AUTHOR=Bian Shi-Zhu , Zhang Chen , Rao Rong-Sheng , Ding Xiao-Han , Huang Lan TITLE=Systemic Blood Predictors of Elevated Pulmonary Artery Pressure Assessed by Non-invasive Echocardiography After Acute Exposure to High Altitude: A Prospective Cohort Study JOURNAL=Frontiers in Cardiovascular Medicine VOLUME=Volume 9 - 2022 YEAR=2022 URL=https://www.frontiersin.org/journals/cardiovascular-medicine/articles/10.3389/fcvm.2022.866093 DOI=10.3389/fcvm.2022.866093 ISSN=2297-055X ABSTRACT=Background and Aim Elevated pulmonary artery pressure (ePAP) in response to high-altitude hypoxia is a critical physiopathologic factor in 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. Methods A total of 154 participants were transported to high altitude (3700 m) from sea level within two hours. 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. Results The mPAP increased significantly from sea level to high altitude (19.79 ± 6.53 to 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 altitude were independently associated with ePAP. Conclusions The 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 altitude may contribute to the development of ePAP.