Hang Liang-Wen, Finnsson Eysteinn, Ágústsson Jón S, Sands Scott A, Cheng Wan-Ju
College of Medicine, China Medical University, Taichung, Taiwan.
Sleep Medicine Center, Department of Pulmonary and Critical Care Medicine, China Medical University Hospital, Taichung, Taiwan.
ERJ Open Res. 2025 Aug 4;11(4). doi: 10.1183/23120541.01283-2024. eCollection 2025 Jul.
Smoking is a known risk factor for obstructive sleep apnoea (OSA). However, the specific pathological mechanism linking smoking to OSA remains unclear. This study aims to explore the endotypic traits of OSA among current and former smokers.
We prospectively collected polysomnographic data from 980 patients with an apnoea-hypopnoea index (AHI) ≥15 h from a single clinical sleep centre. Smoking status was determined through self-reported questionnaires completed prior to polysomnography. Endotypic traits (including arousal threshold, collapsibility, loop gain, circulatory delay, ventilatory response to arousal and upper airway compensation) were estimated using polysomnographic signals. Adjusted multivariate linear regression analysis was conducted to investigate the association between smoking and endotypic traits.
Compared with nonsmokers, current smokers were associated with a 7.6 h higher AHI, an 8.8% eupnoea higher arousal threshold, a 4.0% eupnoea lower ventilation at the eupnoeic drive (V), a 6.7% eupnoea lower ventilation at arousal threshold (V), a 0.03 higher loop gain, and a 0.64 lower delay during non-rapid eye movement sleep. During rapid eye movement sleep, current smokers showed an 11.1% eupnoea higher arousal threshold, a 6.5% eupnoea lower V, a 4.6% eupnoea lower median ventilation observed at minimal ventilatory drive (V), a 0.05 higher loop gain, and a 0.57 lower delay. Former smokers exhibited a 5.7% eupnoea lower upper airway compensation and a 6.7% eupnoea lower V during rapid eye movement sleep compared with nonsmokers. Smoking amount and duration since quitting were not linearly associated with AHI or endotypic traits.
Smoking is associated with increased upper airway collapsibility and loop gain among patients with OSA. These effects may be reversible following smoking cessation.
吸烟是阻塞性睡眠呼吸暂停（OSA）已知的风险因素。然而，吸烟与OSA之间的具体病理机制仍不清楚。本研究旨在探讨当前吸烟者和既往吸烟者中OSA的内型特征。
我们前瞻性地收集了来自单一临床睡眠中心的980例呼吸暂停低通气指数（AHI）≥15次/小时患者的多导睡眠图数据。吸烟状况通过多导睡眠图检查前完成的自我报告问卷确定。使用多导睡眠图信号估计内型特征（包括觉醒阈值、可塌陷性、环路增益、循环延迟、对觉醒的通气反应和上气道代偿）。进行调整后的多变量线性回归分析以研究吸烟与内型特征之间的关联。
与不吸烟者相比，当前吸烟者的AHI高7.6次/小时，在平静呼吸时觉醒阈值高8.8%，在平静呼吸驱动（V）时通气低4.0%，在觉醒阈值时通气低6.7%，环路增益高0.03，在非快速眼动睡眠期间延迟低0.64。在快速眼动睡眠期间，当前吸烟者的觉醒阈值高11.1%，V低6.5%，在最小通气驱动时观察到的中位通气低4.6%，环路增益高0.05，延迟低0.57。与不吸烟者相比，既往吸烟者在快速眼动睡眠期间上气道代偿低5.7%，V低6.7%。吸烟量和戒烟后的持续时间与AHI或内型特征无线性关联。
吸烟与OSA患者上气道可塌陷性增加和环路增益增加有关。戒烟后这些影响可能是可逆的。
