Ting-Chun Huang1,2,3, Li-Wei Lo1,4, Shinya Yamada1,5, Yu-Hui Chou1, Wei-Lun Lin1,4, Shih-Lin Chang1,4, Yenn-Jiang Lin1,4, Shin-Huei Liu1,4, Wen-Han Cheng1,4, Tsung-Ying Tsai1,4, Ping-Yen Liu2,3, Shih-Ann Chen1,4. 1. Division of Cardiology, Department of Medicine, Taipei Veterans General Hospital, Taipei, Taiwan. 2. Division of Cardiology, Department of Internal Medicine, National Cheng Kung University Hospital, College of Medicine, National Cheng Kung University, Tainan, Taiwan. 3. Institute of Clinical Medicine, College of Medicine, National Cheng Kung University, Tainan, Taiwan. 4. Institute of Clinical Medicine and Cardiovascular Research, National Yang-Ming University, Taipei, Taiwan. 5. Department of Cardiovascular Medicine, Fukushima Medical University, Fukushima, Japan.
Abstract
BACKGROUND: The relationship between gastroesophageal reflux disease (GERD) and atrial fibrillation (AF) has been previously reported. However, the detailed mechanism remains unknown. In this study, we investigated the effects of acid reflux on the intrinsic cardiac autonomic nervous system, atrial/ventricular electrophysiology, and AF inducibility. METHODS: Eighteen rabbits were randomized into three groups: acid reflux (group 1, n = 6), control (group 2, n = 6), and acid reflux with periesophageal vagal blockade (group 3, n = 6). Atrial and ventricular effective refractory periods (ERPs) and AF inducibility were checked at baseline and then hourly until 5 hours after the experiment. RESULTS: Three hours after the experiment, atrial ERP prolongation was noted in groups 2 and 3 (P < .05), whereas shortening of the atrial ERPs was observed in group 1, compared with the baseline. However, no changes were observed in ventricular ERPs in the three groups. The AF inducibility was higher in group 1 than in groups 2 and 3. Pathological examination showed clear esophageal mucosal breaks in groups 1 and 3. CONCLUSIONS: In this study, we found that the antimuscarinic blockade prevents GERD induced changes to atrial electrophysiology and susceptibility to AF-making it highly likely that autonomic activity is important in mediating this effect.
BACKGROUND: The relationship between gastroesophageal reflux disease (GERD) and atrial fibrillation (AF) has been previously reported. However, the detailed mechanism remains unknown. In this study, we investigated the effects of acid reflux on the intrinsic cardiac autonomic nervous system, atrial/ventricular electrophysiology, and AF inducibility. METHODS: Eighteen rabbits were randomized into three groups: acid reflux (group 1, n = 6), control (group 2, n = 6), and acid reflux with periesophageal vagal blockade (group 3, n = 6). Atrial and ventricular effective refractory periods (ERPs) and AF inducibility were checked at baseline and then hourly until 5 hours after the experiment. RESULTS: Three hours after the experiment, atrial ERP prolongation was noted in groups 2 and 3 (P < .05), whereas shortening of the atrial ERPs was observed in group 1, compared with the baseline. However, no changes were observed in ventricular ERPs in the three groups. The AF inducibility was higher in group 1 than in groups 2 and 3. Pathological examination showed clear esophageal mucosal breaks in groups 1 and 3. CONCLUSIONS: In this study, we found that the antimuscarinic blockade prevents GERD induced changes to atrial electrophysiology and susceptibility to AF-making it highly likely that autonomic activity is important in mediating this effect.