Levy Patrick, Tamisier Renaud, Arnaud Claire, Monneret Denis, Baguet Jean Philippe, Stanke-Labesque Francoise, Dematteis Maurice, Godin-Ribuot Diane, Ribuot Christophe, Pepin Jean-Louis
INSERM U 1042, Hypoxia PathoPhysiology Laboratory, Joseph Fourier University, Grenoble, France.
Front Biosci (Elite Ed). 2012 Jan 1;4(6):2007-21. doi: 10.2741/521.
Sleep dramatically influences cardiovascular regulation. Changes in sleep duration or quality as seen in sleep disorders may prevent blood pressure to fall during sleep as expected in human physiology. This supports the increased prevalence of hypertension and drug-resistant hypertension in those with sleep loss. Other cardiovascular outcomes i.e. coronary lesions seem to be associated with sleep duration. Systemic inflammation, oxidative stress and endothelial dysfunction seem to be associated with both sleep loss and sleep disorders. The most critical example is Obstructive Sleep Apnea (OSA). Sympathetic activation, oxidative stress and systemic inflammation are the main intermediary mechanisms associated with sleep apnea and intermittent hypoxia. There are now convincing data regarding the associations between hypertension, arrhythmias, stroke, coronary heart disease, increased cardiovascular mortality and OSA. There are also data in OSA and in animal models supporting the link between sleep apnea and atherosclerosis and dysmetabolism. Whether treating sleep apnea enables the reversal of chronic cardiovascular and metabolic consequences of OSA, remains to be studied in adequately designed studies, particularly in comparison with usual treatment strategies.
睡眠对心血管调节有着显著影响。睡眠障碍中所见的睡眠时间或质量变化可能会阻止血压在睡眠期间如人体生理学所预期的那样下降。这支持了睡眠不足人群中高血压和难治性高血压患病率增加的现象。其他心血管结局，即冠状动脉病变，似乎与睡眠时间有关。全身炎症、氧化应激和内皮功能障碍似乎与睡眠不足和睡眠障碍都有关。最关键的例子是阻塞性睡眠呼吸暂停（OSA）。交感神经激活、氧化应激和全身炎症是与睡眠呼吸暂停和间歇性缺氧相关的主要中介机制。现在有令人信服的数据表明高血压、心律失常、中风、冠心病、心血管死亡率增加与OSA之间存在关联。在OSA和动物模型中也有数据支持睡眠呼吸暂停与动脉粥样硬化和代谢紊乱之间的联系。治疗睡眠呼吸暂停是否能逆转OSA的慢性心血管和代谢后果，仍有待在设计充分的研究中进行探讨，特别是与常规治疗策略进行比较。
