Alterations in left ventricular three-dimensional dynamic geometry and systolic function during acute right ventricular hypertension in the conscious dog.

Fifteen chronically instrumented, conscious dogs were studied to determine whether, in the intact circulation, mechanical interactions dictated by the anatomic contiguity of the two ventricles significantly alter left ventricular (LV) dynamic geometry and systolic function during acute right ventricular (RV) hypertension. The three-dimensional geometry of the left ventricle was monitored with three pairs of ultrasonic dimension transducers; ventricular pressures were measured with micromanometers. Data collected during pulmonary artery constriction (RV pressure 68 +/- 8/7 +/- 4 mm Hg) were compared with control data collected at matched heart rates (RV pressure 32 +/- 8/4 +/- 4 mm Hg). During pulmonary artery constriction, mean calculated LV end-diastolic volumes decreased from 69.2 +/- 20.0 to 56.2 +/- 21.3 cm3 (p less than or equal to 0.05). Mean systolic stroke volume decreased from 20.6 +/- 5.5 to 14.0 +/- 6.3 cm3 (p less than or equal to 0.05). These changes were entirely accounted for by alterations in the behavior of the LV septal-free wall minor axis and rearrangements in LV equatorial geometry. When the pulmonary artery was constricted, elongation of the septal-free wall axis occurred during isovolumic systole and was accompanied by a reciprocal decrease in anterior-posterior dimension. Most of the decrease in septal-free wall dimension occurred during relaxation and early diastole rather than during ejection. Mean septal-free wall end-diastolic dimension decreased from 5.45 +/- 0.69 to 4.90 +/- 0.75 cm (p less than or equal to 0.05). The mean systolic decrease in septal-free wall dimension fell from 0.36 +/- 0.18 to 0.14 +/- 0.22 cm (p less than or equal to 0.05). The end-diastolic dimensions and systolic shortening of the LV anterior-posterior minor axis and base-apex major axis were not significantly altered by pulmonary artery constriction. These findings suggest that during acute RV hypertension, impairment of LV systolic function and rearrangements in LV dynamic geometry are primarily the result of the anatomic contiguity of the two ventricles.