Background: Classical electrophysiological studies involve inducing a tachycardia to prove mechanism, ablating the target and then confirming non-inducibility. This has not been the case in atrial fibrillation (AF) as the mechanisms are not known. We postulated that ablation of ectopy-triggering ganglionated plexus (ET-GP) sites that trigger AF would also terminate AF, thus proving their role in the pathophysiology of AF.
Objective: To determine whether sustained AF triggered by high frequency stimulation (HFS) at a GP site can be terminated by ablation of GPs.
Methods: Patients with paroxysmal AF were recruited and underwent left atrial mapping for ET-GP with short bursts of HFS within the local refractory period at each site. An ET-GP was defined as any response that triggered ectopy or atrial arrhythmia (Fig 1A). Any ET-GP that triggered AF which sustained for >2mins was identified as a 'non-terminating AF' and underwent ET-GP ablation (Fig 1B).
Results: 18/32 (56%) patients underwent ablation of ET-GP sites that triggered non-terminating AF. 11/18 (61%) reverted to sinus rhythm, either with ET-GP ablation alone or with additional cardioversions.7/18 (39%) patients remained in non-terminating AF despite ET-GP ablation. In total, there were 45 sustained AF episodes. 15/18 patients had more than 1 episode of non-terminating AF. In total, there were 45 non-terminating AF episodes triggered by ET-GP. 22 (49%) of these episodes were successfully terminated by ablation of 1 or more ET-GP sites. The remaining 23 (51%) episodes failed to terminate with ET-GP ablation. The average time from start of ablation to termination of AF was 6 minutes 30 seconds.
Conclusion: For the first time, we have demonstrated that AF triggered and sustained by stimulation of an ET-GP site and can be ablated to terminate AF and restore sinus rhythm. This is a compelling finding that ET-GP contribute to the autonomic activity in the triggering and maintenance of AF.
