Abstract

High altitude (HA) exposure has been considered as a cardiac stress and might impair ventricular diastolic function. Atrial contraction is involved in ventricular passive filling, however the atrial performance to HA exposure is poorly understood. This study aimed to evaluate the effect of short-term HA exposure on bi-atrial function. Physiological and 2D-echocardiographic data were collected in 82 healthy men at sea level (SL, 400 m) and 4100 m after an ascent within 7 days. Atrial function was measured using volumetric and speckle-tracking analyses during reservoir, conduit and contractile phases of cardiac cycle. Following HA exposure, significant decreases of reservoir and conduit function indexes were observed in bi-atria, whereas decreases of contractile function indexes were observed in right atrium (RA), estimated via RA active emptying fraction (SL 41.7 ± 13.9% vs. HA 35.4 ± 12.2%, p = 0.001), strain during the contractile phase [SL 13.5 (11.4, 17.8) % vs. HA 12.3 (9.3, 15.9) %, p = 0.003], and peak strain rate during the contractile phase [SL − 1.76 (− 2.24, − 1.48) s−1 vs. HA − 1.57 (− 2.01, − 1.23) s−1, p = 0.002], but not in left atrium (LA). In conclusion, short-term HA exposure of healthy individuals impairs bi-atrial performance, mostly observed in RA. Especially, atrial contractile function decreases in RA rather than LA, which seems not to compensate for decreased ventricular filling after HA exposure. Our findings may provide a novel evidence for right-sided heart dysfunction to HA exposure.

Highlights

  • An increasing number of lowlanders visit high altitude (HA) for work or leisure

  • We aimed to investigate the effect of short-term HA exposure on bi-atrial function using speckle-tracking echocardiography (STE) and identify the related factors

  • For right ventricular (RV) parameters, significantly decreased EDA index while unchanged ESA index, and decreased RV fractional area change (FAC) were recorded at HA

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Summary

Introduction

HA exposure challenges cardiac function to meet the tissue metabolic demand for oxygen under hypoxic conditions [1]. It has been well established that the cardiac response to HA exposure presents preserved ventricular systolic function, impaired ventricular diastolic function, and elevated pulmonary arterial pressure [2]. Atrial contraction is the final component during ventricular diastole and contributes approximately 15% to 20% of stroke volume as a compensatory mechanism [3,4,5]. Evidence is lacking regarding atrial response to HA exposure. It takes several days to acclimate to HA conditions with cardiac output returning to normal through a higher heart rate and lower stroke volume [8].

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