BACKGROUND: Atrial tachycardia (AT) may develop after biatrial surgical ablation of atrial fibrillation. However, the mechanism has not been determined in detail. OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
BACKGROUND:Atrial tachycardia (AT) may develop after biatrial surgical ablation of atrial fibrillation. However, the mechanism has not been determined in detail. OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.