0431 PATHOPHYSIOLOGIC ASPECTS OF SLEEP DISORDERED BREATHING AND PAROXYSMAL ATRIAL FIBRILLATION

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Although associations of sleep disordered breathing (SDB) and continuous atrial fibrillation (AF) have been well-characterized, the relationship of SDB and paroxysmal AF (PAF), an earlier stage in the AF evolution, is not well understood. We sought to examine the association of SDB and its attendant pathophysiologic attributes in relation to PAF. We leverage a case control study designed to examine the underlying mechanisms of SDB and PAF: the Sleep Apnea and Atrial Fibrillation Biomarkers and Electrophysiological Atrial Triggers (SAFEBEAT, NCT02576587). Cases were >18 years with PAF1:1 matched to controls without AF by age (±5 years), sex, race and body mass index (BMI±5kg/m2) who underwent 16-channel research-grade polysomnography. SDB was defined by apnea hypopnea (>3% desaturation) index (AHI), central apnea index (CAI), percentage sleep time <90% oxygen saturation (TST<90) and arousal index (AI). Conditional logistic regression models were used to assess relationships of SDB measures and PAF. Multivariable models were further adjusted for hypertension, diabetes, myocardial infarction history, dyslipidemia and depression (odds ratio and 95% confidence intervals presented). The analytic sample was comprised of 300 participants (n=150 cases, n=150 controls): age 61.9 ± 11.9 years, 63.3% male, and BMI 31.4 ± 6.7kg/m2. Unadjusted analyses demonstrate a statistically significant inverse association of AHI and PAF (OR=0.95, 95%CI: 0.93–0.97) which persisted in the multivariable model (OR=0.95, 95%CI: 0.93–0.98). High blood pressure had a significant association with PAF (OR= 1.97, 95%CI: 1.013–3.82). No significant associations were observed for CAI, AI and TST<90 relative to PAF. The current findings demonstrate a 5% decreased odds of PAF per single unit increase in AHI consistent with an unanticipated inverse association. Given existing data showing increased risk of mainly continuous AF in SDB, it is possible that SDB may exert variable influences (beneficial versus detrimental) depending upon the extent of cardiac remodeling and stage of AF evolution. NHLBI RO1 1 R01 HL 109493, Clinical and Translational Science Collaborative of Cleveland,UL1TR000439 from the National Center for Advancing Translational Sciences (NCATS) component of the National Institutes of Health and NIH roadmap for Medical Research.