Cardiac autonomic ganglia ablation suppresses atrial fibrillation in a canine model of acute intermittent hypoxia.

Atrial fibrillation (AF) is associated with hypoxia in which cardiac autonomic nerve system (ANS) plays an important role. Our previous studies indicated that ANS is activated in an intermittent hypoxia model and contributes to AF initiation. This study aimed to investigate the effects of cardiac ganglionated plexus (GP) ablation on AF in this model.

In thirteen anesthetized male dogs, GP ablation was applied after 1h of intermittent hypoxia in the first group (n=7) and before that in the second group (n=6). The heart rate (HR), blood pressure (BP), arterial blood gases, heart rate viability indices, atrial effective refractory period (ERP) and window of vulnerability (WOV), the sum of WOVs (ΣWOV) were measured. In both groups, HR, BP increased and then declined during hypoxia, and not significantly affected by GP ablation. Hypoxemia, hypercapnia and acidosis were observed after intermittent hypoxia. In the first group, both of low frequency power (LF) and high frequency power (HF) increased during hypoxia. At the end of intermittent hypoxia, LF/HF ratio decreased, ERP shortened and ΣWOV increased. The following GP ablation resulted in increases in LF, LF/HF, ERP and decreases in HF, ΣWOV. In the second group, GP ablation caused increases in LF, LF/HF, ERP and decrease in HF. Subsequently, ERP shortened at several sites after intermittent hypoxia. However, there were no significant changes in LF/HF ratio or ΣWOV.

Cardiac ANS plays an important role in hypoxia-induced AF. AF associated with hypoxia might be prevented or reversed by GP ablation.