In our approach to dynamic cardiomyoplasty, which consists of wrapping a skeletal muscle around the heart and stimulating the former in synchrony with heart contractions to augment ventricular contractility, we have transferred a latissimus dorsi muscle flap to the heart by way of a partial resection of the second rib and subsequently suturing the muscle flap around the ventricles. The muscle flap is stimulated by a Cardio-Myostimulator burst-pulse generator (Medtronic SP 1005) connected to intramuscular electrodes. In preclinical animal research, the latissimus dorsi muscle flap was shown to maintain adequate contractile force and to increase its fatigue resistance by gradual conversion of glycolytic-fatigue-sensitive-to-oxidative-fatigue-resistant muscular fibers (100%). Histochemical and biochemical studies of chronically stimulated muscles showed a total transformation of muscle fast myosin to slow myosin with characteristics similar to those of myocardium. Electron microscopy showed preserved myofibrillar cytoarchitecture and increased mitochondrial density in the cell. At 9 months, cardiac output and ultrasonic Doppler studies showed a significant increase in ventricular function (cardiac output, +21%; peak blood velocity, +40% -80%; and stroke volume, +98% -102%) during muscle stimulation. In the clinical situation, long-term (range of follow-up interval, 4-42 months) beneficial cardiac effects of cardiomyoplasty have been documented in eight patients with various pathologies (ventricular tumor, left ventricular aneurysm, ischemic disease, and dilated cardiomyopathy). Our current understanding of this process is that dynamic cardiomyoplasty acts in two ways: 1) it promotes more vigorous systolic contraction, and 2) it appears to limit heart dilatation.