Background: Obstructive sleep apnea (OSA) is closely associated with atrial fibrillation (AF). Hence OSA-treatment by continuous positive airway pressure (CPAP) is believed to reduce the atrial fibrillation burden in OSA-patients. Yet, atrial electrophysiological consequences due to CPAP-therapy remain to be unknown. In pigs, we investigated differential atrial effects of obstructive respiratory events, simulated by intermittent negative upper airway pressure (INAP) and increasing levels of CPAP-applications.

Methods: In spontaneously breathing pigs, obstructive respiratory events were simulated by intermittent negative upper airway pressure (INAP) applied via a pressure device connected to the intubation tube. INAP was applied for 75 seconds with a 10 minute resting period in-between. After four INAP-applications, during which atrial electrophysiological responses to INAP were recorded, continuous positive airway pressure was applied in increasing pressure stages for a duration of 20 minutes each pressure level (4,8,12 and16 mbar). Atrial effective refractory periods (AERP) were acquired at the free wall of the right atrium (RA) and in the distal area of the coronary sinus (CS) before (Pre-INAP), during (INAP) and after (Post-) INAP and every 10 minutes throughout the stepwise increase of CPAP.

Results: AERP shortened due to INAP application in the RA (Pre-INAP 136±6ms vs. INAP 94±6ms; p=0.0025), but only moderately in the CS (Pre-INAP 130±7ms vs. 106±9ms; p=0.07). Stepwise increases of CPAP-application up until 12 mbar did neither result in changes of RA- nor CS-AERP. Only CPAP-application at 16 mbar (CPAP16) resulted in transiently shortened CS-AERP (CPAP-baseline 140±6ms versus CPAP16 115±10ms; p=0.0081), but not RA-AERPs (p=0.31).

Conclusion: In pigs, simulation of obstructive respiratory events by INAP are associated with shortening of atrial refractoriness, predominantly in the right atrium. High-pressure CPAP-application results in transient shortening of refractoriness in the coronary sinus, representing impairment of left atrial electrophysiology. If high pressure CPAP-therapy relevantly impairs human atrial electrophysiology, remains to be further investigated.