Growing Evidence Linking OSA During Rapid Eye Movement Sleep to Systemic Hypertension.
Growing Evidence Linking OSA During Rapid Eye Movement Sleep to Systemic Hypertension.
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越来越多的证据表明快速眼动睡眠期间的 OSA 与全身性高血压有关。
DOI：
10.1016/j.chest.2016.03.047
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发表时间：
2016
期刊：
影响因子：
9.6
通讯作者：
Carter,JasonR
中科院分区：
文献类型：
--
作者：
Mokhlesi,Babak;Carter,JasonR
大约60年前，芝加哥大学的两位研究人员纳撒尼尔·克莱特曼（Nathaniel Kleitman）和尤金·阿塞林斯基（Eugene Aserinsky）发现了快速眼动（REM）睡眠，这是一个睡眠阶段，约占健康成年人总睡眠时间的四分之一。[1]迄今为止，对快速眼动睡眠的研究主要集中在记忆、情感和认知方面。然而，在过去的几年里，人们越来越有兴趣了解睡眠的两个主要阶段（REM和非REM睡眠）中OSA的后果。尽管REM睡眠期间的OSA与白天过度嗜睡或生活质量降低无关，但重要的是要认识到REM睡眠期间存在重要的自主神经系统和心肺变化，这支持了REM OSA可能比非REM OSA具有更差的心脏代谢后果的观点。[4]从病理生理学的角度来看，胆碱能介导的舌下神经抑制导致颏舌肌张力的抑制，从而大大增加了REM睡眠期间上呼吸道塌陷的倾向。这种情况反过来又会导致REM主导型OSA或在REM睡眠期间变得更严重的OSA。此外，与非REM睡眠相比，REM睡眠与更大的交感神经活动，更低的迷走神经张力和更多的心血管不稳定性有关。快速眼动睡眠的特征还在于低氧和高碳酸血症的呼吸驱动的减少。这些生理现象可以部分解释为什么REM睡眠期间的阻塞性呼吸暂停和呼吸不足持续时间较长，与显着更大的氧去饱和度，并导致更大的血压波动相比，阻塞性事件在非REM睡眠。最近对威斯康星州睡眠队列研究的分析表明，快速眼动睡眠期的阻塞性睡眠呼吸暂停与普遍的和偶发的全身性高血压以及偶发的夜间血压非下降独立相关。7，8在这个基于人群的队列中，REM呼吸暂停低通气指数（AHI）$15事件/h具有临床显著的阈值效应。有趣的是，非REM AHI与高血压无关。从代谢的角度来看，REM AHI升高与2型糖尿病患者的血糖控制不良和基于社区的睡眠心脏健康研究中的胰岛素抵抗独立相关。[10]尽管REM OSA和心脏代谢健康之间存在这些重要的联系，但还需要更多的证据。
It was nearly six decades ago when two University of Chicago investigators, Nathaniel Kleitman and Eugene Aserinsky, discovered rapid eye movement (REM) sleep, a stage of sleep that accounts for approximately one-quarter of total sleep time in healthy adults. 1 To date, the preponderance of research on REM sleep has focused on memory, affect, and cognition. In the last few years, however, there has been a growing interest in understanding the consequences of OSA during the two main stages of sleep (REM and non-REM sleep). Although OSA during REM sleep has not been associated with excessive daytime sleepiness or reduced quality of life, 2, 3 it is important to recognize that there are important autonomic nervous system and cardiorespiratory changes during REM sleep supporting the notion that REM OSA may have worse cardiometabolic consequences than non-REM OSA. 4 From a pathophysiologic point of view, cholinergic-mediated inhibition of the hypoglossal nerve results in the suppression of genioglossus muscle tone and thus substantially increases propensity for upper airway collapse during REM sleep. This scenario in turn can lead to either REM-predominant OSA or simply OSA that becomes more severe during REM sleep. Moreover, REM sleep is associated with greater sympathetic activity, lower vagal tone, and more cardiovascular instability compared with non-REM sleep. 5 REM sleep is also characterized by a reduction in the hypoxic and hypercapnic ventilatory drive. These physiologic phenomena may in part explain why obstructive apneas and hypopneas during REM sleep are longer in duration, associated with significantly greater oxygen desaturation, and lead to greater fluctuations in BP compared with obstructive events in non-REM sleep. 5, 6Recent analysis of the Wisconsin Sleep Cohort has shown that OSA during REM sleep is independently associated with prevalent and incident systemic hypertension as well as with incident nondipping of nocturnal BP. 7, 8 In this population-based cohort, the REM apnea-hypopnea index (AHI) $15 events/h had a clinically significant threshold effect. Interestingly, the non-REM AHI was not associated with hypertension. From a metabolic standpoint, elevated REM AHI has been independently associated with worse glycemic control in patients with type 2 diabetes 9 and with insulin resistance in the community-based Sleep Heart Health Study. 10 Despite these important associations between REM OSA and cardiometabolic health, additional evidence is needed.