Sleep Disorders Centre and Pulmonary Division, University Hospital of Zurich, Raemistrasse 100, 8091 Zurich, Switzerland.
Nat Rev Cardiol. 2010 Dec;7(12):677-85. doi: 10.1038/nrcardio.2010.145.
Obstructive sleep apnea (OSA) is characterized by repetitive apnea-hypopnea cycles during sleep, which are associated with oxygen desaturation and sleep disruption. Up to 30% of the adult population in Western countries are thought to be affected by asymptomatic OSA and approximately 2-4% by symptomatic OSA (also known as obstructive sleep apnea syndrome, or OSAS). Controlled trials have demonstrated that OSAS causes hypertension and prospective epidemiological studies have indicated that OSAS might be an independent risk factor for stroke and myocardial ischemia. Three biological mechanisms are thought to underpin the association of OSA with endothelial dysfunction and arterial disease: intermittent hypoxia leading to increased oxidative stress, systemic inflammation, and sympathetic activity; intrathoracic pressure changes leading to excessive mechanical stress on the heart and large artery walls; and arousal-induced reflex sympathetic activation with resultant repetitive blood-pressure rises. More clinical interventional trials are needed to determine the magnitude of the effect OSA has on cardiovascular damage and to enable a comparison with conventional vascular risk factors.
阻塞性睡眠呼吸暂停（OSA）的特征是睡眠期间反复出现呼吸暂停-低通气循环，与氧饱和度下降和睡眠中断有关。据认为，多达 30%的西方国家成年人受到无症状 OSA 的影响，约 2-4%受到有症状 OSA（也称为阻塞性睡眠呼吸暂停综合征，或 OSAS）的影响。对照试验已经证明 OSAS 会导致高血压，前瞻性流行病学研究表明 OSAS 可能是中风和心肌缺血的独立危险因素。有三种生物学机制被认为是 OSA 与内皮功能障碍和动脉疾病相关的基础：间歇性低氧导致氧化应激增加、全身炎症和交感神经活性增加；胸腔内压力变化导致心脏和大动脉壁过度机械应力；以及觉醒引起的反射性交感神经激活导致反复血压升高。需要更多的临床干预试验来确定 OSA 对心血管损害的影响程度，并与传统的血管危险因素进行比较。
