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Impairment of left atrial mechanics does not contribute to the reduction in stroke volume after active ascent to 4559 m
Author(s) -
Sareban Mahdi,
Perz Tabea,
Macholz Franziska,
Reich Bernhard,
Schmidt Peter,
Fried Sebastian,
Mairbäurl Heimo,
Berger Marc M.,
Niebauer Josef
Publication year - 2019
Publication title -
scandinavian journal of medicine and science in sports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.575
H-Index - 115
eISSN - 1600-0838
pISSN - 0905-7188
DOI - 10.1111/sms.13325
Subject(s) - preload , cardiology , medicine , stroke volume , effects of high altitude on humans , diastole , stroke (engine) , blood pressure , heart rate , hemodynamics , anatomy , mechanical engineering , engineering
Hypoxia challenges left ventricular (LV) function due to reduced energy supply. Conflicting results exist whether high‐altitude exposure impairs LV diastolic function and thus contributes to the high altitude‐induced increase in systolic pulmonary artery pressure (sPAP) and reduction in stroke volume (SV). This study aimed to assess LV diastolic function, LV end‐diastolic pressure (LVEDP), and LA mechanics using comprehensive echocardiographic imaging in healthy volunteers at 4559 m. Fifty subjects performed rapid (<20 hours) and active ascent from 1130 m to 4559 m (high). All participants underwent echocardiography during baseline examination at 424 m (low) as well as 7, 20 and 44 hours after arrival at high altitude. Heart rate (HR), sPAP, and comprehensive volumetric‐ and Doppler‐ as well as speckle tracking‐derived LA strain parameters were obtained to assess LV diastolic function, LA mechanics, and LVEDP in a multiparametric approach. Data for final analyses were available in 46 subjects. HR (low: 64 ± 11 vs high: 79 ± 14 beats/min, P < 0.001) and sPAP (low: 24.4 ± 3.8 vs high: 38.5 ± 8.2 mm Hg, P < 0.001) increased following ascent and remained elevated at high altitude. Stroke volume (low: 64.5 ± 15.0 vs high: 58.1 ± 16.4 mL, P < 0.001) and EDV decreased following ascent and remained decreased at high altitude due to decreased LV passive filling volume, whereas LA mechanics were preserved. There was no case of LV diastolic dysfunction or increased LVEDP estimates. In summary, this study shows that rapid and active ascent of healthy individuals to 4559 m impairs passive filling and SV of the LV. These alterations were not related to changes in LV and LA mechanics.