The following is a summary of “Sleep‐Disordered Breathing, Hypoxia, and Pulmonary Physiologic Influences in Atrial Fibrillation,” published in the November 2023 issue of Cardiology by Heinzinger et al.
In this study, using a substantial clinical cohort, researchers investigated the link between sleep-disordered breathing, sleep-related hypoxia, and atrial fibrillation (AF) development. The relationship between sleep-related hypoxia, pulmonary physiology, and their contributions to the onset of AF remains ambiguous, prompting the comprehensive analysis. Their retrospective cohort comprised patients undergoing sleep studies at Cleveland Clinic between January 2, 2000, and December 30, 2015. Using Cox proportional hazards models, they assessed various parameters, including apnea-hypopnea index, oxygen saturation levels, and end-tidal carbon dioxide about incident AF, adjusting for multiple factors. The cohort of 42,057 individuals, with a median age of 50.7 years and diverse demographic characteristics, saw 4.6% developing AF within 5 years. Elevated apnea-hypopnea index, reduced oxygen saturation levels, and increased carbon dioxide were associated with heightened AF risk. Specifically, a 10-unit increase in the apnea-hypopnea index led to a 2% higher risk, while similar changes in oxygen saturation levels were linked to a 6% to 30% increased AF risk.
After considering spirometry factors, sleep-related hypoxia remained significantly associated with incident AF, indicating a substantial role in AF development independent of pulmonary physiological impairment. These findings underscore the substantial impact of sleep-related hypoxia on AF incidence, highlighting its significance even when accounting for pulmonary physiological factors.
Source: ahajournals.org/doi/10.1161/JAHA.123.031462
