CLINICAL-STUDY OF THE EFFECTS OF LATISSIMUS-DORSI MUSCLE FLAP STIMULATION AFTER CARDIOMYOPLASTY

Background Beneficial hemodynamic effects after dynamic cardiomyoplast y have been inconsistently demonstrated, and the effects seen may be d ue to the wrap itself, to flap stimulation, or both. The aim of this s tudy was to determine whether flap stimulation per se acts as a systol ic active process after cardiomyoplasty. Methods and Results Catheteri zations were performed in 13 patients 14.4+/-7 months after cardiomyop lasty. New York Heart Association functional class decreased from 3.3 to 2.1 after the procedure (P=.0005). Hemodynamic evaluations were fir st 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 stimulat ion was stopped, there was no change (P>.05) in indexes of systolic or diastolic LV function (peak systolic LV pressure, LV ejection fractio n, peak positive dP/dt, peak negative dP/dt, or tau). Pulmonary capill ary wedge pressure and cardiac index were unchanged when stimulated an d 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 deter iorated in 2 patients, but a slight improvement was noted in 3 patient s. Cardiothoracic ratio, echocardiographic LV end-diastolic dimension, and fractional shortening remained unchanged between immediate (<1 mo nth) and long-term (36.7+/-25.9 months) postoperative evaluations. Con clusions In the majority of our patients, there was no short-term hemo dynamic benefit of flap stimulation; therefore, we conclude that the e fficacy of cardiomyoplasty may be a consequence of a passive ''girdlin g effect,'' which limits the progression of ventricular enlargement an d further deterioration of ejection fraction.