Key result
High-altitude trekking to 5085 m increased pulmonary artery systolic pressure from 13.1 to 26.6 mmHg (P<0.001) and enhanced left ventricular contractility and untwisting efficiency.
Why the study?
While cardiac responses to acute hypoxic exposure have been thoroughly investigated, the effects of high-altitude trekking on biventricular mechanics, including LV subendocardial and subepicardial function, remained uninvestigated.
Does high-altitude trekking alter biventricular mechanics and function in healthy subjects?
Observational (n=20)
Does high-altitude trekking alter biventricular mechanics and function in healthy subjects?
Absolute Event Rate: 26.6% vs 13.1%
p-value: p=<0.001
High-altitude trekking induces major changes in LV mechanics, including increased contractility and untwisting efficiency, which play a key role in preserving cardiac function despite increased pulmonary pressures.
NEW FINDINGS: What is the central question of this study? This study is the first to investigate the effects of high-altitude trekking on biventricular mechanics, including measurements of left ventricular subendocardial and subepicardial function. What is the main finding and its importance? We provide new evidence that an increased contractility and untwisting efficiency, a key element of diastolic function, probably plays a key role in preservation of cardiac function during high-altitude trekking. Persistent increased loading conditions during several weeks at high altitude might have a key role in the appearance of left or right ventricular dysfunction. ABSTRACT: Cardiac responses to acute hypoxic exposure have been thoroughly investigated. We analysed the effects of high-altitude trekking (i.e. prolonged hypoxic exposure) on biventricular function, including the evaluation of subendocardial and subepicardial function in the left ventricle (LV). Resting evaluations of LV and right ventricular (RV) function and mechanics were assessed by speckle tracking echocardiography on 20 subjects at sea level and at high altitude (5085 m, after a 10 day ascent). Pulmonary artery systolic pressure was increased at high altitude (sea level, 13.1 ± 5.9 mmHg; high altitude, 26.6 ± 10.8 mmHg; P < 0.001). Left ventricular volumes were decreased, whereas RV volumes were increased at high altitude. Alterations in pulmonary artery systolic pressure and cardiac volumes were correlated with hypoxaemia. We observed neither RV nor LV systolic dysfunction, including analysis of LV subendocardial and subepicardial function. Left ventricular systolic strain rates were enhanced at high altitude. Transmitral and transtricuspid diastolic filling ratios were decreased at high altitude. Diastolic apical rotational rate, untwisting rate and untwisting rate/peak twist ratio (i.e. untwisting efficiency) were enhanced at high altitude. We observed no echocardiographic signs of LV and RV pathological dysfunction at rest at high altitude. In contrast, our data highlighted major changes in the LV mechanics, with an increased LV contractility and a higher untwisting efficiency at high altitude. Biventricular interaction, alterations in loading conditions and an increase in plasma catecholamine concentration might partly explain these modifications. Thus, we demonstrated that LV mechanics (i.e. increased strain rates and untwisting efficiency) have a key role in preservation of cardiac function during high-altitude trekking.
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Maufrais et al. (2019) conducted an observational in High-altitude exposure (n=20). High-altitude trekking (5085 m) vs. Sea level baseline was evaluated on Pulmonary artery systolic pressure (p=<0.001). High-altitude trekking to 5085 m increased pulmonary artery systolic pressure from 13.1 to 26.6 mmHg (P<0.001) and enhanced left ventricular contractility and untwisting efficiency.
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