Obstructive Sleep Apnea An Emerging Risk Factor for Atherosclerosis
Obstructive Sleep Apnea An Emerging Risk Factor for Atherosclerosis
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DOI：
10.1378/chest.10-2223
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发表时间：
2011-08-01
期刊：
影响因子：
9.6
通讯作者：
Lorenzi-Filho, Geraldo
中科院分区：
文献类型：
--
作者：
Drager, Luciano F.;Polotsky, Vsevolod Y.;Lorenzi-Filho, Geraldo
阻塞性睡眠呼吸暂停（OSA）与心血管疾病（包括心肌梗死和中风）的死亡独立相关。心肌梗死和中风是动脉粥样硬化的并发症;因此，在过去的十年中，研究人员试图解开OSA和动脉粥样硬化之间的关系。阻塞性睡眠呼吸暂停可通过加重关键的致动脉粥样硬化危险因素而加速动脉粥样硬化。例如，阻塞性睡眠呼吸暂停综合症是公认的高血压的次要原因，并可能导致胰岛素抵抗、糖尿病和血脂异常。此外，动物模型中的临床数据和实验证据表明，OSA可具有直接促动脉粥样硬化作用，诱导全身炎症、氧化应激、血管平滑肌细胞活化、粘附分子表达增加、单核细胞/淋巴细胞活化、巨噬细胞中脂质负荷增加、脂质过氧化和内皮功能障碍。几项横断面研究一致表明，阻塞性睡眠呼吸暂停与过早动脉粥样硬化的替代标志物独立相关，其中大多数在颈动脉床。此外，正如随机临床试验所示，持续气道正压通气治疗OSA可减轻颈动脉粥样硬化。本文综述了阻塞性睡眠呼吸暂停在动脉粥样硬化形成中的作用，并强调了这一重要研究领域的未来前景。胸部2011; 140（2）：534-542
Obstructive sleep apnea (OSA) is independently associated with death from cardiovascular diseases, including myocardial infarction and stroke. Myocardial infarction and stroke are complications of atherosclerosis; therefore, over the last decade investigators have tried to unravel relationships between OSA and atherosclerosis. OSA may accelerate atherosclerosis by exacerbating key atherogenic risk factors. For instance, OSA is a recognized secondary cause of hypertension and may contribute to insulin resistance, diabetes, and dyslipidemia. In addition, clinical data and experimental evidence in animal models suggest that OSA can have direct proatherogenic effects inducing systemic inflammation, oxidative stress, vascular smooth cell activation, increased adhesion molecule expression, monocyte/lymphocyte activation, increased lipid loading in macrophages, lipid peroxidation, and endothelial dysfunction. Several cross-sectional studies have shown consistently that OSA is independently associated with surrogate markers of premature atherosclerosis, most of them in the carotid bed. Moreover, OSA treatment with continuous positive airway pressure may attenuate carotid atherosclerosis, as has been shown in a randomized clinical trial. This review provides an update on the role of OSA in atherogenesis and highlights future perspectives in this important research area. CHEST 2011; 140(2):534-542