BACKGROUND: 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.
METHODS: 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.
RESULTS: 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.
CONCLUSION: 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.