Effect of Obstructive Sleep Apnea on the Sleep Architecture in Cirrhosis
Effect of Obstructive Sleep Apnea on the Sleep Architecture in Cirrhosis
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DOI：
10.5664/jcsm.2488
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发表时间：
2013-01-01
影响因子：
4.3
通讯作者：
Bajaj, Jasmohan S.
中科院分区：
文献类型：
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作者：
Kappus, Matthew R.;Leszczyszyn, David J.;Bajaj, Jasmohan S.
研究目的：肝硬化的睡眠障碍被认为是由于肝性脑病（HE）。尚未评估肝硬化、既往HE和阻塞性睡眠呼吸暂停（OSA）之间的相互作用。我们的目的是评估额外的影响，肝硬化和不事先HE的睡眠结构和感知睡眠障碍的OSA patients.Methods：OSA患者进行多导睡眠图（PSG）在肝移植中心的病例对照审查进行。合并肝硬化的OSA患者（有/无既往HE）与不合并肝硬化的OSA患者年龄匹配1：1。睡眠质量，白天嗜睡，睡眠质量和睡眠结构进行了比较groups.Results：49 OSA肝硬化患者（年龄57.4 +/- 8.3岁，模型为终末期肝病（MELD）8.3 +/- 5.4，51%的HCV，20%的前HE）的年龄匹配1：1的OSA患者无肝硬化。阻塞性睡眠呼吸暂停低通气指数、觉醒指数、睡眠效率、日间嗜睡以及嗜睡对日常活动的影响在阻塞性睡眠呼吸暂停伴/不伴肝硬化患者之间相似。睡眠结构，包括%慢波睡眠（SWS），也没有组间差异。MELD与早期（N1）时间呈正相关（r = 0.4，p = 0.03）。与其他患者相比，所有既往HE患者（n = 10）的结构均向早期非恢复性睡眠转变（较高的% [N2]期[66 vs 52%，p = 0.005]，较低的% SWS [0 vs 29%，p = 0.02]，较低的REM潜伏期[95 vs 151分钟，p = 0.04]）。酒精性病因与N1/N2睡眠的潜伏期较高，但没有其他影响睡眠architecture.Conclusions：阻塞性睡眠呼吸暂停可以有助于睡眠障碍肝硬化，应考虑在肝硬化的睡眠障碍的鉴别。先前的HE可能与OSA协同恶化睡眠结构。
Study Objectives: Sleep disturbances in cirrhosis are assumed to be due to hepatic encephalopathy (HE). The interaction between cirrhosis, prior HE, and obstructive sleep apnea (OSA) has not been evaluated. We aimed to evaluate the additional effect of cirrhosis with and without prior HE on the sleep architecture and perceived sleep disturbances of OSA patients.Methods: A case-control review of OSA patients who underwent polysomnography (PSG) in a liver-transplant center was performed. OSA patients with cirrhosis (with/without prior HE) were age-matched 1:1 with OSA patients without cirrhosis. Sleep quality, daytime sleepiness, sleep quality, and sleep architecture was compared between groups.Results: Forty-nine OSA cirrhotic patients (age 57.4 +/- 8.3 years, model for end-stage liver disease (MELD) 8.3 +/- 5.4, 51% HCV, 20% prior HE) were age-matched 1:1 to OSA patients without cirrhosis. Apnea-hypopnea index, arousal index, sleep efficiency, daytime sleepiness, and effect of sleepiness on daily activities were similar between OSA patients with/without cirrhosis. Sleep architecture, including % slow wave sleep (SWS), was also not different between the groups. MELD was positively correlated with time in early (N1) stage (r = 0.4, p = 0.03). All prior HE patients (n = 10) had a shift of the architecture towards early, non-restorative sleep (higher % [N2] stage [66 vs 52%, p = 0.005], lower % SWS [0 vs 29%, p = 0.02], lower REM latency [95 vs 151 minutes, p = 0.04]) compared to the rest. Alcoholic etiology was associated with higher latency to N1/N2 sleep, but no other effect on sleep architecture was seen.Conclusions: OSA can contribute to sleep disturbance in cirrhosis and should be considered in the differential of sleep disturbances in cirrhosis. Prior HE may synergize with OSA in worsening the sleep architecture.