Pulmonary Vascular: Original Research
The Effect of a 2-Day Stay at High Altitude (2,500 m) on Right Ventricular Afterload and Oxygen Delivery in Patients With Pulmonary Vascular Disease: A Randomized Controlled Crossover Trial
Julian Müller, Simon R. Schneider, Meret Bauer, et al
Chest 2026 Available online 3 July 2026
https://doi.org/10.1016/j.chest.2026.06.032
Background
High altitude may adversely affect patients with pulmonary vascular disease (PVD), but acute cardiopulmonary effects remain unclear.
Research Question
How does 2-day high-altitude exposure affect pulmonary hemodynamics and oxygen delivery in patients with PVD defined as pulmonary arterial or chronic thromboembolic pulmonary hypertension?
Study Design and Methods
In this randomized, controlled crossover trial, stable, low-risk patients with PVD without resting hypoxemia at 470 m were transported by cable car to 2,500 m, where they stayed for 2 days. Systolic pulmonary arterial pressure (sPAP), total pulmonary resistance (TPR), right ventricular (RV) arterial coupling, pulmonary arterial elastance (EA), and pulmonary arterial compliance (PAC) were assessed by echocardiography, whereas oxygen content was measured in arterial blood gases.
Results
Twenty-seven patients with PVD (44% female; mean [SD] age, 61 [14] years) were included. Altitude exposure was associated with an increase in sPAP of 18 mm Hg (40%; 95% CI, 9-28 mm Hg; P < .001) and TPR of 2.8 Wood units (WU; 32%; 95% CI, 0.7-4.9 WU; P = .007). RV arterial coupling, assessed by tricuspid regurgitation velocity (TAPSE) to sPAP ratio, decreased from a mean (SD) of 0.55 (0.04) mm/mm Hg to 0.38 (0.04) mm/mm Hg (–31%; 95% CI, –0.27 to –0.07 mm/mm Hg; P < .001). EA increased by 0.2 mm Hg/mL (33%; 95% CI, 0.07-0.33 mm Hg/mL; P < .001) and PAC decreased by 1.6 mL/mm Hg (38%; –2.7 to –0.6 mL/mm Hg; P = .002). Although oxygen content was lower at high altitude, oxygen delivery was similar at both altitudes.



Interpretation
Our results show that 2-day exposure to 2,500 m in stable, low-risk patients with PVD increases RV resistive and pulsatile afterload and decreases TAPSE to sPAP ratio, indicating reduced RV arterial coupling. Despite attenuated cardiac adaptation, overall function seems to be sufficient to maintain oxygen delivery and to compensate partially for hypoxemia.
Clinical Trial Registration
ClinicalTrials.gov; No.: NCT05107700; URL: www.clinicaltrials.gov