The effect of chronic pulmonary hypertension on left ventricular size, function, and interventricular septal motion

Abstract

The effect of right ventricular pressure overload secondary to chronic pulmonary arterial hypertension on left ventricular size and function and on interventricular septal motion was studied in 13 patients in whom coronary artery disease, hypertension, and hypoxemia were excluded. Regional and global left ventricular function were assessed by computer-assisted analysis of two-dimensional directed M-mode echocardiograms obtained within 24 hours of a hemodynamic study. Septal position and motion were further analyzed by delineating seven points along the right and left sides of the septum during a single cardiac cycle. All echocardiographic data were compared to those of 10 normal subjects. Mean values for right ventricular systolic, mean pulmonary artery and puimonary capillary wedge pressures were: 71 ± 26 mm Hg, 46 ± 16 mm Hg, and 7 ± 1 mm Hg, respectively. Septal motion was interpreted from the M-mode echocardiograms as normal in seven patients (group I) and abnormal in the remaining six patients (group II). The only hemodynamic parameter which distinguished these two patterns was ΔP, the transseptal systolic pressure gradient across the interventricular septum, which was significantly different (p < 0.02) in group I (ΔP = 65 ± 16 mm Hg) from that of group II (ΔP = 21 ± 24 mm Hg). As a result of abnormal septal position, the septal-free wall dimensions of the left ventricle were reduced, but there was no evidence of depressed left ventricular performance in these patients. We conclude that resting left ventricular function is well preserved in patients with pulmonary hypertension, despite significant alterations in septal position and left ventricular size. Abnormal septal motion in patients with right ventricular pressure overload is related to changes in the pressure gradient across the interventricular septum.