Abstract
STUDY OBJECTIVES: To examine the unclear, inconsistent role of sleep architectural disruption in atrial fibrillation (AF) development. METHODS: Patients (age ≥ 18 years) who underwent in-laboratory sleep studies at Cleveland Clinic 2000-2015 were examined (follow-up: 7.8 ± 3.5 years). Primary predictors were arousal index and total sleep time. Secondary predictors included sleep efficiency, wakefulness after sleep onset, sleep and REM latency, and percentage of each sleep stage. Predictors were fit to Cox proportional hazard models predicting time from sleep study to AF by diagnosis code. Covariates included demographics, anthropometrics, tobacco use, sleepiness, apnea-hypopnea index, sleep apnea-specific hypoxic impact, cardiovascular risk factors and disease, mood disorders, medications, and positive airway pressure. RESULTS: In our cohort (n = 27 232, age: 49.4 ± 14.5 years, 43.7% male, 73.9% white), 2077 (7.6%) developed incident AF. Arousal index was not associated with AF incidence. For every hour of decreased total sleep time, AF incidence increased 8% (HR = 1.08, 95% CI = 1.04 to 1.11). For every 10-unit decrease in sleep efficiency, AF incidence increased 6% (HR = 1.06, 95% CI = 1.04 to 1.09). For every hour of increased wakefulness after sleep onset, AF incidence increased 11% (HR = 1.11, 95% CI = 1.05 to 1.16). For every 10-unit increase in percent N1, AF incidence increased 6% (HR = 1.06, 95% CI = 1.01 to 1.10). CONCLUSIONS: Less sleep time and greater sleep disruption were associated with increased incident AF in this large clinical cohort. These results suggest that sleep macro-architecture can influence AF development. Mechanistic and prospective studies are needed to verify whether sleep disruption is a novel target for AF prevention.