Toraldo D M, DE Nuccio F, DE Benedetto M, Scoditti E
"V. Fazzi" Hospital Rehabilitation Dept, Respiratory Care Unit, ASL Lecce, Italy;
Laboratory of Human Anatomy and Neuroscience, Dept. of Biological and Environmental Sciences and Technologies, University of Salento, Lecce, Italy;
Acta Otorhinolaryngol Ital. 2015 Apr;35(2):69-74.
Obstructive sleep apnoea syndrome (OSAS) is associated with severe cerebro-cardiovascular morbidity and mortality. It is an independent risk factor for atherosclerosis, arterial thrombosis and metabolic syndrome, and recently has been associated with an increased incidence of cancer and death. A causal link between OSAS and atherosclerosis has been partially established. Recent research on atherosclerosis in OSAS has focused on thrombotic tendency and blood viscosity, providing new insight into disease mechanisms. Hypoxia is a critical pathophysiological element in OSAS that leads to intensive sympathetic activity, in association with inflammation, oxidative stress and procoagulant activity. Hypoxia and the induction of oxidative stress can simultaneously represent an underlying mechanism in the pathogenesis of cancer development and progression. This mini-review will discuss the latest findings on the association and potential relationship between OSA and pathological vascular sequelae.
阻塞性睡眠呼吸暂停综合征(OSAS)与严重的心脑血管发病率和死亡率相关。它是动脉粥样硬化、动脉血栓形成和代谢综合征的独立危险因素,最近还与癌症发病率和死亡率的增加有关。OSAS与动脉粥样硬化之间的因果关系已部分确立。最近关于OSAS中动脉粥样硬化的研究集中在血栓形成倾向和血液粘度上,为疾病机制提供了新的见解。缺氧是OSAS中的一个关键病理生理因素,它会导致强烈的交感神经活动,并伴有炎症、氧化应激和促凝活性。缺氧和氧化应激的诱导可能同时是癌症发生和发展的潜在发病机制。本综述将讨论OSA与病理性血管后遗症之间关联和潜在关系的最新发现。