Department of Internal Medicine, Excellence Cluster Cardio-Pulmonary Institute (CPI), Member of the German Center for Lung Research (DZL), Justus Liebig University of Giessen, Aulweg 130, 35392 Giessen, Germany.
Department of Mountain and Sleep Medicine and Pulmonary Hypertension, National Center of Cardiology and Internal Medicine, Bishkek 720040, Kyrgyzstan.
Int J Environ Res Public Health. 2021 Feb 10;18(4):1692. doi: 10.3390/ijerph18041692.
Alveolar hypoxia is the most prominent feature of high altitude environment with well-known consequences for the cardio-pulmonary system, including development of pulmonary hypertension. Pulmonary hypertension due to an exaggerated hypoxic pulmonary vasoconstriction contributes to high altitude pulmonary edema (HAPE), a life-threatening disorder, occurring at high altitudes in non-acclimatized healthy individuals. Despite a strong physiologic rationale for using vasodilators for prevention and treatment of HAPE, no systematic studies of their efficacy have been conducted to date. Calcium-channel blockers are currently recommended for drug prophylaxis in high-risk individuals with a clear history of recurrent HAPE based on the extensive clinical experience with nifedipine in HAPE prevention in susceptible individuals. Chronic exposure to hypoxia induces pulmonary vascular remodeling and development of pulmonary hypertension, which places an increased pressure load on the right ventricle leading to right heart failure. Further, pulmonary hypertension along with excessive erythrocytosis may complicate chronic mountain sickness, another high altitude maladaptation disorder. Importantly, other causes than hypoxia may potentially underlie and/or contribute to pulmonary hypertension at high altitude, such as chronic heart and lung diseases, thrombotic or embolic diseases. Extensive clinical experience with drugs in patients with pulmonary arterial hypertension suggests their potential for treatment of high altitude pulmonary hypertension. Small studies have demonstrated their efficacy in reducing pulmonary artery pressure in high altitude residents. However, no drugs have been approved to date for the therapy of chronic high altitude pulmonary hypertension. This work provides a literature review on the role of pulmonary hypertension in the pathogenesis of acute and chronic high altitude maladaptation disorders and summarizes current knowledge regarding potential treatment options.
肺泡缺氧是高原环境中最显著的特征，对心肺系统有明显的影响，包括肺动脉高压的发展。由于缺氧性肺血管收缩过度而导致的肺动脉高压导致了高原肺水肿（HAPE），这是一种危及生命的疾病，发生在未经适应的健康个体的高海拔地区。尽管使用血管扩张剂预防和治疗 HAPE 具有很强的生理学依据，但迄今为止，尚未对其疗效进行系统研究。钙通道阻滞剂目前被推荐用于有反复 HAPE 病史的高危个体的药物预防，这是基于硝苯地平在易感个体中预防 HAPE 的广泛临床经验。慢性缺氧会导致肺血管重塑和肺动脉高压的发展，这会增加右心室的压力负荷，导致右心衰竭。此外，肺动脉高压和过度红细胞增多症可能会使慢性高山病（另一种高原适应不良疾病）复杂化。重要的是，除了缺氧之外，其他原因也可能导致高原地区的肺动脉高压，例如慢性心脏病和肺部疾病、血栓形成或栓塞性疾病。在肺动脉高压患者中使用药物的广泛临床经验表明，它们可能具有治疗高原性肺动脉高压的潜力。一些小型研究已经证明了它们在降低高原居民肺动脉压力方面的疗效。然而，迄今为止，没有药物被批准用于治疗慢性高原性肺动脉高压。本研究对肺动脉高压在急性和慢性高原适应不良疾病发病机制中的作用进行了文献综述，并总结了目前关于潜在治疗选择的知识。
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