Obstructive Sleep Apnea Is a Distinct Physiological Endotype in Individuals with Comorbid Insomnia and Sleep Apnea (COMISA)

With up to 40% of individuals with either insomnia or obstructive sleep apnea (OSA) demonstrating clinically significant symptoms of the other disorder, the high degree of comorbidity amongst the two most common sleep disorders suggests a bi-directional relationship and/or shared underpinnings. Whilst the presence of insomnia disorder is believed to influence the underlying pathophysiology of OSA, this influence is yet to be examined directly. To investigate whether the four OSA endotypes (upper airway collapsibility, muscle compensation, loop gain, and the arousal threshold) are different in OSA patients with and without comorbid insomnia disorder. Using the ventilatory flow pattern captured from routine polysomnography, the four OSA endotypes were measured in 34 OSA patients who met diagnostic criteria for insomnia disorder (COMISA) and 34 OSA patients without insomnia (OSA-only). Patients demonstrated mild-to-severe OSA (AHI: 25.8±2.0 events/h) and were individually matched according to age (50.2±1.5 years) sex (42M:26F), and body mass index (29.3±0.6 kg/m2). Compared to OSA patients without comorbid insomnia, COMISA patients demonstrated significantly lower respiratory arousal thresholds (128.9 [118.1-137.1] vs. 147.7 [132.3-165.0] %Veupnea, U=261, 95%CI[-38.3, -13.9], d=1.1, p