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Editorial |

Growing Evidence Linking OSA During Rapid Eye Movement Sleep to Systemic Hypertension

Babak Mokhlesi, MD, FCCP; Jason R. Carter, PhD
Author and Funding Information

FINANCIAL/NONFINANCIAL DISCLOSURES: The authors have reported to CHEST the following: B. M. is supported by National Institutes of Health [Grant R01HL119161] and has served as a consultant to Philips Respironics and has received research support from Philips Respironics; he has also received honorarium from Zephyr Medical Technologies and has served on the advisory board of Itamar Medical. J. R. C. is supported by the National Heart, Lung, and Blood Institute (Grant HL-122919-01). Both authors are supported by the Merck Investigator Studies Program.

aDepartment of Medicine, Section of Pulmonary and Critical Care, Sleep Disorders Center, University of Chicago, Chicago, IL

bSleep, Metabolism and Health Center, University of Chicago, Chicago, IL

cDepartment of Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, MI

CORRESPONDENCE TO: Babak Mokhlesi, MD, FCCP, Section of Pulmonary and Critical Medicine, Department of Medicine, University of Chicago, 5841 S Maryland Ave, MC6076/Room M630, Chicago, IL 60637


Copyright 2016, American College of Chest Physicians. All Rights Reserved.


Chest. 2016;150(3):475-477. doi:10.1016/j.chest.2016.03.047
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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. 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,, 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. 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. 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.,

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