0471 Simplified Endotyping Using Home Sleep Study Data to Inform Targeted Therapy for Obstructive Sleep Apnea

Abstract Introduction Obstructive sleep apnea (OSA) pathogenesis is heterogenous with important contributions from at least 4 key endotypes: 1) impaired pharyngeal anatomy, 2) unstable breathing control (high loop gain), 3) poor pharyngeal dilator muscle responsiveness and 4) waking up too easily to minor airway narrowing (low respiratory arousal threshold). Gold standard physiology assessments in a relatively small number of well-characterized participants indicate wide interindividual variability in pharyngeal collapsibility (impaired upper airway anatomy) and that ~30% of people with OSA have impairment in each of the three non-anatomical endotypes. Overall, ~70% have impairment in one or more non-anatomical endotypes which has implications for targeted therapy decisions. We recently developed a simplified model to estimate OSA endotypes from standard in-laboratory polysomnography and clinical data (Dutta et al, Annals ATS, 2021). In this study, we applied this model to estimate OSA endotypes in a large clinical population. Methods OSA endotypes were estimated using standard sleep study outputs and clinical data (i.e., age and BMI) from 6,500 consecutive home-based diagnostic studies (Sleep Profiler PSG- Advanced Brain Monitoring). All participants had an apnea/hypopnea index (AHI) 5 events/h. The proportion of participants who were estimated to have impairment in one or more OSA endotypes was calculated according to previously published physiological cutoffs. Results On average, participants (39% female) had moderately severe OSA (AHI=28±23 events/h (Mean±SD), were middle aged (49±15 years) and obese (BMI=32±7 kg/m2). 29% were estimated to have only mild anatomical compromise (Pcrit -2cmH2O). 23% had poor dilator muscles, 31% high loop gain and 29% had a low arousal threshold. 62% of participants had impairment in one or more non-anatomical endotypes. Conclusion These data highlight the feasibility for simplified OSA endotyping using home sleep study recordings at scale. In addition, consistent with smaller, more detailed physiology studies, a substantial proportion of the clinical OSA patient population have only minor anatomical impairment. Furthermore, approximately two thirds have impairment in one or more non-anatomical endotypes. These findings highlight the potential for simplified OSA endotyping to inform targeted non-CPAP therapy selection for a large proportion of people diagnosed with OSA. Support (if any) DJE is funded by a National Health and Medical Research Investigator Grant (1196261).