Lavie Lena
Lloyd Rigler Sleep Apnea Research Laboratory, Unit of Anatomy and Cell Biology, The Ruth and Bruce Rappaport Faculty of Medicine, Technion-Israel Institute of Technology, Haifa, Israel.
Front Biosci (Elite Ed). 2012 Jan 1;4(4):1391-403. doi: 10.2741/469.
Obstructive sleep apnea syndrome (OSA) is a breathing disorder in sleep. In recent years, this entity has emerged as a major public health problem due to its high prevalence and the profound impact on patients' health and quality of life. A large body of evidence identified OSA as an independent risk factor for cardiovascular morbidity and mortality. Also an association was demonstrated with additional cardiovascular risk factors. This has led to intensive research on the mechanisms involved. The main characteristics of OSA are the recurrent pauses in respiration which result in intermittent hypoxia (IH) and hypercapnia, accompanied by decreased blood oxygen saturation and arousals during sleep. The associations of OSA with cardiovascular morbidities rely on the cyclic nature of the IH, and implicate the apnea related multiple cycles of hypoxia/reoxygenation with increased production of reactive oxygen species (ROS), thereby initiating inflammation. This review summarizes the main findings in oxidative stress/inflammation in the context of OSA and its consequences to possible cardiovascular outcomes through the development of endothelial dysfunction and early clinical signs of atherosclerosis.
阻塞性睡眠呼吸暂停综合征（OSA）是一种睡眠呼吸障碍。近年来，由于其高患病率以及对患者健康和生活质量的深远影响，这一病症已成为一个主要的公共卫生问题。大量证据表明OSA是心血管疾病发病和死亡的独立危险因素。此外，还证实了它与其他心血管危险因素有关联。这引发了对其中涉及机制的深入研究。OSA的主要特征是呼吸反复暂停，导致间歇性缺氧（IH）和高碳酸血症，同时伴有睡眠期间血氧饱和度下降和觉醒。OSA与心血管疾病的关联依赖于IH的周期性本质，并涉及与呼吸暂停相关的多个缺氧/复氧循环，以及活性氧（ROS）生成增加，从而引发炎症。本综述总结了在OSA背景下氧化应激/炎症的主要发现，以及通过内皮功能障碍的发展和动脉粥样硬化的早期临床症状，其对可能的心血管结局的影响。
