Abstract
BACKGROUND: Autonomic dysfunction plays a significant role in initiating postoperative atrial fibrillation (POAF) by causing atrial ectopic triggers, potentially through mechanisms such as increased sympathetic activity and altered vagal tone. These atrial ectopic triggers can easily induce POAF, especially in the presence of vulnerable substrates such as pericardial inflammation or structural remodeling. OBJECTIVE: To test the hypothesis that autonomic dysfunction causes atrial ectopic triggers or POAF in the canine sterile pericarditis model. METHODS: Ten sterile pericarditis dogs were studied on postoperative Days 2-3. Autonomic dysfunction was induced by stellate ganglion nerve stimulation (SNS, 5-15 mA; 4-10 Hz; pulse width 0.5-5 ms) with or without vagus nerve stimulation (VNS, 15 mA; 20 Hz; pulse width 0.5-2 ms) performed during sinus rhythm for up to 2 h. Atrial ectopic triggers and heart rate (HR) were assessed during autonomic dysfunction. RESULTS: Sustained POAF by burst pacing was induced in 5 of 10 animals (50%). During sinus rhythm (HR 109 ± 14 bpm), autonomic dysfunction using SNS (±VNS) changed the HR from 151 ± 18 bpm (SNS alone) to 72 ± 10 bpm (SNS+VNS) (mean HR fluctuation 79 ± 16 bpm). Atrial ectopic triggers were observed in 1 of 10 animals (10%), originating from either right or left atrium, yet these triggers did not induce POAF. CONCLUSION: Atrial ectopic triggers associated with autonomic dysfunction were observed in only 10% of animals in the postoperative period and did not induce POAF. The low incidence of atrial ectopic triggers in this model may provide mechanistic insights into the lower observed incidence of POAF in patients undergoing coronary artery bypass grafting (CABG) compared to those undergoing valvular heart surgery.