Abstract
The aims of this study were to explore the effect of high-altitude (HA) exposure on the incidence, determinants, and impacts of right ventricular dyssynchrony (RVD). In our study, 108 healthy young men were enrolled, and physiological and echocardiographic variables were recorded at both sea level and 4,100 m. By using two-dimensional speckle-tracking echocardiography, RVD was evaluated by calculating the R–R interval-corrected standard deviation of the time-to-peak systolic strain for the four mid-basal RV segments (RVSD4) and defined by RVSD4 > 18.7 ms. After HA exposure, RVSD4 was significantly increased, and the incidence of RVD was approximately 32.4%. Subjects with RVD showed lower oxygen saturation (SaO2) and RV global longitudinal strain and higher systolic pulmonary artery pressure than those without RVD. Moreover, myocardial acceleration during isovolumic contraction was increased in all subjects and those without RVD, but not in those with RVD. Multivariate logistic regression revealed that SaO2 is an independent determinant of RVD at HA (odds ratio: 0.72, 95% CI: 0.56–0.92; P = 0.009). However, the mean pulmonary artery pressure was linearly correlated with the magnitude of RVD in the presence of Notch. No changes were found in RV fractional area change, tricuspid annular motion, or tricuspid s’ velocity between subjects with and without RVD. Collectively, we demonstrated for the first time that HA exposure could induce RVD in healthy subjects, which may be mainly attributed to the decline in SaO2 as well as RV overload; the incidence of RVD was associated with reduced RV regional function and blunted myocardial acceleration.
Highlights
Traveling to a high altitude (HA) for sports, work, or recreational purposes is becoming popular but poses some physiological challenges to the cardiovascular system, leading to hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, and increases in pulmonary artery pressure (PAP) (Xu and Jing, 2009)
It has been proposed that right ventricular (RV) systolic function is well preserved and that its diastolic function is sometimes altered under acute HA hypoxia (Naeije, 2010), exposure to HA at 8,000 m or acute hypoxia results in RV dilatation, an increased RV Tei index, and a decreased RV free wall longitudinal systolic strain (Kurdziel et al, 2017; Netzer et al, 2017)
SaO2 is an independent determinant of right ventricular dyssynchrony (RVD) at HA; (3) mean PAP (mPAP) is linearly correlated with the magnitude of RVD in the presence of Notch; and (4) the presence and magnitude of RVD at HA result in reduced RV global longitudinal strain (RVGLS) and blunted tricuspid IVA
Summary
Traveling to a high altitude (HA) for sports, work, or recreational purposes is becoming popular but poses some physiological challenges to the cardiovascular system, leading to hypoxic pulmonary vasoconstriction, pulmonary vascular remodeling, and increases in pulmonary artery pressure (PAP) (Xu and Jing, 2009). It has been proposed that RV systolic function is well preserved and that its diastolic function is sometimes altered under acute HA hypoxia (Naeije, 2010), exposure to HA at 8,000 m or acute hypoxia results in RV dilatation, an increased RV Tei index, and a decreased RV free wall longitudinal systolic strain (Kurdziel et al, 2017; Netzer et al, 2017). Significant decreases in tricuspid annular plane systolic excursion (TAPSE) and RV global longitudinal strain (RVGLS) have been found in healthy lowlanders after ascending to an HA of 5,050 m, suggesting that RV longitudinal systolic function is impaired (Stembridge et al, 2014). Elevated PAP and HA hypoxia may potentially threaten RV performance, the effects of acute HA exposure on RV global or regional functions are controversial and inconclusive
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