Effects of high-dose supplemental oxygen therapy on pulmonary haemodynamics at 3250 m in high-altitude residents at risk for pulmonary hypertension.

QUESTION ADDRESSED BY THE STUDY: Hypoxic pulmonary vasoconstriction increases systolic pulmonary artery pressure (sPAP) and may contribute to high-altitude pulmonary hypertension (HAPH). While supplemental oxygen therapy (SOT) lowers sPAP during acute hypoxic exposure, its haemodynamic effects in permanent high-altitude residents remain unclear. In particular, the relative contribution of fixed vascular remodelling to chronically elevated sPAP is uncertain.

PARTICIPANTS AND

METHODS

In this open-label, non-randomised, sequential interventional trial, Kyrgyz highlanders living >2500 m with tricuspid regurgitation velocity >2.8 m/s underwent echocardiography under ambient air and after >15 min of high-dose SOT (FiO₂≈0.95, 10 L/min) at 3250 m.

RESULTS

48 participants (56% females, mean±SD age 53±12 years) completed the study per-protocol. SOT reduced sPAP from 45±11 to 31±5 mm Hg, cardiac output (CO) from 5.1±1.2 to 4.3±1.4 L/min and total pulmonary resistance (TPR) from 9.2±2.7 to 7.5±1.5 WU (all p<0.001). In an exploratory subanalysis, a larger sPAP decrease was associated with higher baseline sPAP and younger age.

ANSWER TO THE QUESTION: High-dose SOT acutely lowers sPAP in high-altitude residents at risk for HAPH. The decrease in sPAP is driven by reductions in both CO and TPR. The decline in TPR indicates a largely reversible hypoxic-vasoconstrictor component, whereas the contribution of fixed vascular remodelling to elevated PAP appears minimal. These findings underscore the physiological potential of short-term high-dose oxygen to reduce right ventricular afterload and improve pulmonary haemodynamics in this high-altitude population at risk for HAPH.

TRIAL REGISTRATION NUMBER: NCT06489756.