|
|
||||||||
Ann Thorac Surg 1997;64:85
© 1997 The Society of Thoracic Surgeons
Department of Surgery, MCP/Hahnemann School of Medicine, Allegheny University of the Health Sciences, 320 E North Ave, Pittsburgh, PA 15212-4772
From its inception, cardiomyoplasty was by definition a dynamic procedure. It is by nature a sound concept, a "do-able" intervention, and still a promising surgical therapeutic measure for patients with otherwise irreversible congestive heart failure. The ventricular systolic augmentation intended by the synchronous contraction of an onlaid "conditioned" skeletal muscle, as much as the limitation of progressive cardiac dilatation and the eventual ventricular remodeling, are all dynamic components. In cardio-myo-plasty there is no room for a "static" component, not even as a concept. It would be the negation of the very foundation on which the symbiotic relation of cardiac and skeletal muscles is built for this and other procedures using the same principle.
Vaynblat and colleagues report on an experimental study "to test the potential benefit of wrapping the heart ...with the hope of ...preserving ventricular function in an animal model of rapidly progressive heart failure." The benefit of cardiac binding was limited to preventing biventricular dilatation and to significantly attenuating the increase in left ventricular end-diastolic pressure over a term of 7 weeks. So much for the benefits of the "static component" of cardiomyoplasty.
The traditional mechanical approach that muscle alternates from a biologically "active" state during contraction to a biologically "resting" state during relaxation has been criticized in the past [1]. Thermodynamically, the live skeletal muscle is never at rest. It may be quiet, but it is not static. The sustained tension maintained by the myofibers during mechanical relaxation is, by thermodynamic standards, a highly active phase, whereas during mechanical contraction the muscle switches into a thermodynamically passive state. Because investigators have disregarded for more than a decade the basic principles of energy conservation, present-day cardiomyoplasty devices and stimulation protocols have failed to keep muscle flaps in optimal working condition for any significant period. In long-term survivors, the result is, at its best, the equivalent of cardiac binding with an artificial membrane, and the initially achieved systolic augmentation is lost forever. Cardiac binding has the potential for being another (albeit different) positive contribution toward the surgical treatment of advanced congestive heart failure, but it is no match for the inherent potential of a cardiomyoplasty with a muscle stimulation program devised from the beginning to safeguard the long-term (10 years or more) integrity and working capabilities of the "converted" myofibers. One must not ignore the fact that the survival of the patient is contingent on the survival of the heart-muscle binomial unit created by cardiomyoplasty, or that the long-term success of the procedure depends, next to a dedicated cardiologist, on the long-term expected rendition of the skeletal muscle flap. It seems that more ambitious results at a much earlier stage have precluded scientists from reaching that goal.
Reference
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |