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炎症会加速阻塞性睡眠呼吸暂停综合征(OSAS)中的动脉粥样硬化进程。

Inflammation accelerates atherosclerotic processes in obstructive sleep apnea syndrome (OSAS).

机构信息

Division of Cardiology, Geneva University Hospital, Geneva, Switzerland.

出版信息

Sleep Breath. 2010 Sep;14(3):261-9. doi: 10.1007/s11325-010-0338-3. Epub 2010 Mar 3.

DOI:10.1007/s11325-010-0338-3
PMID:20198512
Abstract

Obstructive sleep apnea syndrome (OSAS) is an often underestimated sleep disorder that has been associated with cardiovascular disease. OSAS is characterized by cycles of apnea and/or hypopnea during sleep caused by the collapse of the upper airways. Intermittent hypoxia deriving from the cycles of apnea/arousals (to retrieve the ventilation) plays a pivotal role in the pathogenesis of the disease. Obesity is the most frequent predisposing condition of OSAS. Recent evidence suggests that OSAS could be considered as a pro-atherosclerotic disease, independently of visceral fat amount. Oxidative stress, cardiovascular inflammation, endothelial dysfunction, and metabolic abnormalities in OSAS could accelerate atherogenesis. The present review is focused on the possible pathophysiological mediators which could favor atherosclerosis in OSAS.

摘要

阻塞性睡眠呼吸暂停综合征(OSAS)是一种常被低估的睡眠障碍,与心血管疾病有关。OSAS的特征是上呼吸道塌陷导致睡眠期间出现呼吸暂停和/或呼吸不足的循环。呼吸暂停/觉醒(以恢复通气)引起的间歇性缺氧在疾病发病机制中起着关键作用。肥胖是 OSAS 最常见的易患条件。最近的证据表明,OSAS 可被视为动脉粥样硬化疾病,与内脏脂肪量无关。OSAS 中的氧化应激、心血管炎症、内皮功能障碍和代谢异常可加速动脉粥样硬化的形成。本综述重点讨论可能有利于 OSAS 中动脉粥样硬化形成的病理生理介质。

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