Background and goal of study: Acute hypoxia, as it occurs with high altitude exposure or during acute respiratory distress syndrome (ARDS), causes hypoxic pulmonary vasoconstriction and consequently pulmonary hypertension. The resulting increase in right ventricular afterload has been suggested to impair left ventricular (LV) diastolic function by shifting the ventricular septum towards the LV. This study evaluated physiologic variables and comprehensive echocardiographic indices of LV diastolic function following rapid ascent (<22 hours) to 4559 m in healthy volunteers.
Methods: Fifty subjects ascended in groups of 10 from 1130 to 4559 m within 22 hours including an overnight stay at 3611m. All participants underwent 2D echocardiography during baseline examinations at low altitude (424 m, Salzburg, Austria) and after 7, 20 and 44 hours at high altitude. Heart rate (HR), mean arterial pressure (MAP), and systolic pulmonary artery pressure (sPAP) were assessed and comprehensive volumetric-, spectral Doppler-, tissue Doppler- as well as speckle tracking derived strain-indices for LV diastolic function were obtained.  
Results and Discussion: HR (HRlow: 64.2±11.2 vs. HRhigh: 79.1±14.2 min-1, p<.001), MAP (MAPlow: 88.9±5.9 vs. MAPhigh: 91.7±7.0 mmHg, p=.002); and sPAP (sPAPlow: 24.4±3.8 vs. sPAPhigh: 38.5±8.2 mmHg, p<.001) increased significantly following ascent and remained elevated at high altitude. Left atrial (LA) reservoir Strain (ε) (εlow: 44.6±9.4 vs. εhigh: 49.6±12.6%, p<.05) increased significantly following ascent, remained elevated at high altitude and did not correlate with changes in physiologic variables. Spectral-Doppler derived index for LV filling (E/Alow: 1.7±0.5 vs. E/Ahigh: 1.4±0.5, p<.001) changed significantly due to a significant increase in late diastolic filling (Alow: 43.3±9.0 vs. Ahigh: 53.1±12.2 cm·sec-1). Changes in E/A correlated with changes in HR (r=.46, p<.001) but did not correlate with changes in sPAP or MAP. E/E’ as an estimate of LV filling pressure and LV diastolic function did not change. 
Conclusion: Rapid ascent of healthy individuals to 4559 m increased sPAP but did not impair LV diastolic function, possibly due to increasing global LA performance. As functional LA reserve might be required for maintaining diastolic integrity at high altitude, individuals with pre-existing LA or LV disease may be at increased risk for left heart failure and high altitude pulmonary edema following rapid ascent to high altitude.

07 / Rapid ascent to high altitude (4559 m) does not impair left ventricular diastolic function in healthy volunteers