Systemic Blood Predictors of Elevated Pulmonary Artery Pressure Assessed by Non-invasive Echocardiography After Acute Exposure to High Altitude: A Prospective Cohort Study

Abstract

AimElevated pulmonary artery pressure (ePAP) in response to high-altitude hypoxia is a critical physiopathological factor in the hypoxic adaptation that may lead to high-altitude pulmonary edema in the acute phase or high-altitude pulmonary hypertension in the long term. However, the sea-level predictors of risk factors for altitude-induced ePAP have not been examined. Thus, we aimed to identify the baseline systemic blood predictors of ePAP after acute high-altitude exposure.Materials and MethodsA total of 154 participants were transported to a high altitude 3,700 m from sea level within 2 h. Echocardiography examinations were performed to assess the mean pulmonary artery pressure (mPAP) and hemodynamics at both altitudes. All the individuals underwent blood tests to determine the concentrations of vascular regulatory factors. Univariate and adjusted logistic regression analyses were performed to identify the independent predictors of ePAP and factors related to ePAP.ResultsThe mPAP increased significantly from sea level to high altitude (19.79 ± 6.53–27.16 ± 7.16 mmHg, p < 0.05). Increased levels of endothelin (ET-1), Ang (1–7), Ang II, and bradykinin were found after high-altitude exposure, while the levels of nitric oxide (NO), prostaglandin E2 (PEG2), and serotonin decreased sharply (all p-values < 0.05). At high altitude, 52.6% of the subjects exhibited ePAP, and the mPAP was closely correlated with the baseline Ang II level (r = 0.170, p = 0.036) and follow-up levels of NO (r = −0.209, p = 0.009), Ang II (r = 0.246, p = 0.002), and Ang (1–7) (r = −0.222, p = 0.006) and the left atrial inner diameter (LAD, r = 0.270, p < 0.001). Both the baseline and follow-up NO and Ang II levels were significantly different between the ePAP and non-ePAP groups. Finally, we identified the baseline Ang II and NO concentrations as two independent predictors of ePAP (p < 0.05). We also found that two vascular regulatory factors with inverse roles, namely, Ang (1–7) and Ang II, at high altitudes were independently associated with ePAP. Additionally, ET-1, NO, PEG2, and LAD were associated with ePAP.ConclusionThe baseline concentrations of Ang II and NO at sea level are two independent predictors of ePAP after acute high-altitude exposure. Furthermore, Ang (1-7) and Ang II combined with ET-1, NO, PEG2, and LAD at high altitudes may contribute to the development of ePAP.

Hyperbaric oxygen preconditioning for prevention of acute high-altitude diseases: Fact or fiction?

“…At high altitude, the body reacts to hypoxia by hyperventilating, which is known as the hypoxic ventilatory response. In hypoxic conditions, the reduced supply of nitric oxide (NO) and prostaglandin E2 ( Bian et al, 2022 ) can cause excessive rise in pulmonary artery pressure (PAP). Increased PAP prior to the development of edema is the key pathophysiological factor of HAPE ( Mulchrone et al, 2020 ).…”

Effect of ubiquinol on cardiorespiratory fitness during high-altitude acclimatization and de-acclimatization in healthy adults: the Shigatse CARdiorespiratory fitness study design

“…Arterial oxygenation reduction is attributed to decreased partial pressure inspiratory oxygen and altered coupling of convectional and diffusional oxygen transport systems (7). Meanwhile, the elevated pulmonary vascular resistance is explained through hypoxia-induced pulmonary vasoconstriction and increased cardiac afterload in the right ventricle (8,9). Although multiple reports have illustrated that the impairment of cardiorespiratory fitness is the main course of decreased physical performance capacity (10)(11)(12), there is far less information regarding the characteristics of cardiorespiratory fitness in the process of highaltitude acclimatization and de-acclimatization.…”