Abstract:Pulmonary hypertension (PH) has been shown to be associated with regional inhomogeneity (or dyssynchrony) of right ventricular (RV) contraction. Right ventricular dyssynchrony is an independent predictor of decreased survival in advanced PH, but has also been reported in patients with only mildly elevated pulmonary artery pressure (PAP). The mechanisms of RV dyssynchrony in PH remain uncertain. Our aim was to evaluate RV regional function in healthy subjects during acute hypoxia and during exercise. Seventeen … Show more
“…Not surprisingly, the absence of RV overload as a contributor to the incidence of RVD may be explained by the fact that the elevated PAP during the first few days at HA was moderate. Consistently, recent results also showed that acute hypoxia for several minutes, but not exercise, could induce regional inhomogeneity (or dyssynchrony) of RV contraction, although both acute hypoxia and exercise led to a comparable increase in RV afterload, suggesting that acute hypoxia was the main determinant of RVD but not RV afterload (Pezzuto et al, 2018). Hypobaric hypoxia is the main characteristic of the HA environment but may result in the reduction in cardiac phosphocreatine (PCr)/ATP in healthy volunteers (Holloway et al, 2011).…”
Section: Determinants Of Ha Exposure-induced Rvdmentioning
confidence: 55%
“…In patients with pulmonary hypertension (PH), the presence of RVD is always associated with the symptomatology, functional state, exercise performance, and clinical outcomes (Murata et al, 2017;Rehman et al, 2018). Recent evidence also showed that RVD occurred during hypoxia but not during exercise, suggesting the combined contributions of mechanical (RV afterload) and systemic (hypoxia) factors (Pezzuto et al, 2018). Based on these reasons, we hypothesize that RVD is present under acute HA exposure and can be explained by HA hypoxia or increased RV afterload.…”
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 intervalcorrected 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 (SaO 2) 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 SaO 2 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 SaO 2 as well as RV overload; the incidence of RVD was associated with reduced RV regional function and blunted myocardial acceleration.
“…Not surprisingly, the absence of RV overload as a contributor to the incidence of RVD may be explained by the fact that the elevated PAP during the first few days at HA was moderate. Consistently, recent results also showed that acute hypoxia for several minutes, but not exercise, could induce regional inhomogeneity (or dyssynchrony) of RV contraction, although both acute hypoxia and exercise led to a comparable increase in RV afterload, suggesting that acute hypoxia was the main determinant of RVD but not RV afterload (Pezzuto et al, 2018). Hypobaric hypoxia is the main characteristic of the HA environment but may result in the reduction in cardiac phosphocreatine (PCr)/ATP in healthy volunteers (Holloway et al, 2011).…”
Section: Determinants Of Ha Exposure-induced Rvdmentioning
confidence: 55%
“…In patients with pulmonary hypertension (PH), the presence of RVD is always associated with the symptomatology, functional state, exercise performance, and clinical outcomes (Murata et al, 2017;Rehman et al, 2018). Recent evidence also showed that RVD occurred during hypoxia but not during exercise, suggesting the combined contributions of mechanical (RV afterload) and systemic (hypoxia) factors (Pezzuto et al, 2018). Based on these reasons, we hypothesize that RVD is present under acute HA exposure and can be explained by HA hypoxia or increased RV afterload.…”
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 intervalcorrected 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 (SaO 2) 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 SaO 2 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 SaO 2 as well as RV overload; the incidence of RVD was associated with reduced RV regional function and blunted myocardial acceleration.
“…International Ltd, Southam, UK), producing a fraction of inspired oxygen (F iO 2 ) of 12%. This degree of hypoxia corresponds to an altitude of 4500 m and has been shown to be well tolerated with minimal changes in arterial P CO 2 (Pezzuto et al, 2018).…”
Regional heterogeneity in timing of right ventricular (RV) contraction (RV dyssynchrony; RVD) occurs when pulmonary artery systolic pressure (PASP) is increased during acute hypoxia. Interestingly, RVD is not observed during exercise, a stimulus that increases both PASP and venous return. Therefore, we hypothesised that RVD in healthy humans is sensitive to changes in venous return, and examined whether (i) increasing venous return in acute hypoxia lowers RVD and (ii) if RVD is further exaggerated in sustained hypoxia, given increased PASP is accompanied by decreased ventricular filling at high altitude. RVD, PASP and right ventricular end-diastolic area (RVEDA) were assessed using transthoracic two-dimensional and speckle-tracking echocardiography during acute normobaric hypoxia (F iO 2 = 0.12) and sustained exposure (5-10 days) to hypobaric hypoxia (3800 m). Venous return was augmented with lower body positive pressure at sea level (LBPP; +10 mmHg) and saline infusion at high altitude. PASP was increased in acute hypoxia (20 ± 6 vs. 28 ± 7,
“…At high altitude, in resting conditions, signs of altered diastolic but preserved or enhanced systolic RV function have been described in chronic [61] or acute hypoxic conditions [62,63]. RV seems thus to tolerate hypoxic conditions.…”
Section: Right Ventriclementioning
confidence: 99%
“…RV seems thus to tolerate hypoxic conditions. However, a recent study showed inhomogeneous RV contraction in hypoxia but not during exercise, suggesting that hypoxic stress is not trivial [63]. How much this could account for altered RV maximal outflow remains unknown as studies on right ventricular function during hypoxic exercise are sorely lacking [64].…”
Pulmonary circulation has long been known to have specific proprieties of recruitment and distention to keep the hemodynamic pressure low even when facing very high blood flow. Aerobic exercise especially at high intensity has the particularity to increase considerably the cardiac output. The ability of the pulmonary circulation to face high blood flow with maintaining low pressures is considered as the pulmonary vascular reserve. Furthermore, high pulmonary vascular reserve has been shown to be characterized by low pulmonary vascular resistance, high pulmonary vascular distensibility, high pulmonary capillary volume, and high lung diffusing capacity allowing for lower ventilation at a same metabolic cost. The pulmonary vascular reserve thus reflects the capacity of the pulmonary circulation, including the capillary network, to adapt to high exercise levels. Interestingly, a high pulmonary vascular reserve is an advantage as it is associated with a superior aerobic exercise capacity (VO 2 max). This observation strongly suggests that exercise capacity is modulated by the functional state of the pulmonary circulation. However, why or when pulmonary vascular reserve may be related to a higher aerobic exercise capacity remains incompletely understood. The present chapter will discuss the role of each component of the pulmonary vascular reserve during exercise and develop the factors able to influence the pulmonary vascular reserve in heathy individuals.
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