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Ann Thorac Surg 2001;71:2077-2078
© 2001 The Society of Thoracic Surgeons
a Department of Cardiothoracic Surgery, Allegheny General Hospital, Pittsburgh, Pennsylvania, USA
Address reprint requests to Dr Magovern, Department of Cardiothoracic Surgery, Allegheny General Hospital, 320 East North Ave, Pittsburgh, PA 15212
e-mail: jmagover{at}wpahs.org
Abstract
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.
The article cited above outlined the experimental effects of right latissimus dorsi cardiomyoplasty on left ventricular function. This operation was subsequently done on a total of 16 patients. The early data on this group of patients confirmed our experimental results. At 6 weeks after surgery, the mean left ventricular ejection fraction (LVEF) increased from 25 ± 1.6% to 35 ± 3%, and the mean left ventricular end diastolic volume decreased from 365 ± 18 to 307 ± 24 mL (p < 0.05) [1]. During a long-term follow-up period of 2 years, the procedure stabilized left ventricular size and prevented dilatation, but the initial improvements in LVEF were not maintained. However, the LVEF in long-term survivors remained equal to or slightly higher than the preoperative level, which is further evidence of stabilization of left ventricular function [2]. The operative mortality was low at 6% (1/16), but survival was only 62% at 1 year and 50% at 2 years, due to a significant incidence of sudden death. The net result was that cardiomyoplasty using the right latissimus dorsi muscle had results very similar to that using the left muscle. The primary long-term effect was to prevent left ventricular dilation and maintain LVEF by a biologic girdling effect.
Despite some promising experimental and clinical results, interest in clinical application of cardiomyoplasty has waned in recent years. There are several reasons for this, but the most important is that heart-failure cardiologists were not sufficiently convinced by the data to refer patients for surgery, noting that the clinical benefits were modest, the surgical morbidity was significant, and that survival was not improved. In addition, pharmacologic therapy for congestive heart failure has advanced tremendously in the past decade. Recent randomized clinical trials have shown improved survival using ß-blockers, angiotensin-converting enzyme inhibitors, aldosterone antagonists, and angiotensin II receptor blockers. These trials have given heart failure specialists many options for the treatment of patients with mild to moderate heart failure. For all these reasons, recruitment of patients to a randomized clinical trial comparing cardiomyoplasty with medical therapy was very slow, which in turn resulted in loss of corporate interest in this procedure before the muscle-stimulator technology gained FDA approval.
Surgical therapy for chronic congestive heart failure remains an active area for research and entrepreneurial activity. Initial enthusiasm for the left ventricular reduction procedure has now vanished, but passive girdling and cardiac compression devices are under development. These concepts seek to replicate the beneficial aspects of cardiomyoplasty, but without the need for such a major operative procedure. The concept of using a mechanical left ventricular assist device as a bridge to recovery of cardiac function is gaining support, but remains a research project rather than a proven therapy. Various cellular and molecular approaches to heart failure management are also underway, including cytokine blocking drugs and gene transfection techniques.
At this point, cardiomyoplasty has been eclipsed by other approaches, but several centers continue with research efforts. We have demonstrated improved skeletal muscle strength and viability when muscle stimulation protocols are used that allow muscle rest periods [3]. Santamore and associates have shown impressive hemodynamic results in animals with heart failure when the latissimus dorsi muscle viability is improved by an initial vascular delay period [4]. In many ways, cardiomyoplasty remains an attractive concept, and it may very well return to clinical prominence in the future after additional research and development in the laboratory.
References
This article has been cited by other articles:
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  R. F. Padera Jr. and F. J. Schoen Pathology of Cardiac Surgery Card. Surg. Adult, January 1, 2008; 3(2008): 111 - 178. [Full Text]
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F. J. Schoen and R. F. Padera Jr. Cardiac Surgical Pathology Card. Surg. Adult, January 1, 2003; 2(2003): 119 - 185. [Full Text]
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