O053 Obstructive sleep apnea is a distinct physiological phenotype in individuals with comorbid insomnia and sleep apnea (COMISA)

INTRODUCTION: Obstructive sleep apnea (OSA) pathophysiology varies among individuals, though the influence of comorbid insomnia on this pathophysiology is unknown. We examined whether upper airway collapsibility, muscle compensation, loop gain, and the arousal threshold differ between OSA patients with and without comorbid insomnia disorder. METHODS: We noninvasively determined the four traits using the ventilatory flow pattern captured from standard polysomnography in 34 comorbid insomnia and obstructive sleep apnea (COMISA) and 34 OSA patients without insomnia (OSA-only). Participants had mild-to-severe OSA ( AHI: 25.8±2.0 events/h) and were matched according to age (50.2±1.5 years) sex (42M:26F), and body mass index (29.3±0.6 kg/m²). RESULTS: COMISA patients had significantly lower respiratory arousal thresholds (128.9 [118.1–137.1] vs. 147.7 [132.3–165.0] %Veupnea, U=261, p<.001), less collapsible upper airways (i.e., higher VPASSIVE: 88.2 [85.5–94.6] vs. 72.9 [64.7–79.2] %Veupnea, U=1081, p<.001) and more stable ventilatory control (i.e., lower loop gain: 0.51 [0.44–0.56] vs. 0.58 [0.49–0.70], U=402, p=.03) relative to OSA-only controls. Muscle compensation did not significantly differ between groups. DISCUSSION: OSA patients with comorbid insomnia appear to have OSA driven more by heightened nocturnal arousability than by the contribution of anatomical factors, compared to OSA patients without insomnia. Heightened nocturnal arousability as the driver of apneic events in COMISA suggests the conditioned arousal perpetuating insomnia may also increase risk or severity of OSA. Further research should investigate whether targeting increased arousal propensity (e.g., through CBT-I) provides therapeutic benefit to individuals with COMISA.