Po-02-149 effect of right and left-sided programmed atrial extrasystoles on conduction across bachmann’s bundle and initiation of atrial fibrillation

Atrial extrasystoles (AES) originating from the pulmonary veins are notorious for triggering episodes of atrial fibrillation (AF). However, non-pulmonary vein triggers, emerging from e.g. the superior vena cava, left atrial posterior free wall, left atrial appendage (LAA), terminal crest and interatrial septum, play also an important role in a significant part of AF patients. AES provoke conduction disorders due to (dispersion in) refractoriness and enhanced non-uniform anisotropy of atrial tissue, which are related to initiation and perpetuation of AF. Bachmann’s bundle (BB) is the main route for interatrial conduction and plays a key role in AF development. However, the exact mechanistic effects of AES on BB in AF initiation are still unknown. To examine the impact of programmed electrical stimulation (PES) from the left and right atrium on activation and electrophysiological features of BB. Intra-operative high-resolution epicardial mapping of BB was performed during sinus rhythm (SR) in 32 patients (29 male, 66±10 years). PES included a S1 sequence of 400 ms followed by a S2 of 300, 250 and 200 ms provided from the left and right atrial appendage (LAA/RAA). Electrophysiological features included unipolar voltage, conduction velocity, potential type (single, short/long double and fractionated) and conduction delay/block (CDCB). Features of the shortest captured S2 were compared to the S1 sequence. The average cycle length during SR was 967 [883–1213] ms. Compared to SR, during S1 pacing from both the RAA and LAA, voltage and conduction velocity decreased, and the amount of fractionation increased (see Table). In addition, CDCB increased specifically during RAA S1 pacing, while total activation time increased during LAA pacing. Applying the maximal captured S2, 11 patients had a refractory period of 250 ms, 16 patients of 200 ms and 5 patients <200 ms. In 4 patients, AF was induced by a S2 of 250 or 200 ms from either RAA or LAA. During both RAA and LAA S2 pacing, voltage and conduction velocity decreased, while total activation time and CDCB increased. Specifically, the maximal length of CDCB lines increased remarkably during LAA S2 pacing and even more during RAA S2 pacing. Premature AES affect interatrial conduction via BB by enhancing conduction disorders. This indicates that BB is involved in AF initiation by ectopic beats, independently of their origin from the right or left atrium.