The effect of pulmonary artery hypertension on right-ventricular performance in patients with chronic obstructive pulmonary disease (COPD) is unclear. Decreased values of right-ventricular ejection fraction (RVEF) have been reported, but most patients with stable COPD are not in cardiac failure and have normal or even increased cardiac outputs. We therefore hypothesized that RVEF may be afterload dependent, and thus a poor parameter of cardiac function, and that right-ventricular contractility may be normal even in COPD patients with pulmonary hypertension. We therefore studied 24 COPD patients using a combined hemodynamic and radionuclide approach. RVEF and thermodilution stroke volume index were measured simultaneously at rest in all 24 patients and also during bicycle ergometry in 9 patients. We then calculated end-diastolic and end-systolic volume indices and derived right-ventricular systolic pressure-volume relations in all and the slopes (E) of the pressure-volume line in 9 patients. RVEF was normal in COPD patients without pulmonary hypertension, but was reduced in those with pulmonary hypertension. A strong inverse linear relation between RVEF and mean pulmonary artery pressure (r = -0,73; p < 0.001) and pulmonary vascular resistance (r = -0.69; p < 0.001) could be demonstrated, indicating RVEF to be highly afterload dependent. Right-ventricular end-diastolic volume index was significantly higher in patients with pulmonary hypertension, indicating increased preload as the major mechanism to maintain adequate stroke volume in the face of an increased afterload. Right-ventricular end-systolic pressure-volume relations, a good parameter to define right-ventricular contractility independent of systolic loading conditions, were not different between COPD patients with or without pulmonary hypertension, nor did the slopes of the pressure-volume lines in the 9 patients studied during exercise show any difference. From these data we conclude that (a) RVEF is a poor indicator of overallright-ventricular function; (b) right-ventricular contractility is well preserved in stable COPD patients; (c) the major mechanism of maintaining stroke volume in the face of increased right-ventricular afterload seems to be preload augmentation.