The effect of a two-day stay at high altitude (2500 m) on right ventricular afterload and oxygen delivery in patients with pulmonary vascular disease A randomized controlled crossover trial.

Abstract

High altitude may adversely affect patients with pulmonary vascular disease (PVD), but acute cardiopulmonary effects remain unclear. How does two-day high-altitude exposure affect pulmonary hemodynamics and oxygen delivery in patients with PVD defined as pulmonary arterial or chronic thromboembolic pulmonary hypertension? In this randomized, controlled crossover trial, stable, low-risk patients with PVD without resting hypoxemia at 470 m were transported by cable car to 2500 m, where they stayed for two days. Systolic pulmonary arterial pressure (sPAP), total pulmonary resistance (TPR), right ventricular (RV) -arterial coupling, pulmonary arterial elastance (E_A) and compliance (PAC) were assessed by echocardiography, while oxygen content was measured in arterial blood gases. Twenty-seven patients with PVD (44% women, 61±14 years) were included. Altitude exposure was associated with an increase in sPAP of 18 mmHg (40%, 95%CI: 9 to 28 mmHg, p<0.001) and TPR of 2.8 WU (32%, 0.7 to 4.9 WU, p=0.007). RV-arterial coupling, assessed by TAPSE/sPAP ratio, decreased from 0.55±0.04 to 0.38±0.04 mm/mmHg (-31%, -0.27 to -0.07 mm/mmHg, p<0.001). E_A increased by 0.2 mmHg/mL (33%, 0.07 to 0.33 mmHg/mL, p<0.001) and PAC decreased by 1.6 mL/mmHg (38%, -2.7 to -0.6 mL/mmHg, p=0.002). Although oxygen content was lower at high altitude, oxygen delivery was similar at both altitudes. Two-day exposure to 2500 m in stable, low-risk patients with PVD increases RV resistive and pulsatile afterload and decreases TAPSE/sPAP, indicating reduced RV-arterial coupling. Despite attenuated cardiac adaptation, overall function appears sufficient to maintain oxygen delivery and partially compensate for hypoxemia. Clinicaltrials.gov (NCT05107700).