Abstract Rationale Obstructive Sleep Apnea (OSA) and asthma are prevalent and comorbid disorders that share some similar risk factors. The interaction between pathological mechanisms in the upper and lower airway may explain how each disease impacts the other. Nocturnal asthma may potentiate phenotypic traits such as low arousal threshold or pharyngeal upper airway collapsibility and small airways obstruction may lead to more obstructive events. Leveraging a technique to measure pathophysiological traits underlying OSA from routine sleep studies in a large clinical cohort, we tested the hypotheses that i) OSA severity and traits differ in patients with asthma vs OSA-alone, and ii) pulmonary function test (PFT) abnormalities in these patients are also associated with OSA traits (e.g., airflow obstruction and low arousal threshold/high loop gain). Methods The San Diego Multi-Outcome OSA Endophenotype (SNOOzzzE) cohort includes 3,319 consecutive adults who underwent a clinical in-laboratory polysomnography at the UCSD sleep clinic between 1/2017-12/2019. We included patients who had OSA (AHI5/h, with 50% central events) in whom we were able to quantify key pathophysiological traits including anatomical upper airway collapsibility (Vmin and Vpassive; lower=more collapsible), arousal threshold (lower=waking up easier), loop gain (higher=more ventilatory instability), and pharyngeal dilator muscle recruitment (Vcomp; lower=less recruitment) via a published polysomnography-based algorithm. Subjects with OSA and an Asthma diagnosis (confirmed by pulmonologist review) were matched with OSA-only controls based on age (±5years), sex, body mass index (BMI, ±3kg/m2) in a 1:3 ratio. Using mixed-effects, linear regression we compared OSA severity (primary: AHI; secondary: markers of hypoxia) and traits across both groups. Results To date, we included 168 patients with Asthma+OSA. The 504 OSA-only controls were overall well matched for key demographic characteristics, although the asthma+OSA group was more likely to identify as Hispanic, with some additional racial differences observed (Table). Sleep apnea severity was comparable between groups (mean±SD AHI 31±23 34±28, P = 0.18). In univariable analyses, patients with asthma+OSA exhibited a significantly less collapsible upper airway (Vmin, P = 0.02) and a lower arousal threshold (P = 0.007). Multivariable models adjusting for race/ethnicity, as well as analyses examining associations between physiologic traits and pulmonary function test measures, are pending. Conclusion Preliminary findings suggest that among patients with asthma, OSA may be driven primarily by a low arousal threshold, which counterbalances a relatively less collapsible upper airway. This combination may result in an overall OSA severity similar to that observed in matched patients with OSA but without asthma. This abstract is funded by: Partially funded by the NIH, see below
Jimenez et al. (Fri,) studied this question.