Obstructive apneas immediately impact atrial hemodynamics and arrhythmias

Obstructive sleep apnea (OSA) and atrial fibrillation (AF) often coexist. OSA causes intrathoracic pressure fluctuations, which act as mechanical stimuli to the thin-walled atria. Atrial stretching facilitates AF.

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.

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 multislice computer tomography scans (n = 84) at baseline, during apnea and on release.

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 < .010; pigs = 27). During apnea release, right atrial volume was 30% and left atrial volume 32% larger than at baseline (pigs = 5; P < .05 baseline vs release). Right atrial pressure increased from 5 ± 4 mmHg at baseline to 9 ± 6 mmHg in apnea release (P < .05). Especially in the right atrium, the estimated atrial transmural pressure was higher during and on apnea release. While assuming atrial sphericity, this led to a higher estimated wall tension index.

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.