Characteristics and Possible Mechanisms of AEPVR
The distal insertion sites of AEPVR were mostly discovered between the ipsilateral PVs. The connection on the left atrial posterior wall traversed over the prior lesion, suggesting endocardial block with epicardial sparing. According to the anatomical literature, the interpulmonary area is covered with the thickest myocardium around PVs composed of overlapping layers of differently aligned fibers[17,18]. Myocardial strands here cross commonly in an oblique direction before connected to the longitudinally descending fibers on the posterior wall[19, 20], compatible with the mapping results in our study (Graphical Abstract). The subjects in AEPVR group had a smaller atrial size and a shorter DAT, indicating an earlier disease stage which may be associated with healthier myocardium which required higher energy to create transmural lesion. Although the presence of residual epicardial connection was reported mainly associated with anatomical issues[9-11], we have found multiple ablation parameters in relation to AEPVR. In multivariable analysis, the presence of AEPVR was generally associated with a lower energy output and tissue response reflected by AI and impedance drop, respectively. It was further validated by the integrated model in ROC containing multiple parameters which showed the best predictive ability for AEPVR. The relative inadequate energy applied at the posterior wall could be explained by the inevitable concerns of complication e.g., esophageal damage, gastric immobility, and cardiac tamponade[21,22](Figure 4A).
Besides the failure to create durable transmural lesion, another possible mechanism could be the delayed manifestation of a secondary connection after the preferential conduction was blocked. This was especially suitable to explain the reconnection between the right anterior carina and right atrium, which was not affected by prior circumferential ablation and also commonly present in the repeat procedures (Supplementary Figure 2 & Supplementary Video 1). The mechanism was similar to the late presence of an additional accessory pathway (AP) found after successful ablation of the first AP[23]. The anterior carina was preferentially activated by the wavefront from Bachmann bundle or fossa ovalis[24]. ICB conduction could be only revealed until the rest pathways are blocked. When it played the role of an AP with delayed appearance, it could be left unnoticed without sufficient waiting time and detailed remapping (Supplementary Figure 1).