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Ann Thorac Surg 1995;60:1461-1462
© 1995 The Society of Thoracic Surgeons

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Correspondence

Anabolic Hormones in Cardiomyoplasty

Cardiomyoplasty Laboratory, Sinai Samaritan Medical Center, 945 North 12th St, Po Box 342 W419, Milwaukee, Wi 53201

To the Editor:

I congratulate Dirk Fritzsche and associates on an excellent article [1]. It is true that the hemodynamic benefit of cardiomyoplasty depends on two variables: the force capacity and the thickness of the latissimus dorsi muscle. All who perform clinical cardiomyoplasty know that the values of both of these variables decline significantly in the course of the conditioning process: force capacity and thickness are sacrificed in favor of increased resistance to fatigue. This is especially important when cardiomyoplasty is performed for patients with chronic heart failure. In these patients exercise capacity, fatigue, and dyspnea correlate poorly with the extent of left ventricular dysfunction. There is significant depression of the oxidative capacity and a reduction in the activity of enzymes of the skeletal muscle [2]. This makes the effectiveness of using the latissimus dorsi muscle of such patients for dynamic cardiomyoplasty questionable.

The results obtained by Dirk Fritzsche and associates are very impressive. The administration of anabolic steroid led to an increase in the force capacity and in the muscle mass of the conditioned latissimus dorsi muscle and an overall improvement in hemodynamic functioning. Although anabolic steroids have acquired some notoriety as a result of their use in sports, it is necessary to investigate their effect on skeletal muscle in critically ill patients. I would like to lend my support to these investigations that were performed at the Clinic for Cardiovascular Surgery, University of Leipzig (Germany). Side effects of anabolic steroids are expected for young people and growing organisms. When one focuses on the age of patients for whom cardiomyoplasty is a clinical option, the dangerous side effects of anabolic steroids lose their significance, especially when compared with the benefits received from their pharmacologic effect on the latissimus dorsi muscle.

My colleagues and I performed an analogous investigation at the Milwaukee Heart Project (Milwaukee, WI). An electrical stimulation training protocol for 6 sheep was initiated for 8 weeks (Myostim 7220 stimulator; Telectronics, Englewood, CO). Localized anabolic steroid (nandrolone decanoate) was administrated for the 8-week period via an osmotic pump placed in a subcutaneous pocket with a catheter introduced into the latissimus dorsi muscle. We studied the contractile force of the electrically stimulated muscle and the unstimulated contralateral control muscle. Baseline data were calculated as 100% and all other data were corrected to baseline. After 4 weeks there was no decrease in contractile force. The change was from 88% to 100% with different preloads (10, 15, and 20 g/kg) and amplitudes of impulses (5 and 10 V). After 8 weeks, the latissimus dorsi muscle was more powerful than before electrical stimulation. The change was 97% to 133%. Usually after 8 weeks of electrical stimulation alone, contractile force decreases to 70% to 75%. During a fatigue test (30 min, 100 bpm, ripple frequency, 10 V amplitude, and 6 impulses per burst) after 8 weeks of our protocol, the latissimus dorsi muscle lost only 12% of its initial force, whereas control muscle lost 40%. Thus local anabolic administration made the latissimus dorsi muscle stronger and more useful for cardiomyoplasty.

Of course, for future investigations it will be necessary to more carefully study the side effects of anabolic steroids in patients with end-stage congestive heart disease. However, I think that the expected life expectancy after cardiomyoplasty and the benefits of using anabolic steroid administration will overcome the possible side-effects.

References

1. Fritzsche D, Krakor R, Asmussen G, et al. Anabolic steroids (metenolone) improve muscle performance and hemodynamic characteristics in cardiomyoplasty. Ann Thorac Surg 1995;59:961–70.[Abstract/Free Full Text]
2. Karlsson J, Diamant B, Folkers K, et al. Ischemic heart disease, skeletal muscle fibers and exercise capacity. Eur Heart J 1992;13:758–62.[Abstract/Free Full Text]

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