Mechanically increased right ventricular afterload alters left ventricular configuration, not contractility, in neonatal lambs

Left ventricular dysfunction has been observed in human infants with pulmonary hypertension. The purpose of this study was to establish whether mechanically increased right ventricular afterload alters left ventricular performance by altering its contractility, configuration, or both. Six neonatal 3- to 7-d-old lambs were acutely instrumented with micromanometer-tipped catheters and two pairs of ultrasonic crystals to measure left ventricular pressure and anterior-posterior and septal-free wall dimensions. The product of these two dimensions, denoted left ventricular area, was used as an index of left ventricular volume. Two levels of mechanically increased right ventricular afterload were induced with a closed pericardium under three levels of left ventricular preload produced by whole-blood transfusions. Four brief increases in left ventricular afterload were induced by constricting the aorta under each right ventricular afterload and preload condition. Using multiple linear regression, we found that the slope of the end-systolic pressure-area relationship, an index of contractility, was unchanged [0.90 +/- 0.11 mm Hg/mm2 (SEM)], and stroke area (65.8 +/- 7 mm2) and cardiac output (the product of stroke area and heart rate) (13,400 +/- 1,660 mm2/min) were maintained. However, the area intercept of the pressure-area line at zero pressure (499 +/- 13 mm2) shifted significantly to the left in the presence of both levels of increased right ventricular afterload (by -39.2 +/- 13 and -76.2 +/- 15 mm2, respectively). Mechanically increased right ventricular afterload alters left ventricular configuration and causes a shift in the operating volume (area) range of the ventricle with no change in contractility in 3- to 7-d-old lambs.