Multiple atrial tachycardias after atrial fibrillation ablation: the importance of careful mapping and observation.

A combination of pulmonary vein isolation (PV), electrogram-based ablation, and linear lesions have been demonstrated to result in medium-term freedom from atrial fibrillation (AF) in the majority of patients with persistent AF in several studies. Such an extensive ablation is associated with a high incidence of postablation atrial tachycardia (AT), which is often complex and multiple. Deductive mapping strategy,1,2 which consists of activation mapping and entrainment mapping, can identify the mechanism and/or source of the postablation AT rapidly and accurately. However, careful mapping and close observation to identify subtle changes between the ATs are necessary. Postpacing interval (PPI) mapping is a useful technique, with some limitation for focal AT.3–5 We present a case that demonstrated multiple postablation ATs requiring careful mapping for identifying each of them. It also demonstrated the utility of PPI mapping in the precise diagnosis of the sources of focal ATs. A 47-year-old man with an 8-year history of paroxysmal lone AF, not controlled with amiodarone, was admitted to our institution with persistent AT for his third catheter ablation procedure. At the first procedure, 7 years ago, PV isolation was performed. Six months ago, reisolation of PVs, electrogram-based ablation, and linear ablation of left atrial (LA) roof and left mitral isthmus for inducible AT were performed, which completely blocked both lines. The AT cycle length (ATCL) was 275 ms during the start of the third procedure. A steerable decapolar catheter was inserted into the coronary sinus (CS), and an externally irrigated ablation catheter (Thermocool, Biosense Webster) was advanced into the LA via a transseptal puncture. Oral anticoagulation therapy was discontinued 3 days before the procedure. After transseptal puncture, a bolus of 50 IU/kg of heparin was administered. No PV reconnection was observed. Mapping revealed the mechanism of clinical AT as a …