Unveiling Orthostatic Hypotension and Its Hemodynamic Mechanisms in Precapillary Pulmonary Hypertension

Purpose Investigate the prevalence, subtypes (initial, delayed recovery, classic), and hemodynamic mechanisms of orthostatic hypotension in patients with pulmonary arterial hypertension or chronic thromboembolic pulmonary hypertension. Methods Orthostatic hypotension was assessed using a 10-min active standing maneuver from supine baseline, with heart rate (HR; electrocardiogram) and arterial pressure (volume clamp finger photoplethysmography) measured beat-by-beat. Stroke volume was estimated from the arterial pressure waveform, while cardiac output and total peripheral resistance were calculated. Results Among 60 patients, 31 (52%) had orthostatic. Patients with and without orthostatic did not differ in sex, age, resting pulmonary hemodynamics, resting systemic arterial pressure, medications, functional class, and aerobic exercise capacity (all P > 0.050). Heart rate, stroke volume, cardiac output, and total peripheral resistance responses (% change from supine baseline) were not different between groups with and without initial orthostatic hypotension (P > 0.05). However, stroke volume decay was greater in the group with than without delayed recovery (-31 ± 21 vs. -19 ± 14%; P = 0.033). Additionally, a compensatory increase in total peripheral resistance was blunted in the group with classic orthostatic hypotension than without orthostatic hypotension (-6 ± 21 vs. 7 ± 15%; P = 0.023). Conclusion Orthostatic hypotension is common in patients with pulmonary arterial hypertension or chronic thromboembolic pulmonary hypertension but is not associated with specific clinical characteristics. Initial orthostatic hypotension lacks a clear hemodynamic cause, whereas delayed recovery and classic orthostatic hypotension are linked to impaired stroke volume and total peripheral resistance responses to standing, respectively.