CARDIOMYOPLASTY - HEMODYNAMIC BENEFIT TO NORMAL AND DEPRESSED CANINE LEFT-VENTRICULAR FUNCTION

This study examined the effects of cardiomyoplasty with vascular delay on canine normal and depressed left ventricular (LV) function. To imp rove viability of the latissimus dorsi muscle (LDM), vascular delay wa s performed 2 weeks before cardiomyoplasty in 10 mongrel dogs. Two wee ks after cardiomyoplasty, LV function was evaluated by simultaneously measuring LV and aortic pressure, and aortic flow. The LDM was stimula ted at a ratio of 1:4-1:7 synchronously with ventricular systole. Micr ospheres (90 mu) were sequentially injected into the left coronary art ery to depress LV function. Data were acquired and analyzed on a beat to beat basis. Results were as follows: LDM stimulation significantly augmented LV systolic pressure (LVSP) from 138 +/- 2 to 161 +/- 2 mmH g, the peak rate of change of LV pressure (+dP/dt) from 1888 +/- 46 to 2584 +/- 43 mmHg/sec, aortic systolic pressure (AoSP) from 140 +/- 2 to 159 +/- 2 mmHg, stroke volume (SV) from 11.2 +/- 0.3 to 13.3 +/- 0.3 mi, stroke work (SW) from 19 +/- 1 to 26 +/- 1* gm.m, peak aortic flow (P Oa) from 5542 +/- 142 to 7190 +/- 161 ml/min, and decreased -dP/dt from -1683 +/- 31 to -1689 +/- 49 mmHg/sec (* = p < 0.05). Mic rosphere injections depressed LV function, but did not affect the magn itude of the net changes between stimulated and nonstimulated beats. H owever, the percent changes significantly increased. Preconditioning o f LDM with vascular delay augments cardiac function in LDM assisted be ats. This improved performance was present in both normal as well as d epressed LV function groups. Thus, investigations of cardiomyoplasty m ay not necessarily require a model of severe myocardial dysfunction. V ascular delay offers an important preconditioning method of LDM to aug ment cardiac function in cardiomyoplasty.