Obstructive apneas immediately impact atrial hemodynamics and arrhythmias

BACKGROUND: Obstructive sleep apnea (OSA) and atrial fibrillation (AF) often co-exist. OSA causes intra-thoracic pressure fluctuations, which act as mechanical stimuli to the thin-walled atria. Atrial stretching facilitates AF. OBJECTIVE: To provide a comprehensive mapping on how onset and release of obstructive apnea impact atrial arrhythmia occurrence and bi-atrial hemodynamics in an animal model. METHODS: We simulated obstructive apnea by administrating intermittent negative upper airway pressure (-60 mbar) for 75 seconds in anesthetized, spontaneously breathing pigs. We quantified atrial premature complexes on electrocardiography. We assessed atrial hemodynamics by intra-atrial pressures and repetitive dynamic multi-slice computer tomography scans (n = 84) at baseline, during apnea and upon release. RESULTS: Atrial premature complexes were most frequent during the release period after apnea (0.16±0.27 arrhythmias/second vs. 0.04 ± 0.08 at baseline, p < 0.010; pigs = 27). During apnea release, right atrial volume was 30% and left atrial volume 32% larger than at baseline (pigs = 5; p < 0.05 baseline vs. release). Right atrial pressure increased from 5 ± 4 mmHg at baseline to 9 ± 6 mmHg in apnea release (p < 0.05). Especially in the right atrium, the estimated atrial transmural pressure was higher during and upon apnea release. While assuming atrial sphericity, this led to a higher estimated wall tension index. CONCLUSION: Release of an obstructive apnea associates with marked changes in atrial hemodynamics and arrhythmia burden in a porcine model. This has implications for understanding disease-mechanisms for OSA-related AF in humans.