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).