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Ann Thorac Surg 1997;64:408-409
© 1997 The Society of Thoracic Surgeons

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Invited Commentary

Invited Commentary

Department of Human Anatomy and Cell Biology, University of Liverpool, The New Medical School, Ashton Street, Liverpool L69 3GE, United Kingdom

See also page 404.

A surgical approach to cardiac assistance based on redeployment of the patient's own skeletal muscle is an attractive prospect. It offers a biological solution to heart failure that is free from the risks, debilitating side-effects, and costs associated with long-term immunosuppression; it is not limited by donor availability; and it allows the patient's own heart and all the associated neuroregulatory circuits to be retained intact. The costs are mainly those associated with the surgical procedure itself, including the implantable stimulator used to activate the grafted muscle. One route to the implementation of skeletal muscle assist is cardiomyoplasty, and this has provided the main clinical experience to date. Commercial pressures, and the need to conform to fixed protocols for multicenter trials, have tended to inhibit systematic optimization of this technique. This is unfortunate because transposition, reconfiguration and electrical stimulation pose a challenge to the long-term integrity of the muscle graft that clinical protocols have never adequately taken into account [1–3]. This article by You and colleagues is to be welcomed for taking a critical look at one part of the existing protocol: the postoperative delay that precedes the commencement of stimulation.

It is difficult to predict the extent to which the grafted latissimus dorsi muscle might undergo changes during this period. A muscle whose tendon has been cut suffers a total loss of resting tension, and the atrophy and histopathology associated with this tenotomized state has been known for more than 30 years (see [1] for references). However, this is not the full situation in cardiomyoplasty. It is true that a cardiomyoplasty wrap cannot be made at the muscle's physiologic resting tension, or it would impede refilling of the ventricles during diastole; on the other hand, tension in the wrap is not zero, and it may be modulated rhythmically by the filling and emptying of the ventricles. So what happens to a muscle that is left in this condition without stimulation for 2 weeks? This is the crucial question and unfortunately it is one that the present article leaves unanswered. In their experimental group, You and colleagues cut the humeral insertion of the latissimus dorsi muscle but the muscle was then left for 2 weeks in situ. The changes are therefore those that are already well-documented for tenotomy, and the only real difference from previous work is that the tension-generating capacity of each muscle was assessed by configuring it for cardiomyoplasty, rather than adopting a more conventional linear force measurement procedure. Ligation of the collateral circulation certainly introduces an additional factor, but the experimental design was regrettably asymmetric in this respect, collateral ligation taking place 4 weeks before the terminal experiment in the "atrophy" group and only 2 weeks beforehand in the control group. Finally, the muscles in the study had not been conditioned (by chronic electrical stimulation) to become resistant to fatigue, an essential step in harnessing skeletal muscle power for cardiac assistance. The conditioning process is associated with profound changes not only in fatigue resistance but also in force–velocity and power–velocity relationships. How an unconditioned muscle performs during propanolol-induced heart failure is therefore a somewhat academic issue [1].

You and colleagues clearly appreciate at least some of these shortcomings, and one would not disagree with their broad conclusions, which are in line with previous recommendations [1]. However, their work leaves open the tantalizing question: would muscles left as unstimulated cardiomyoplasty wraps show similar or less deterioration than those detached but left in situ, as in the present study? It is to be hoped that this question will not be too long in receiving an answer.

References

1. Salmons S, Jarvis JC. Cardiomyoplasty: a look at the fundamentals. In: Carpentier A, Chachques JC, Grandjean PA, eds. Cardiomyoplasty. Mount Kisco, NY: Futura 1991:3–17.
2. El Oakley RM, Jarvis JC, Barman D, et al. Factors affecting the integrity of latissimus dorsi muscle grafts: implications for cardiac assistance from skeletal muscle. J Heart Lung Transplant 1995;14:359–65.[Medline]
3. Salmons S. Damage in functional grafts of skeletal muscle. In: Salmons S, ed. Muscle damage. Oxford: Oxford University Press, 1997:215–33.

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