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Mechanisms of cardiomyoplasty: comparative effects of adynamic versus dynamic cardiomyoplasty.

BACKGROUND: The apparent paradox seen in patients who have undergone dynamic cardiomyoplasty and shown substantial clinical and functional improvements with only modest hemodynamic changes may be due to inappropriate end points chosen for study, a result of incomplete understanding of mechanisms involved. The purpose of this study was to compare the relative role of the passive "girdling effect" and the dynamic "systolic squeezing effect" of the wrapped muscle in cardiomyoplasty. METHODS: The control group of 6 dogs underwent 4 weeks of rapid pacing (250 beats/min) to induce severe heart failure followed by 8 weeks of observation without rapid pacing. The trajectory of recovery in hemodynamics and cardiac dimensions was followed with echocardiography and Swan-Ganz catheters. In the "adynamic" cardiomyoplasty group (n=4), the left latissimus dorsi muscle was wrapped around the ventricles and allowed to stabilize and mature for 4 weeks. This was followed by rapid pacing and recovery as in the control group. In the "dynamic" cardiomyoplasty group (n=3), the same protocol for the adynamic group was followed except that a synchronizable cardiomyostimulator was attached to the thoracodorsal nerve of the muscle wrap. This allowed the latter to be transformed during the rapid-pacing phase and permitted dynamic squeezing of the muscle wrap to be generated by burst stimulation synchronized with cardiac contraction in a 1:2 ratio. RESULTS: Baseline data were comparable in all groups prior to rapid pacing. After 4 weeks of rapid pacing, the left ventricular ejection fraction was higher in the adynamic (27.0%+/-3.9%; p < 0.05) and dynamic (33.3%+/-2.3%; p < 0.02) cardiomyoplasty groups compared with controls (18.8%+/-8.3%). Similarly, ventricular dilatation in both systole and diastole was less in the adynamic (51.8+/-8.7 mL, [p < 0.002] and 38.2+/-7.2 mL [p < 0.001], respectively) and dynamic (62.0+/-7.2 [p < 0.02] and 41.3+/-3.5 mL [p < 0.005], respectively) cardiomyoplasty groups compared with controls. In the dynamic group, on and off studies were carried out after cessation of rapid pacing while the heart was still in severe failure, and they demonstrated a systolic squeezing effect in stimulated beats. Only this group recovered fully to baseline after 8 weeks. CONCLUSIONS: By reducing myocardial stress, both the passive girdling effect and the dynamic systolic squeezing effect have complementary roles in the mechanisms of dynamic cardiomyoplasty.

Animals↗

Cardiomyoplasty and implantable cardioverter defibrillator: efficacy and safety of concomitant device implantation: sudden death and cardiomyoplasty.

Sudden death represents a common event in the natural history of patients affected by chronic heart failure. Such an outcome also has been shown to characterize the follow-up of the cardiomyoplasty procedure. We report two cases of patients who had cardiomyoplasty and experienced witnessed episodes of ventricular arrhythmia at variable times after surgery (2 years and 2 months, respectively). In the first case, an implantable cardioverter defibrillator (ICD) was implanted subsequent to the arrhythmic episode, whereas the second patient had a combined cardiomyoplasty and ICD implantation procedure. In particular, this patient underwent a modified wrapping technique, herein described, because of a large left ventricular dilatation. In both cases, ventricular defibrillation did not affect the correct functioning of the implanted cardiomyostimulator. Our article confirms that ventricular arrhythmia is common in cardiomyoplasty patients. The combined use of a skeletal muscle stimulator and implantable defibrillator may therefore be effective in preventing arrhythmia-related sudden death without any concurrent effect on the correct functioning of the wrapped muscle/heart circuit, with likely benefit on long-term cardiomyoplasty patient survival.

Aged↗

Latissimus dorsi cardiomyoplasty: a chronic experimental porcine model. Feasibility study of cardiomyoplasty in Danish Landrace pigs and Göttingen minipigs.

Cardiomyoplasty is an experimental treatment for end-stage heart failure. We hypothesized that the porcine latissimus dorsi muscle (LDM) in an experimental porcine model is a suitable surrogate for a clinically relevant evaluation of this concept. Fourteen Danish Landrace (DL) pigs and six Göttingen minipigs (GM) were studied. The LDM was evaluated immediately after surgical dissection and in various phases: phase 1 (n = 4)--outcome of a partial vascular isolation (vascular delay), 2 to 3 weeks prior to heart wrapping in DL pigs; phase 2 (n = 6)--long-term flap survival of nonstimulated LDM cardiomyoplasty in DL pigs; phase 3 (n = 6)--outcome of nonstimulated cardiomyoplasty in GM; phase 4--one DL pig had dynamic cardiomyoplasty performed and was subjected to low-intensity LDM stimulation for 8 months. Isolation of the LDM of DL pigs and GM as a pedicled graft had no acute deleterious impact on the global blood supply. In phase 1a, partial vascular isolation and in situ recovery of the LDM resulted in a muscle encapsulated in fibrotic tissue, which hampered a later heart wrap. In phase 1b, a less extensive dissection diminished fibrosis and allowed subsequent wrapping. In phase 2, after 6 weeks of nonstimulated LDM cardiomyoplasty, the LDM of DL pigs was viable, with excellent heart-muscle integration. In phase 3, the same procedure applied in GM yielded the same result as that in DL pigs, but with a higher success rate owing to the learning phase.

Animals↗

Retrospective risk analysis for early heart-related death after cardiomyoplasty. The Worldwide Cardiomyoplasty Group.

BACKGROUND: Dynamic cardiomyoplasty is an evolving treatment for heart failure that uses an electrically stimulated latissimus dorsi muscle wrapped around the heart to improve cardiac function. Preoperative patient characteristics and deaths after cardiomyoplasty have been recorded during the past 5 years in a cumulative database representing worldwide experience of 42 medical centers. METHODS: Statistical models of hazards (monthly death rates) were used to identify risk factors for transiently increased risk of cardiovascular mortality within 2 months after cardiomyoplasty. RESULTS: Actuarial survival (n = 261) was 88%, 80%, and 76% at 1, 3, and 6 months after cardiomyoplasty, respectively. The peak hazard of 6% dying per month occurred during the first month after the surgical procedure. Lower ejection fraction, increased number of major coronary arteries with > or = 70% stenotic lesions, and lower chronotropic responses during exercise were independent risk factors for the transient increase in early cardiovascular mortality. Early risk of cardiovascular mortality was significantly reduced as centers gained experience with more than 3 patients. CONCLUSION: Early survival after cardiomyoplasty has improved with experience and might be reduced further by preoperative assessments that identify patients at highest risk.

Actuarial Analysis↗

Multicenter trial of dynamic cardiomyoplasty for chronic heart failure. The American Cardiomyoplasty Group.

OBJECTIVES: The purpose of this study was to prospectively assess the effect of dynamic cardiomyoplasty in patients with symptomatic chronic heart failure. BACKGROUND: Since the first procedure was performed in 1985, dynamic cardiomyoplasty has been developed for use in patients with chronic heart failure. The aging population in developed countries has made heart failure a growing public health concern. Heart transplantation is appropriate or available for only a small proportion of these patients because of limited donor supply. Effective alternatives to transplantation are needed. METHODS: Eight centers in North and South America performed 68 cardiomyoplasty procedures between May 1991 and September 1993. Data were prospectively collected every 6 months and compared with preoperative values using paired t tests, chi-square tests and actuarial survival analyses. RESULTS: Patients had a mean (+/- SD) age of 57 +/- 1 years and were predominantly male (53 [78%] of 68). Heart failure etiology was classified as idiopathic in 47 (69%) of 68 patients and ischemic in 21 (31%). The in-hospital mortality rate was 12% (8 of 68), and the survival rate at 6 and 12 months was 75 +/- 5% and 68 +/- 6%, respectively. Objective improvements were seen at 6 months (n = 49) in left ventricular ejection fraction (23 +/- 1% vs. 25 +/- 1%, p = 0.05), stroke volume (50 +/- 2 vs. 56 +/- 3 ml/beat, p = 0.02) and left ventricular stroke work index (26 +/- 1 vs 30 +/- 2 g/m2 per beat, p = 0.01). Improvements in mean New York Heart Association functional class (3 +/- 0.04 vs. 1.8 +/- 0.1, p = 0.0001) and activity of daily living score (59 +/- 3 vs. 80 +/- 2, p = 0.0001) were also observed. There were no significant changes at 6 months in peak oxygen consumption (15 +/- 1 vs. 16 +/- 1 ml/kg per min), cardiac index (2.26 +/- 0.08 vs. 2.33 +/- 0.08 liters/min per m2), pulmonary capillary wedge pressure (19 +/- 2 vs. 18 +/- 1 mm Hg) or heart rate (87 +/- 2 vs. 82 +/- 3 beats/min). CONCLUSIONS: These data suggest that dynamic cardiomyoplasty improves ventricular systolic function, reduces symptoms of heart failure and improves objective measures of quality of life in patients with congestive heart failure. This improvement occurred without changes in peak exercise capacity, ventricular filling pressure or actuarial survival.

Cardiac Output, Low↗

Cardiac function and histological changes after non-dynamic cardiomyoplasty and preliminary study of dynamic cardiomyoplasty.

By means of histological method and ultrasound cardiographic (UCG) examination, the left-right ratio of transectional area of muscle fiber of latissimus dorsi muscle (LDM) after non-dynamic cardiomyoplasty was 77.4 +/- 11.7% in Group I (3 weeks after operation), and 78.4 +/- 11.6% atrophy and hyperplasia of LDM, but the basical structure was retained. The ejection fraction (EF) decreased significantly after operation (P < 0.05), but the difference between two groups was non- significant. Also, dynamic cardiomyoplasty was performed on a sheep. UCG showed the increased cardiac systolic function after operation. ATPase, succinodehydrogenase (SDH) and PAS examination implied the strengthening of fatigue-resistant ability in skeletal muscles after long-term electrical stimulation. So cardiomyoplasty is suggested to be a supplementary measure in treating end-stage heart failure.

Animals↗

Maintained benefits and improved survival of dynamic cardiomyoplasty by activity-rest stimulation: 5-year results of the Italian trial on "demand" dynamic cardiomyoplasty.

OBJECTIVE: Latissimus dorsi (LD) muscular degeneration caused by continuous electrical stimulation has been the main cause of the poor results of dynamic cardiomyoplasty (DCMP) and its exclusion from the recent international guidelines on heart failure. To avoid full transformation of the LD and to improve results, a new stimulation protocol was developed; fewer impulses per day are delivered, providing the LD wrap with daily periods of rest ("demand" stimulation), based on a heart rate cut-off. The aim of this work is to report the results at 5 years of follow-up of the Italian Trial of Demand Dynamic Cardiomyoplasty and to discuss their impact on the destiny of this type of cardiac assistance. METHODS: Twelve patients with dilated myocardiopathy (M/F=11/1, mean age 58.2+/-5.8 years, sinus rhythm/atrial fibrillation=11/1) were submitted during the period 1993-1996 to DCMP and at different intervals to demand protocol. Clinical, echocardiographic, mechanographic and cardiac invasive assessments were scheduled before initiating the demand protocol and during the follow-up at 0, 6 and every 12 months. RESULTS: The mean duration of follow-up was 40.2+/-13.8 months (range 18-64). There were no perioperative deaths. The demand stimulation protocol showed a decrease in 5 years in New York Health Association (NYHA) class (3.17+/-0.38-1.67+/-0.77, P=0.0001), an improvement of left ventricular ejection fraction (22.6+/-4.38-32.0+/-7.0, P<0.001), a 5-year actuarial survival of 83.3% (one patient was switched to heart transplantation programme due to clinical worsening and another one died of massive pulmonary embolism). CONCLUSIONS: Demand DCMP maintains over time LD muscular properties, enhances clinical benefits and improves survival of DCMP, thus reopening the debate whether this type of treatment should be considered in patients with end-stage heart failure.

Cardiomyopathy, Dilated↗

A review of the concept of circulatory bioassist focused on the "new" demand dynamic cardiomyoplasty: the renewal of dynamic cardiomyoplasty?

After the initial enthusiasm, the dynamic cardiomyoplasty lost its reputation owing to the poor long-term results, caused by the muscular degeneration subsequent to chronic continuous electrical stimulation of the latissimus dorsi. An activity-rest stimulation protocol that avoids full transformation of the skeletal muscle, maintaining muscular properties over time, has been successfully tried. This "demand" stimulation protocol showed in humans good results improving NYHA class, ejection fraction value, and survival. The discussion about the capability of this and a unique kind of cardiocirculatory bioassist is due to be reopened. In fact, heart transplant, percutaneous circulatory-supporting device, multisites stimulation therapy, and total artificial heart have some drawbacks, one of which is the economic cost. In developing countries the more economic demand dynamic cardiomyoplasty may still play a role.

Cardiomyopathy, Dilated↗

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.

Animals↗

Component analysis of bilateral anterior cardiomyoplasty.

This experiment was designed to analyze the mechanism of ventricular augmentation generated with bilateral anterior cardiomyoplasty by comparing it in an acute setting with its components, the left anterior cardiomyoplasty and the right anterior cardiomyoplasty. Hemodynamic variables were measured in 8 dogs before and after each flap was positioned around the heart. Stimulation was achieved by R-wave synchronous latissimus burst pacing at a ratio of 1:4, an amplitude of 5 V, a frequency of 33 Hz, and a duration of 30% of the R-R interval. Hemodynamic changes were again recorded during latissimus stimulation. Construction of the bilateral anterior wrap (static cardiomyoplasty) caused some depression of baseline hemodynamic function, which was greater than that caused by either the static right or left anterior cardiomyoplasty. With stimulation of the muscles (dynamic cardiomyoplasty), the bilateral wrap caused significant biventricular augmentation. Evaluation of the components of the bilateral wrap demonstrated that dynamic right anterior cardiomyoplasty also provided significant biventricular augmentation, but the dynamic left anterior cardiomyoplasty augmented only right-sided variables. The mechanism of biventricular compression by the bilateral procedure is due mostly to the right wrap. The right anterior cardiomyoplasty may provide significant biventricular compression for treatment of heart failure, without the complexity associated with bilateral anterior cardiomyoplasty.

Animals↗

Dynamic cardiomyoplasty in chronic left ventricular failure: an experimental model.

Dynamic cardiomyoplasty continues to attract interest as a therapeutic option in the management of heart failure. In a large animal model of ischemic heart failure, we have compared dynamic cardiomyoplasty with both adynamic cardiomyoplasty and a control group. Heart failure was induced by coronary artery ligation in sheep, and under the same anesthetic dynamic cardiomyoplasty (n = 5), adynamic cardiomyoplasty (n = 4), or no further procedure was performed (n = 5). After recovery the animals were housed for a further 3 months. The dynamic cardiomyoplasty underwent a recognized muscle transformation protocol during this period. At terminal studies, the animals were hemodynamically assessed, both under baseline conditions and after colloid volume loading. The data at baseline were compared with unpaired t tests, and the function curves created by volume loading were compared by analysis of variance. Although the changes at baseline were small, there were highly significant improvements in the function curves in the dynamic cardiomyoplasty group when the stimulators were turned on compared with stimulators off (p = 0.005) for cardiac output; p = 0.035 for left ventricular end-diastolic pressure; p = 0.002 for pulmonary artery capillary wedge pressure; p = 0.004 for stroke volume; and p = 0.003 for cardiac power). There were also significant improvements in indices of cardiac performance when the dynamic cardiomyoplasty group was compared with both the control and adynamic cardiomyoplasty groups. We conclude that there is experimental evidence that cardiomyoplasty augments cardiac function in a model of chronic left ventricular failure.

Animals↗

Thoracoscopic cardiomyoplasty: a canine feasibility study.

BACKGROUND: Thoracoscopy may be effective in reducing the surgical stress of cardiomyoplasty. The feasibility of thoracoscopy in cardiomyoplasty was investigated. METHODS: Cardiomyoplasty by thoracoscopy and by the open method through a thoracotomy was performed in dogs. After 8 to 10 weeks of preconditioning, the hemodynamic effect of burst stimulation was measured. RESULTS: Cardiomyoplasty by thoracoscopy took 90 +/- 21 minutes (mean +/- standard deviation), whereas cardiomyoplasty by the open method took 67 +/- 10 minutes (p < 0.05). As a result of burst stimulation, aortic pressure, descending aortic flow, and left atrial pressure increased by 15.1% +/- 6.5%, 8.6% +/- 6.3%, and 3.8% +/- 4.6%, respectively, in the dogs that received the cardiomyoplasty by thoracoscopy, whereas those indices increased by 16.5% +/- 6.9%, 9.8% +/- 5.9%, and 4.8% +/- 4.2%, respectively, in dogs that received cardiomyoplasty by the open method. No significant difference between the two groups was shown in any index. CONCLUSIONS: Cardiomyoplasty by thoracoscopy was technically practical, and its hemodynamic effect was similar to that of the open method. The feasibility of cardiomyoplasty by thoracoscopy was thereby suggested.

Animals↗

Improved efficiency of energy transfer to external work in chronic cardiomyoplasty based on the pressure-volume relationship.

OBJECTIVE: Cardiomyoplasty is a surgical procedure to support the failing heart, in which a burst-stimulated latissimus dorsi muscle flap is transposed and wrapped around the ventricles. The effect of dynamic cardiac compression, implemented as cardiomyoplasty, on left ventricular performance remains controversial; the mechanism by which clinical symptoms are improved remains unclear. To investigate the mechanism for improvement of patients' symptoms, it is important to evaluate the effects of cardiomyoplasty on left ventricular energetics and on left ventricular systolic and diastolic function. We therefore evaluated the efficiency of energy transfer from the native pressure-volume area to external work under conditions of 1:3 skeletal muscle burst pacing in an animal model with chronic heart failure. METHODS: In seven Merino-Wether sheep, cardiomyoplasty was performed after stable heart failure was induced by staged coronary embolizations (ejection fraction < 35%). Hemodynamic assessment including the assessment of the pressure-volume relationship was performed 8 weeks after cardiomyoplasty when the latissimus dorsi muscle was fully trained. Instantaneous left ventricular pressure and volume were measured with a catheter-tipped manometer and a conductance catheter during steady-state conditions and after a transient inferior vena cava occlusion. The effect of dynamic cardiac compression on left ventricular systolic function was assessed by comparing pre-assisted and assisted beats and on diastolic function by comparing assisted and post-assisted beats. RESULT: The slope of the end-systolic pressure-volume relationship decreased by 30.5% +/- 27.8% (p = 0.02) during assisted beats. However, left ventricular pump performance improved by increasing stroke volume and external work by 35.9% +/- 36.0% (p = 0.03) and 9.7% +/- 6.8% (p = 0.03), respectively, resulting in a reduction of the volume intercept. As a result, the end-systolic pressure-volume relationship shifted to the left. The efficiency of energy transfer from the native pressure-volume area to the overall external work improved by 7.6% +/- 8.2% (p = 0.04). Cardiomyoplasty did not affect the time constant of left ventricular isovolumic pressure decline or the maximal rate of pressure decay, which suggested that cardiomyoplasty did not affect left ventricular relaxation. CONCLUSIONS: Dynamic cardiac compression in the form of cardiomyoplasty enhanced left ventricular pump performance without interrupting left ventricular filling. The ratio of energy transfer from the native pressure-volume area to the overall external work suggests a myocardial oxygen-sparing effect of cardiomyoplasty.

Animals↗

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.

Adrenergic beta-Agonists↗

Cardiomyoplasty reduces myocardial oxygen consumption: implications for direct mechanical compression.

BACKGROUND: This study investigates the possibility of reducing myocardial oxygen consumption by dynamic cardiomyoplasty in chronic heart failure. The sheep model used is relevant for cardiac assist using direct mechanical cardiac compression. METHODS: In 7 sheep, heart failure was induced by staged intracoronary microembolization followed by dynamic cardiomyoplasty. Six months later, the effect of latissimus dorsi muscle stimulation in the 2:1 mode (on, cardiomyoplasty; off, control) was studied. Left ventricular pressure-volume loops were obtained by conductance, micromanometer, and inferior vena cava occlusion catheter. Myocardial oxygen consumption was derived from left main coronary artery blood flow and oxygen content of arterial and coronary sinus blood. RESULTS: Cardiomyoplasty had no significant effect on left ventricular hemodynamic variables such as end-systolic pressure. However, cardiomyoplasty increased stroke volume and ejection fraction significantly by 11% +/- 12% and 11% +/- 10%, respectively. Although pressure-volume area and external work did not increase with cardiomyoplasty, myocardial oxygen consumption decreased by 21% +/- 11%. Therefore, cardiomyoplasty increased myocardial efficiency (external work/myocardial oxygen consumption) by 16% +/- 13%. CONCLUSIONS: Despite limited hemodynamic improvement from dynamic cardiac compression by cardiomyoplasty in sheep with chronic heart failure, myocardial oxygen consumption was significantly reduced. These findings provide a rationale for reverse remodeling of the failing heart using direct mechanical compression.

Animals↗

Growth potential and left ventricular diastolic function in cardiomyoplasty.

BACKGROUND: Dynamic cardiomyoplasty is an experimental operation for advanced heart failure. Current clinical results bring the possibility of its application to children. This study was designed to obtain information about the relationship between cardiomyoplasty and growth of the heart. METHODS: Six beagles, 9 to 10 weeks old, underwent cardiomyoplasty without electric stimulation (cardiomyoplasty group), and another 5 beagles underwent median sternotomy and pericardiotomy (control group). Six months later, weights of hearts, wrapped latissimus dorsi muscles, and unwrapped right latissimus dorsi muscles and pressure-volume relationships were obtained. RESULTS: Wrapped latissimus dorsi muscles weighed 33 +/- 3 g (mean +/- standard deviation), and unwrapped muscles weighed 68 +/- 5 g. The heart weight was 82 +/- 3 g in the cardiomyoplasty group and 89 +/- 7 g in the control group. Left ventricular maximum elastance was 3.8 +/- 0.8 mm Hg/mL in the cardiomyoplasty group and 3.9 +/- 0.9 mm Hg/mL in the control group. End-diastolic pressure versus end-diastolic volume ratios were 0.52 +/- 0.03 and 0.54 +/- 0.05, respectively. Pathologic examination showed fat infiltration and muscle fiber atrophy in the cardiomyoplasty group. CONCLUSIONS: The wrapped latissimus dorsi muscle flaps were growing and the diastolic function was not impaired. This indicates a potentially safe clinical application of dynamic cardiomyoplasty for children.

Adipose Tissue↗

The effects of prosthetic cardiac binding and adynamic cardiomyoplasty in a model of dilated cardiomyopathy.

OBJECTIVE: Because adynamic cardiomyoplasty, or wrapping skeletal muscle around the heart, had been shown to provide a girdling effect and delay progressive ventricular dilatation in heart failure, a similar girdling effect by the much simpler procedure of cardiac binding, using a prosthetic membrane to wrap the heart, was studied and compared with that of adynamic cardiomyoplasty. METHODS: Twenty-one dogs were divided into control, adynamic cardiomyoplasty, and cardiac binding groups. Cardiac dimension and hemodynamic studies were carried out before and 4 weeks after rapid pacing at 250 beats/min. For adynamic cardiomyoplasty, the left latissimus dorsi muscle was used for the cardiac wrap; for cardiac binding, a Marlex sheet (C. R. Bard, Inc., Murray Hill, N.J.) was used. Serial two-dimensional echocardiography, right heart catheterization, and in the cardiac binding group, left heart catheterization were performed. RESULTS: Four weeks of rapid pacing induced severe heart failure and cardiac dilatation. The magnitude of ventricular dilatation at the end of rapid pacing was less in the cardiac binding group than in the control group and least in the adynamic cardiomyoplasty group. Left ventricular end-diastolic volume, end-systolic volume, and ejection fraction were 82.1 +/- 21.1 ml, 67.1 +/- 16.0 ml, and 17.5% +/- 5.8%, respectively, in the control group; 61.9. +/- 8.1 ml, 44.1 +/- 7.8 ml, and 30.1% +/- 3.6%, respectively, in the cardiac binding group; and 51.8 +/- 8.7 ml, 30.3 +/- 10.4 ml, and 27.0% +/- 4.0%, respectively, in the adynamic cardiomyoplasty group. CONCLUSIONS: Both adynamic cardiomyoplasty and cardiac binding reduced cardiac enlargement and functional deterioration after rapid pacing, with adynamic cardiomyoplasty appearing to be more effective, perhaps because of the adaptive capabilities of the skeletal muscle wrap. However, cardiac binding is a simpler and less invasive procedure, which may be useful as an adjunct to prevent or delay progressive ventricular dilatation in heart failure.

Animals↗