EFFECTS OF FREE-WALL ISCHEMIA AND BUNDLE-BRANCH BLOCK ON SYSTOLIC VENTRICULAR INTERACTION IN DOG HEARTS

Systolic direct ventricular interaction is thought to occur via the ve ntricular septum and the coordinated contraction of common fibers shar ed by both ventricles. The purpose of the present study was to evaluat e the effects of transient free wall ischemia and bundle branch block, which disrupt the coordinated contraction of shared common fibers, on left-to-right systolic ventricular interaction. We produced transient right and left ventricular free wall ischemia by 2-min coronary arter y occlusions and bundle branch block by ventricular pacing in nine in situ dog hearts. To eliminate any confounding effect of series interac tion, we used an abrupt hemodynamic perturbation (aortic constriction) , and we measured systolic interaction gain (IG) as Delta right ventri cular peak systolic pressure/Delta left ventricular peak systolic pres sure (IG(peak)) and instantaneous Delta right ventricular pressure/Del ta left ventricular pressure at matched data sampling times (IG(inst)) , along with changes in right ventricular stroke volume and stroke wor k before and on the beat immediately after the aortic constriction. To achieve equivalence of the interventricular septal pressure transmiss ion contribution to ventricular interaction, the Delta left ventricula r peak systolic pressure produced by the aortic constriction was match ed under all experimental conditions [average increase: 64 +/- 19 (SD) mmHg]. Control IG(peak) was 0.12 +/- 0.05, and control IG(inst) was 0 .11 +/- 0.05. These values did not change with either free wall ischem ia or ventricular pacing, with or without an intact pericardium. The c hanges in right ventricular stroke volume and stroke work produced by the aortic constriction were not different from zero, during either is chemia or ventricular pacing, with or without an intact pericardium. W e conclude that disruption of the coordinated contraction of shared co mmon fibers does not affect direct systolic ventricular interaction wh en assessed during aortic constriction.