Gradients of Atrial Refractoriness and Inducibility of Atrial Fibrillation due to Stimulation of Ganglionated Plexi

Abstract

The mechanism(s) whereby atrial ectopy induces atrial fibrillation (AF) is still poorly understood. In 12 dogs, we determined the refractory period (RP) along the right atrium (RA) and right superior pulmonary vein (RSPV), and AF inducibility with and without concurrent stimulation of the anterior right ganglionated plexi (ARGP) at the base of the RSPV. Multielectrode catheters were attached to the RSPV and RA with the distal electrodes close to ARGP. The RP and window of vulnerability (WOV), i.e., the longest S1-S2 minus the shortest S1-S2 at which AF was induced, were measured before and during incremental levels of ARGP stimulation. Mapping of the onset of AF was performed using the EnSite mapping system (St. Jude Medical, St. Paul, MN, USA) positioned in the RA. A single premature depolarization (PD) from the RSPV that did not induce AF without ARGP stimulation could do so with ARGP stimulation. The onset of AF consistently arose at the myocardium subtending the ARGP. With GP stimulation, the average WOV at the RSPV-atrial junction was significantly wider than at the RA appendage (65 +/- 27 vs. 8 +/- 17 msec, P < 0.05) or further along the RSPV sleeve (48 +/- 39 vs. 10 +/- 20 msec, P < 0.05). Even without GP stimulation, high intensity (10-20 mA) premature stimuli delivered at the RA appendage induced AF, originating from atrial tissue subtending the ARGP, presumably due to axonal conduction that activated the ARGP. GP stimulation, subthreshold for atrial excitation, converts isolated PDs into AF-inducing PDs, suggesting that autonomic tone may play a critical role in the initiation of paroxysmal AF.