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阻塞性睡眠呼吸暂停诱发心血管并发症的临床视角。

Clinical perspective of obstructive sleep apnea-induced cardiovascular complications.

作者信息

Jain Vivek

机构信息

Division of Pulmonary and Critical Care Medicine, GW Medical Faculty Associates, The George Washington University, Washington, District of Columbia 20037, USA.

出版信息

Antioxid Redox Signal. 2007 Jun;9(6):701-10. doi: 10.1089/ars.2007.1558.

DOI:10.1089/ars.2007.1558
PMID:17511585
Abstract

Obstructive sleep apnea (OSA) syndrome is a highly prevalent disorder characterized by recurrent upper airway collapse during sleep, and associated with repetitive episodes of transient oxygen desaturation during sleep. It disrupts normal ventilation and sleep architecture, and is typically associated with excessive daytime sleepiness, snoring, and witnessed apneas. Besides being associated with neurocognitive impairment, mood and behavioral effects, and increased risk for work-related and traffic accidents, OSA has also been implicated in the pathogenesis of various cardiovascular diseases, including systemic hypertension, coronary artery disease, congestive heart failure, pulmonary hypertension, stroke, and cardiac arrhythmias. The mechanisms by which OSA affects the cardiovascular system may involve mechanical effects on intrathoracic pressure, increased sympathetic activation, intermittent hypoxia, and endothelial dysfunction. Therapy with continuous positive airway pressure (CPAP) has been demonstrated to improve cardiopulmonary hemodynamics in patients with OSA and may reverse the endothelial cell dysfunction.

摘要

阻塞性睡眠呼吸暂停(OSA)综合征是一种高度流行的疾病,其特征是睡眠期间上呼吸道反复塌陷,并伴有睡眠期间短暂性氧饱和度下降的反复发作。它会扰乱正常的通气和睡眠结构,通常与白天过度嗜睡、打鼾和观察到的呼吸暂停有关。除了与神经认知障碍、情绪和行为影响以及工作相关和交通事故风险增加有关外,OSA还与各种心血管疾病的发病机制有关,包括系统性高血压、冠状动脉疾病、充血性心力衰竭、肺动脉高压、中风和心律失常。OSA影响心血管系统的机制可能涉及对胸内压的机械作用、交感神经激活增加、间歇性缺氧和内皮功能障碍。持续气道正压通气(CPAP)治疗已被证明可改善OSA患者的心肺血流动力学,并可能逆转内皮细胞功能障碍。

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