Resting evaluations of LV function and mechanics by 2D-strain echocardiography were performed on eleven subjects at sea level (SLPRE), 3h±2h after helicopter transport to altitude (D0), at day 2 (D2), day 4 (D4) and day 6 (D6) at 4350 m and 5h±2h after return to sea level (SLPOST).
Subjects experienced acute mountain sickness (AMS) during the first days and systolic pulmonary arterial hypertension during the six days at high altitude. LV global systolic function, LV strains and LV synchrony were unchanged at high altitude. Peak twist was increased at 4350 m (p<0.05) and was normalized at SLPOST. Early filling decreased at high altitude with a nadir at D2 (SLPRE: 78±13cm.s-1; D2: 66±11cm.s-1, p<0.05) and was normalized at SLPOST. LV filling pressures index was decreased at high altitude with the minimum value obtained at D2 (SLPRE: 4.7±1.2; D2: 3.4±0.6, p<0.05) and remained reduced at SLPOST.
Untwisting was delayed at high altitude (Percentage of untwist during isovolumic relaxation time at SLPREvs D2: 39±31 vs 18±17%, respectively, p=0.08) and was normalized at SLPOST.
High-altitude exposure impaired diastolic function with the greatest effect observed at D2, concomitantly with the occurrence of AMS. The early filling impairments resulted from a decrease in LV filling pressure and a delayed LV untwisting, without changes in LV relaxation. During systole, a progressive increase in LV twist was observed from D0 to D6, probably acting as a compensatory mechanism to maintain ejection fraction and global cardiac performance during high-altitude hypoxia.
The author hereby declares no conflict of interest