Drager Luciano F, Polotsky Vsevolod Y, O'Donnell Christopher P, Cravo Sergio L, Lorenzi-Filho Geraldo, Machado Benedito H
Hypertension Unit, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil; Hypertension Unit, Renal Division, University of São Paulo Medical School, São Paulo, Brazil;
Division of Pulmonary and Critical Care Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland;
Am J Physiol Heart Circ Physiol. 2015 Oct;309(7):H1101-11. doi: 10.1152/ajpheart.00094.2015. Epub 2015 Jul 31.
Obstructive sleep apnea (OSA) is known to be independently associated with several cardiovascular diseases including hypertension, myocardial infarction, and stroke. To determine how OSA can increase cardiovascular risk, animal models have been developed to explore the underlying mechanisms and the cellular and end-organ targets of the predominant pathophysiological disturbance in OSA-intermittent hypoxia. Despite several limitations in translating data from animal models to the clinical arena, significant progress has been made in our understanding of how OSA confers increased cardiovascular risk. It is clear now that the hypoxic stress associated with OSA can elicit a broad spectrum of pathological systemic events including sympathetic activation, systemic inflammation, impaired glucose and lipid metabolism, and endothelial dysfunction, among others. This review provides an update of the basic, clinical, and translational advances in our understanding of the metabolic dysfunction and cardiovascular consequences of OSA and highlights the most recent findings and perspectives in the field.
阻塞性睡眠呼吸暂停(OSA)已知与包括高血压、心肌梗死和中风在内的多种心血管疾病独立相关。为了确定OSA如何增加心血管风险,已开发动物模型来探索潜在机制以及OSA间歇性缺氧中主要病理生理紊乱的细胞和终末器官靶点。尽管将动物模型数据转化到临床领域存在一些局限性,但我们在理解OSA如何增加心血管风险方面已取得重大进展。现在很清楚,与OSA相关的缺氧应激可引发广泛的病理性全身事件,包括交感神经激活、全身炎症、糖脂代谢受损和内皮功能障碍等。本综述提供了我们对OSA代谢功能障碍和心血管后果理解的基础、临床和转化进展的最新情况,并突出了该领域的最新发现和观点。