Influence of right ventricular pressure overload on left and right ventricular filling in cor pulmonale assessed with Doppler echocardiography.

We evaluated the influence of right ventricular (RV) pressure overload on RV and left ventricular (LV) filling using Doppler echocardiography in cor pulmonale. The LV and RV inflow signals were recorded by Doppler flowmetry. The end-diastolic (ED) and end-systolic (ES) LV short axis images were detected by 2-dimensional echocardiography in 20 healthy subjects and in 36 cases of chronic pulmonary disease (CPD) with pulmonary hypertension. We measured (1) the ratio of the peak velocity of inflow due to atrial contraction to the peak velocity of rapid inflow (A/R), (2) the deceleration half-time of rapid inflow (delta TD), (3) the corrected radius of curvature (cRC) of the interventricular septum (IVS) at ES and ED, and (4) the percent change of length of 16 radial grids (%CL) using the fixed method on the ED and ES short axis images. In 17 of 36 patients with CPD, we measured the systolic pulmonary artery pressure (sPAP), the cardiac index (CI), the mean pulmonary capillary wedge pressure (mPCWP), the end-diastolic right ventricular pressure and the partial oxygen pressure of arterial blood (PaO2). The results were as follows: in CPD, (1) both the RV and the LV diastolic behavior were impaired as shown by increased A/R (1.04 +/- 0.20, 0.98 +/- 0.17, respectively) and prolonged delta TD (115 +/- 20, 100 +/- 17 msec, respectively), (2) the IVS was flattened at ED (cRC of IVS = 0.67 +/- 0.12), (3) the IVS wall motion was impaired (%CL of IVS = 133 +/- 13), (4) the sPAP had an adequate correlation with RV A/R (r = 0.80, p less than 0.01), RV delta TD (r = 0.59, p less than 0.05), LV A/R (r = 0.82, p less than 0.01), LV delta TD (r = 0.61, p less than 0.05), cRC of IVS (r = 0.67, p less than 0.01), %CL of IVS (r = -0.59, p less than 0.05). There was no significant correlation between the LV diastolic behavior and the CI, the mPCWP, the PaO2. It is concluded that the impairment of RV diastolic behavior was caused by the decreased RV compliance due to RV free wall hypertrophy. Moreover, the RV pressure overload interfered with the IVS motion during diastole, this regional impairment of diastolic behavior of the IVS subsequently causing impairment of LV diastolic filling.