Abstract
Introduction
There is lack of clarity of sleep disordered breathing (SDB)--including the role of nocturnal hypoxia and confounding influence of obesity--on the clinical course of human coronavirus disease 2019 (COVID-19). We postulate that SDB portends increased risk of adverse COVID-19 clinical outcomes even after accounting for confounding factors.
Methods
A retrospective cohort analysis of COVID-19 and sleep laboratory observational registries March-November 2020 within the Cleveland Clinic health system was performed. Ordinal logistic regression assessed the association of SDB indices and World Health Organization (WHO)-7 COVID-19 clinical outcome (hospitalization, use of supplemental oxygen, non-invasive ventilation, mechanical ventilation/ECMO and death) in an unadjusted model and adjusted for age, sex, race, body mass index(BMI,kg/m2),diabetes mellitus, hypertension, coronary artery disease, heart failure, asthma, chronic obstructive pulmonary disease (COPD), cancer and smoking using SAS software.
Results
Of 19,449 (32%) patients positive for SARS-CoV-2,2,290 (6%) had an available sleep study. The analytic sample included 1788 of which 1,484(64%) had an apnea hypopnea index (AHI, 3–4% hypopnea oxygen desaturation)≥5. The median duration from sleep study to COVID test was 5.8 years (IQR:3.3–9.0). Age was 56.5±14.4 years,50.4% female,28% African American with BMI=35.9±8.9kg/m2. Nine percent of patients were hospitalized,10% with supplemental oxygen,6% used non-invasive ventilation,2% required ECMO or mechanical ventilation and 2% died. For every AHI increase of 5, the odds of a higher WHO-7 level increased 2% (OR=1.02,95%CI1.01-1.04,p=0.005),but the association was mitigated in the adjusted model (OR=1.00,95%CI:0.98,1.02,p=0.80). Per 5% increase in time spent with SaO2<90%, the odds of a higher WHO-7 level increased 10% (OR=1.10,95%CI1.06-1.13,p=<0.001) persisting in the adjusted model(OR=1.06,95%CI:1.02–1.10,p=0.002). For every decrease of 5% mean SaO2, the odds of a higher level WHO-7 increased 56% (OR=0.56,95%CI:0.46–0.67,p<0.001) persisting in the adjusted model(OR=0.72,95%CI:0.58–0.89,p=0.003).
Conclusion
Even after adjustment for obesity, underlying cardiopulmonary disease and smoking, sleep-related hypoxemia was a potential key pathophysiologic mechanism associated with increased morbidity and mortality in COVID-19. Elucidation of sleep-related hypoxemia as a risk stratification measure, particularly given the silent hypoxia inherent to early COVID-19, is critical for future investigation, as is the role of sleep-related hypoxia reversal as a target to improve COVID-19 outcomes.
Support (if any)
Cleveland Clinic Neurologic Institute Resource Development Award
Non-invasive ventilation for sleep-disordered breathing in Smith-Magenis syndrome
