Understanding right and left ventricular systolic function and interactions at rest and with exercise in primary pulmonary hypertension

The effort limitation in primary pulmonary hypertension (PPH) is thought to result from an inability to increase cardiac output with exercise. The precise mechanism, however, is unknown. We studied right ventricular (RV) and left ventricular (LV) function and interactions in 16 patients with PPH with electron beam computed tomography (EBCT) at rest and during supine bicycle exercise. RV and LV volumes and masses were measured at systole and diastole, and ejection fraction and cardiac index computed. Resting RV end-diastolic volume (215 ± 72 ml) and mass (110 ± 45 g) were increased, whereas stroke volume (65 ± 26 ml) and ejection fraction (31 ± 8%) were decreased. LV end-diastolic volume (80 ± 31 ml) was decreased, whereas ejection fraction remained normal (66 ± 9%). Cardiac index was at the lower limit of normal (2.26 ± 0.72 L/min/m2). During exercise, RV end-diastolic volume was unchanged (196 ± 63 ml, p = NS) but stroke volume (52 ± 29 ml, p < 0.05) and ejection fraction (26 ± 10%, p = 0.08) decreased. LV end-diastolic (52 ± 22 ml, p < 0.001), end-systolic (17 ± 8 ml, p < 0.001), and stroke volumes (35 ± 20 ml, p < 0.001) decreased, whereas ejection fraction (65 ± 15%, p = NS) and cardiac index remained unchanged (2.17 ± 0.93 L/min/m2, p = NS). The ratio of RV/LV stroke volume at rest (1.21 ± 1.06) increased with exercise (1.74 ± 1.13, p = 0.09). Patients with PPH have increased RV volume and reduced systolic function with reduced LV volume and normal systolic function. During exercise, RV failure manifested by reduced ejection fraction and worsening tricuspid regurgitation limits cardiac output. LV volume is further reduced due to underfilling rather than direct RV compression.