Mechanisms of postoperative atrial tachycardia following biatrial surgical ablation of atrial fibrillation in relation to the surgical lesion sets

Abstract

Atrial tachycardia (AT) may develop after biatrial surgical ablation of atrial fibrillation. However, the mechanism has not been determined in detail. We aimed to determine the mechanism and treatment of postoperative AT following biatrial surgical ablation in relation to the design and durability of the surgical lesion sets. An electrophysiologic study and radiofrequency ablation were performed in 34 consecutive patients (23 male, mean age of 63 ± 9.4 years) who were referred for AT that developed late after biatrial surgical ablation. The mechanism of a total of 53 ATs was macroreentry in 30, a focal mechanism in 20, and localized reentry in 1, and could not be determined in 2. The cause of the macroreentrant AT was residual conduction across a surgical lesion, most of which was located at the annular end of the mitral (n = 18) or tricuspid isthmus incision (n = 7), where cryoablation was applied during the surgery. We did not find any gaps across the cut-and-sew lesions. Radiofrequency (RF) applications to the gap, or an alternative site to transect the circuit, or the earliest activation site of the focus was effective for 48 ATs (91%). After a total of 1.3 ± 0.6 RF sessions, 27 patients (79%) were free of AT (n = 2) or AF (n = 5) during a follow-up period of 50 ± 49 months. Macroreentry due to a gap in a surgical lesion and focal AT were the major mechanisms of AT in patients after biatrial surgical ablation. Radiofrequency ablation of those ATs is feasible.