Clinical Study of the Effects of Latissimus Dorsi Muscle Flap Stimulation After Cardiomyoplasty

Abstract

Background Beneficial hemodynamic effects after dynamic cardiomyoplasty have been inconsistently demonstrated, and the effects seen may be due to the wrap itself, to flap stimulation, or both. The aim of this study was to determine whether flap stimulation per se acts as a systolic active process after cardiomyoplasty. Methods and Results Catheterizations were performed in 13 patients 14.4±7 months after cardiomyoplasty. New York Heart Association functional class decreased from 3.3 to 2.1 after the procedure ( P =.0005). Hemodynamic evaluations were first performed with the stimulator on in the 2:1 mode and then after the stimulator had been off for at least 24 hours. Left ventricular (LV) ejection fraction increased from 25.1±6% before surgery to 28.2±6.7% with the stimulator on after cardiomyoplasty ( P =.04). When stimulation was stopped, there was no change ( P >.05) in indexes of systolic or diastolic LV function (peak systolic LV pressure, LV ejection fraction, peak positive dP/dt, peak negative dP/dt, or τ). Pulmonary capillary wedge pressure and cardiac index were unchanged when stimulated and nonstimulated settings were compared ( P >.05). However, a remarkable heterogeneity of individual responses was observed. Ejection fraction and cardiac index decreased with the stimulator off in 3 patients, but peak positive dP/dt decreased in 6 patients; diastolic function deteriorated in 2 patients, but a slight improvement was noted in 3 patients. Cardiothoracic ratio, echocardiographic LV end-diastolic dimension, and fractional shortening remained unchanged between immediate (<1 month) and long-term (36.7±25.9 months) postoperative evaluations. Conclusions In the majority of our patients, there was no short-term hemodynamic benefit of flap stimulation; therefore, we conclude that the efficacy of cardiomyoplasty may be a consequence of a passive “girdling effect,” which limits the progression of ventricular enlargement and further deterioration of ejection fraction.