Increased loop gain and upper airway collapsibility among smoking patients with obstructive sleep apnoea

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^-1 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^-1 higher AHI, an 8.8% eupnoea higher arousal threshold, a 4.0% eupnoea lower ventilation at the eupnoeic drive (V_passive), a 6.7% eupnoea lower ventilation at arousal threshold (V_active), 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_active, a 4.6% eupnoea lower median ventilation observed at minimal ventilatory drive (V_min), 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_active 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.