Echocardiographic assessment of cardiac performance in response to high altitude and development of subclinical pulmonary edema in healthy climbers.

Data regarding the effect of high altitude on heart function are sparse and conflicting. We aimed to assess the right and left ventricular responses to altitude-induced hypoxia and the occurrence of subclinical pulmonary edema.Echocardiography was performed according to protocol on 14 subjects participating in an expedition in Nepal, at 3 altitude levels: Montreal (30 m), Namche Bazaar (3450 m), and Chukkung (4730 m). Systematic lung ultrasound was performed to detect ultrasound lung comets.Pulmonary artery systolic pressure increased in all subjects between Montreal and Chukkung (mean 27.4 ± 5.4 mm Hg vs. 39.3 ± 7.7 mm Hg; P < 0.001). Right ventricular (RV) myocardial performance index (MPI) increased significantly (0.32 ± 0.08 at 30 m vs. 0.41 ± 0.10 at 4730 m; P = 0.046). A trend toward deteriorated RV free wall longitudinal strain was observed between Montreal and Chukkung (-25.9 [5.3%] vs. -21.9 [6.4%]; P = 0.092). The left ventricular early diastolic inflow velocity/atrial mitral inflow velocity and early diastolic inflow velocity/mean of the maximal early diastolic mitral annulus tissue doppler velocities ratios remained unchanged. At 4730 m, ultrasound lung comets were seen in all subjects except 1. None had clinical criteria for high-altitude pulmonary edema (HAPE). All altered parameters normalized after return to sea level.Subclinical HAPE is frequent in healthy lowlander climbers. This is the first study to document a trend towards decreased RV free wall strain and MPI increment at high altitude. Whether rising RV MPI is a physiologic adaptive mechanism to hypoxia or a pathologic response identifying HAPE-susceptible subjects needs further study.