Division of Respiratory Medicine, Department of Medicine, Queen Mary Hospital, The University of Hong Kong, Hong Kong.
Respirology. 2012 Feb;17(2):223-36. doi: 10.1111/j.1440-1843.2011.02081.x.
OSA is increasingly recognized as a major health problem in developed countries. Obesity is the most common risk factor in OSA and hence, the prevalence of OSA is undoubtedly rising given the epidemic of obesity. Recent data also suggest that OSA is highly associated with the metabolic syndrome, and it is postulated that OSA contributes to cardiometabolic dysfunction, and subsequently vasculopathy. Current evidence regarding the magnitude of impact on ultimate cardiovascular morbidity or mortality attributable to OSA-induced metabolic dysregulation is scarce. Given the known pathophysiological triggers of intermittent hypoxia and sleep fragmentation in OSA, the potential mechanisms of OSA-obesity-metabolic syndrome interaction involve sympathetic activation, oxidative stress, inflammation and neurohumoral changes. There is accumulating evidence from human and animal/cell models of intermittent hypoxia to map out these mechanistic pathways. In spite of support for an independent role of OSA in the contribution towards metabolic dysfunction, a healthy diet and appropriate lifestyle modifications towards better control of metabolic function are equally important as CPAP treatment in the holistic management of OSA.
阻塞性睡眠呼吸暂停（OSA）在发达国家日益被视为一个主要的健康问题。肥胖是 OSA 最常见的危险因素，因此，鉴于肥胖的流行，OSA 的患病率无疑正在上升。最近的数据还表明，OSA 与代谢综合征高度相关，据推测，OSA 导致心脏代谢功能障碍，进而导致血管病变。目前关于 OSA 引起的代谢失调对心血管发病率或死亡率的影响程度的证据还很缺乏。鉴于 OSA 中间歇性低氧和睡眠片段化的已知病理生理触发因素，OSA-肥胖-代谢综合征相互作用的潜在机制涉及交感神经激活、氧化应激、炎症和神经体液变化。间歇性低氧的人类和动物/细胞模型的研究提供了越来越多的证据来阐明这些机制途径。尽管间歇性低氧在代谢功能障碍中的作用是独立的，但健康饮食和适当的生活方式改变以更好地控制代谢功能与 CPAP 治疗一样，在 OSA 的整体治疗中同样重要。
