were studied. Three dogs underwent right latissimus dorsi adynamic cardiomyoplasty and 3 served as controls. Cardiac and coronary sinus catheterizations were performed at 0 and 6 weeks. A dobutamine stress test was performed at 6 weeks. Myocardial oxygen consumption was not reduced in the cardiomyoplasty group (139.20+/-86.90 Joules/min) compared to the control group (95.10+/-12.60 Joules/min, P = 0.27) at 6 weeks. Mechanical cardiac efficiency was increased in the cardiomyoplasty group (33.15+/-4.40%) compared to the control group (24.50+/-2.70%, P = 0.049) at 6 weeks. Left ventricular end diastolic diameter index was reduced in the cardiomyoplasty group (38.00+/-1.70 mm/m2) compared to the control group (46.30+/-1.55 mm/m2, P = 0.049) at 6 weeks. Indices of diastolic function -dp/dt, and tau were not significantly affected by adynamic cardiomyoplasty. Max dp/dt was increasing more in the cardiomyoplasty group than in the control group (P = 0.07) during dobutamine stress test. Mechanical cardiac efficiency was better preserved by the adynamic cardiomyoplasty. Myocardial contractile reserve might be better preserved with cardiomyoplasty.     

Right ventricular cardiomyoplasty: 10-year follow-up

BACKGROUND: Chronically depressed right ventricular (RV) function presents an unsolved therapeutic challenge in cardiac surgery. Despite recent advances in medical and surgical therapies, prognosis remains poor and patient's quality of life and mortality are frequently unacceptable. The aim of this study is to present the first clinical report and long-term results of RV dynamic cardiomyoplasty applied in patients with RV failure caused by isolated RV cardiomyopathies. METHODS: Seven consecutive patients (5 males, 2 females; mean age, 40 +/- 9 years; range, 15 to 63 years) from a series of 113 cardiomyoplasty procedures performed at Broussais and Pompidou Hospitals were evaluated. The mean duration of follow-up was 10 +/- 3.5 years. All patients had predominant RV dysfunction, associated with tricuspid regurgitation in 6 patients. The cause of RV failure was arrhythmogenic cardiomyopathy (4 patients), ischemic (2 patients), and Uhl's disease (1 patient), and endomyocardial fibrosis (1 patient). Six patients were in preoperative New York Heart Association functional class III and 1 was in intermittent class III/IV. The mean preoperative ejection fraction (measured by isotopic technique) was 18% +/- 5.7% for the right ventricle and 40% +/- 13% for the left ventricle. Right ventricular dynamic cardiomyoplasty consists of wrapping the RV free walls with the left latissimus dorsi muscle flap. The distal part of the latissimus dorsi muscle is fixed to the diaphragm and then electrostimulated. Six patients required associated tricuspid valve surgery. RESULTS: There were no perioperative deaths. The mean duration of follow-up was 10 +/- 3.5 years. Six patients are alive with a remarkable quality of life, 4 are in New York Heart Association functional class I and 2 are in class II. One patient who was in New York Heart Association functional class II died in postoperative year 7 caused by stroke. At last follow-up, mean RV ejection fraction was 33% +/- 11.8% and left ventricular ejection fraction was 52% +/- 12.6%. CONCLUSIONS: The results of this long-term study demonstrate hemodynamic and functional improvements after RV cardiomyoplasty without perioperative mortality, no long-term malignant arrhythmias, and RV dysfunction related deaths. We believe that RV cardiomyoplasty, associated with tricuspid valve surgery when required, could be an effective treatment for severe RV failure.     

Use of tactile stiffness to detect fatigue in the latissimus dorsi muscle

In clinical settings, no method has been established to examine the fatigue of a latissimus dorsi muscle (LDM) preconditioned for cardiomyoplasty. We examined the feasibility of measuring muscle stiffness (tactile stiffness) to evaluate muscle fatigue in situ using our tactile sensor. We stimulated canine LDM with burst pacing and monitored both stiffness and tension to determine their relationship. In both dissected LDM and LDM in situ, the decrements of these parameters during burst pacing were compared between preconditioned and unconditioned LDM. In measurement in situ, the sensor probe was placed on the LDM through a small incision. Strong statistical correlation was shown between stiffness and tension (r = 0.935). In decrements of stiffness in situ, there were statistically significant differences between preconditioned and unconditioned LDM. Our tactile sensor system can provide an efficient method for evaluating fatigue of muscles in situ without measuring muscle tension.     

Voltage-dependent performance of skeletal muscle pouches: implications for cardiomyoplasty.

Cardiomyoplasty, a new therapy for heart failure, uses autologous skeletal muscle to mechanically assist the heart. The success of dynamic cardiomyoplasty is critically dependent on the contraction strength of the assisting skeletal muscle. Unlike cardiac muscle, skeletal muscle contracts in a graded response to electrical stimulation. However, in current cardiomyoplasty practice, no systematic technique exists to set the stimulating voltage effecting skeletal muscle contraction. The stimulating voltage is simply set to some multiple of the "threshold" voltage. Furthermore, researchers do not consider the role of stimulating voltage when they determine the amount of assistance afforded during cardiomyoplasty. To more accurately assess the value of this heuristic voltage-setting technique, we investigated the role of stimulating voltage on the strength of contraction of the latissimus dorsi muscle. Six New Zealand white rabbits had isovolumic hydraulic pouches constructed from the latissimus dorsi muscle. The muscles were wrapped around a compliant balloon in which isovolumic pressure development was measured during tetany-inducing burst (pulse-train) stimulation. The tetanic plateau of the pouch pressure record was used to measure the effects of stimulating voltage on skeletal muscle contraction. Results indicated that (1) increasing stimulating voltage from two to four times the "threshold" voltage increased normalized pouch pressure from 0.38 +/- 0.21 to 0.78 +/- 0.12 (mean +/- SD) (p < 0.05); (2) the threshold-normalized voltage necessary to cause maximal muscle contraction varied widely (5.7 +/- 2.0, mean +/- SD; range, 3.1 to 9.3); and (3) the current achieving maximal pressure development varied from 5.6 to 31.4 mA (19.9 +/- 10.4 mA).(ABSTRACT TRUNCATED AT 250 WORDS)     

Techniques to enhance extramyocardial collateral blood flow after a cardiomyoplasty.

OBJECTIVE: Chronic stimulation of a cardiomyoplasty was combined with low-dose infusion of heparin into the arterial supply of the cardiomyoplasty in order to determine if latissimus-derived collateral blood flow could be further enhanced. SUMMARY BACKGROUND DATA: Acute and chronic stimulation of a latissimus dorsi cardiomyoplasty increased extramyocardial collateral blood flow to 35 +/- 9% and 27 +/- 5%, respectively, of normal myocardial blood flow. METHODS: A model of coronary artery disease was created with an ameroid constrictor in goats, and a cardiomyoplasty was performed. Heparin (15 to 50 U/h) was delivered into the left subclavian artery for a period of 4 weeks. Simultaneously, the latissimus dorsi was chronically stimulated at 2 Hz. RESULTS: Chronic ischemic myocardium received a collateral flow per gram from the skeletal muscle equivalent to 11.8 +/- 5.2% of the blood flow to normal myocardium. The extramyocardial collateral flow correlated with the latissimus muscle flow (r = 0.72). CONCLUSIONS: Enhancement of extramyocardial collateral flow was not found with heparin treatment. In view of the correlation of extra-coronary collateral flow with latissimus muscle flow, the lack of a heparin effect may have been due to low latissimus blood flow. These results suggest that extramyocardial collateral blood flow to the myocardium is highest if the blood flow to the latissimus dorsi muscle is maintained.     

Update 2001: Right latissimus dorsi cardiomyoplasty augments left ventricular systolic performance

As Originally Published in 1993: Right Latissimus Dorsi Cardiomyoplasty Augments Left Ventricular Systolic Performance by Stephen E. Park, MD, Brian L. Cmolik, MD, Robert R. Lazzara, MD, Dennis R. Trumble, MS, and James A. Magovern, MD. Department of Surgery, Allegheny General Hospital, Surgical Research, Allegheny-Singer Research Institute, and Allegheny Campus, The Medical College of Pennsylvania, Pittsburgh, Pennsylvania, USA

We hypothesized that the right latissimus dorsi cardiomyoplasty augments left ventricular performance. Five dogs underwent staged right latissimus dorsi cardiomyoplasty. Ventricular function was studied 1 to 3 weeks later. Left ventricular pressure was measured with a micromanometer and left ventricular dimensions with piezoelectric crystals. Inferior vena caval occlusion was used to vary preload. Pressure-volume data were collected with the muscle unstimulated and stimulated at 1:2 and 1:1 muscle/heart ratios. The end-systolic pressure-volume relation (mm Hg/mL), stroke work, preload recruitable stroke work, left ventricular end-diastolic volume, and the diastolic relaxation constant were calculated and expressed as mean ± standard deviation. Stimulated beats at a 1:2 ratio showed an increase in stroke work of 42.1% (978 ± 381 to 1,390 ± 449 g · cm; p < 0.01) and preload recruitable stroke work of 28.8% (59.4 ± 20.7 to 76.6 ± 11.0 g · cm/cm³; p = 0.05) compared with the unstimulated beats. With the stimulator on at 1:1, smaller changes occurred: stroke work increased 9% (1,167 ± 390 to 1,273 ± 363 g · cm; not significant) and preload recruitable stroke work increased 27% (63.9 ± 22.7 to 80.9 ± 23.1 g · cm/cm³; p = 0.05). There were no significant changes in the end-systolic pressure-volume relation. The diastolic relaxation constant did not change at 1:1 (36 ± 9.7 to 37 ± 6.4 ms; not significant) or 1:2 (36 ± 9.3 to 39 ± 8.2 ms; not significant). Left ventricular end-diastolic volume was unchanged at 1:1 (34 ± 10.7 to 32 ± 10.3 mL) and at 1:2 (31 ± 9.0 to 32 ± 8.7 mL). Right unconditioned latissimus dorsi cardiomyoplasty in anesthetized dogs with normal hearts resulted in enhanced systolic work and contractility with no change in diastolic relaxation at stimulation rates of 1:2 and 1:1.     

A new method of double cardiomyoplasty: "contractile muscular sling".

BACKGROUND: In several experimental studies, double cardiomyoplasty using both latissimus dorsi muscles did not provide sufficient assist to the failing heart and did not clearly show improvement compared with single cardiomyoplasty. This study demonstrated the superior efficacy of our method of double cardiomyoplasty compared with single cardiomyoplasty. METHODS: In 16 dogs, the two latissimus dorsi muscles were crossed in front of the heart and directly sutured to each other behind the heart. Control hemodynamic measurements were obtained, and acute heart failure was induced by intravenous administration of propranolol. After the hemodynamic changes with bilateral latissimus dorsi muscle assistance were measured, single cardiomyoplasty was done in the same dog, and the hemodynamic variables were measured. RESULTS: With our double cardiomyoplasty, aortic systolic pressure increased by 25% (p < 0.001); pulmonary artery systolic pressure, by 40% (p < 0.001); end-systolic elastance, by 155% (p < 0.001); and cardiac output, by 55% (p < 0.001). There were significant increases in aortic pressure, pulmonary artery pressure, end-systolic elastance, stroke volume, and cardiac output with our double cardiomyoplasty compared with single cardiomyoplasty. CONCLUSIONS: In this study, our double cardiomyoplasty provided significant hemodynamic improvement compared with single cardiomyoplasty.     

Increased coronary artery blood flow with aortomyoplasty in chronic heart failure

BACKGROUND: We hypothesized that diastolic counter-pulsation using aortomyoplasty will increase coronary blood flow. METHODS: In dogs (n = 6, 20 to 25 kg), the left latissimus dorsi muscle was isolated, wrapped around the descending thoracic aorta, and conditioned by chronic electrical stimulation. Heart failure was induced by rapid ventricular pacing. In a terminal study, left ventricular and aortic pressures, and blood flow in the left anterior descending coronary artery and descending aorta were measured. The endocardial-viability ratio was calculated. RESULTS: Aortomyoplasty increased mean diastolic aortic pressure (70 +/- 5 to 75 +/- 5 mm Hg, p < 0.05) and reduced peak left ventricular pressure (86 +/- 4 to 84 +/- 4 mm Hg, p < 0.05), leading to a 16% increase in endocardial-viability ratio (1.29 +/- 0.05 to 1.49 +/- 0.05, p < 0.05). Coronary blood flow was increased by 15% (8.2 +/- 1.5 to 9.4 +/- 1.6 mL/min, p < 0.05). During muscle contraction, 2.7 +/- 0.5 mL was ejected from the wrapped aortic segment. CONCLUSIONS: These data demonstrate that aortomyoplasty provides successful diastolic counterpulsation after muscle conditioning and heart failure.     

Evaluation of a compressive-type skeletal muscle pump for cardiac assistance

BACKGROUND: Recent investigations have focused on using the latissimus dorsi muscle for cardiac assistance. Although cardiomyoplasty has been applied clinically, other procedures remain experimental, but promising, modes of cardiac assistance. We assessed the latissimus dorsi muscle as an in situ energy source for circulatory assist devices. METHODS: We developed a pneumatic chamber as a compressive-type muscle actuator. The chamber was implanted under the latissimus dorsi muscle and converted contractile power into pneumatic pressure. The effect of chamber position and size and the influence on muscle blood flow were examined. After muscle conditioning, the pump performance of a circulatory assist device driven by the chamber was evaluated. RESULTS: The chamber functioned better when placed in the proximal position of the latissimus dorsi muscle. The size affected the generated pneumatic pressure, and the higher resting pressure of the chamber reduced the muscle blood flow. The maximum stroke work of the circulatory assist device was greater than that of the right ventricle but less than that of the left ventricle. The chamber could drive the circulatory assist device against the systemic range of afterload in which a high preload was available. Long-term adhesion surrounding the chamber reduced the pressure generation capability. CONCLUSIONS: The compressive-type muscle actuator using the latissimus dorsi muscle generated acceptable hemodynamic work for right ventricular bypass or aortic counterpulsation.