DELAYED STIMULATION OF THE LATISSIMUS-DORSI MAY RESULT IN DISUSE ATROPHY

Background. The latissimus dorsi is usually left unstimulated for 2 we eks after cardiomyoplasty to allow the muscle to recover from the loss of the collateral circulation. To determine whether the 2-week delay may cause muscle atrophy, we randomized 15 mongrel dogs to a control g roup or a disuse atrophy group. Methods. The collateral circulation to the latissimus dorsi was ligated in all animals before cardiomyoplast y to reduce the risk of ischemic injury to the muscle during mobilizat ion. Two weeks after collateral ligation, the atrophy group had the te ndinous attachment of the latissimus dorsi severed and then 2 weeks la ter underwent cardiomyoplasty. The control group had a 2-week delay af ter collateral ligation followed by cardiomyoplasty. Biopsies were per formed before collateral ligation and before cardiomyoplasty. After he art failure was induced, hemodynamic function was assessed during sync hronized contraction of the latissimus dorsi by measuring the maximum systolic elastance, stroke volume, preload recruitable stroke work ind ex, and diastolic compliance. Results. Comparison of muscle morphology between the two groups demonstrated the presence of muscle atrophy in those animals that had been randomized to the atrophy protocol. Durin g synchronized contraction of the latissimus dorsi, there was no signi ficant increase in maximum systolic elastance in either group. However , both stroke volume and pulmonary recruitable stroke work index were significantly higher in the control animals during assisted beats. The left ventricle was less compliant in the atrophy group, suggesting th at muscle atrophy had adversely affected diastolic function. Conclusio ns. Delayed electrical stimulation of the latissimus dorsi may result in atrophy and loss of function. (C) 1997 by The Society of Thoracic S urgeons.