Abstract
We hypothesized that acute electrical stimulation of a latissimus dorsi Cardiomyoplasty would augment the collateral blood flow delivered by the skeletal muscle to the heart. This hypothesis was tested in an animal model (13 goats) of coronary artery disease. Six weeks after a Cardiomyoplasty was performed, myocardial collateral blood flow derived from the latissimus dorsi muscle was measured with colored microspheres when the muscle was at rest and during electrical stimulation of the thoracodorsal nerve at 1.25 Hz. The area at risk for ischemia averaged 13.37 ± 2.08 g (mean ± standard error), or 18.4% of left ventricular mass (n = 13). At rest, significant skeletal muscle-derived collaterals developed in 9 animals, and formed predominantly to chronic ischemic myocardium (mean ± standard error, 0.07 ± 0.02 mL · g<sup>-1</sup> · min<sup>-1</sup>; n = 9), rather than infarct (0.03 ± 0.02 mL · g<sup>-1</sup> · min<sup>-1</sup>; n = 5), or normal myocardium (0.0005 ± 0.0001 mL · g<sup>-1</sup> · min<sup>-1</sup>; n = 9). Stimulation increased skeletal muscle-derived collateral blood flow to chronic ischemic areas to 0.38 ± 0.09 mL · g<sup>-1</sup> · min<sup>-1</sup> (n = 9) (p < 0.05). During stimulation, the collateral flow was greater in the epicardium (0.46 ± 0.11 mL · g<sup>-1</sup> · min<sup>-1</sup>) than in endocardium (0.14 ± 0.09 ml · g<sup>-1</sup> · min<sup>-1</sup>) (p < 0.05). This study demonstrates that electrical stimulation of a latissimus dorsi cardiomyoplasty increases extramyocardial collateral blood flow to chronic ischemic myocardium. © 1993.