Abstract 18783: Unique Connections Between Specific Atrial Locations and the Ventricular Outflow-Tracts Identified as Putative Effectors in the Arrhythmogenesis of Outflow-Tract-Related Ventricular Arrhythmias

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Abstract

The arrhythmogenic mechanism of idiopathic ventricular arrhythmia (IVA) from the outflow tracts (OT) has been described to be triggered activity. However, it is not completely understood why this focal mechanism originates almost exclusively in the OTs, and what specific factors can initiate it.

The complex nature of this mechanism is supported by observations describing the co-existence of supraventricluar tachycardia with OT-IVA; and our previous reports on the parallel abolishment of OT-IVA after accessory pathway-ablation. We hypothesized that specific pathways with preferential conduction might exist between certain atrial locations and the OT regions, which might play a role in the genesis of OT-IVA.

We report here on the electrophysiological (EP) study of eight patients, who were referred to our center because of OT-related premature ventricular contractions (OT-PVC). Using programmed atrial stimulation at the interatrial septum or within the coronary sinus, we show that atrial stimulation was capable of evoking OT-PVCs with an ECG-morphology quasi-identical to the clinical PVC. Of note, these PVCs occur after an evident atrial capture with an A to V interval in the range of 40-80 msec. (All patients exhibited spontaneous PVCs with low frequency (1-2 PVC/5 min) during the EP study; hence co-incidental occurrence during atrial stimulation was excluded).

Our findings suggest that unique connections might exist between specific atrial locations and the OTs, the activation of which could result in triggering PVCs from the presumed exit point of these pathways in the OT. This is also supported by previous findings describing discrete pre-potentials preceding the ventricular electrogram of PVCs at specific locations within the OTs. Remnants of the embryologic AV conduction system (referred to as "dead-end-tract") might serve as a preferential pathway, through which the atrial activation wavefront might occasionally "leak out" towards the OT regions to trigger PVCs.

Our results could have the potential to transform the current approach of OT-IVA-ablation, and might introduce a novel strategy of extending mapping into the atrium, to identify/ablate the presumed entry-sites of the "dead-end-tract", through which the arrhythmia can be triggered.

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