Background-Atrial arrhythmias are common early after atrial fibrillation (AF) ablation. We hypothesized that empirical antiarrhythmic drug (AAD) therapy for 6 weeks after AF ablation would reduce the occurrence of atrial arrhythmias. Methods and Results-We randomized consecutive patients with paroxysmal AF undergoing ablation to empirical antiarrhythmic therapy (AAD group) or no antiarrhythmic therapy (no-AAD group) for the first 6 weeks after ablation. In the no-AAD group, only atrioventricular nodal blocking agents were prescribed. All patients wore a transtelephonic monitor for 4 weeks after discharge and were reevaluated at 6 weeks. The primary end point of the study was a composite of (1) atrial arrhythmias lasting more than 24 hours; (2) atrial arrhythmias associated with severe symptoms requiring hospital admission, cardioversion, or initiation/change of antiarrhythmic drug therapy; and (3) intolerance to antiarrhythmic agent requiring drug cessation. Of 110 enrolled patients (age 55Ϯ9 years, 71% male), 53 were randomized to AAD and 57 to no-AAD. There was no difference in baseline characteristics between groups. During the 6 weeks after ablation, fewer patients reached the primary end point in the AAD compared with the no-AAD group (19% versus 42%; Pϭ0.005). There remained fewer events in the AAD group (13% versus 28%; Pϭ0.05) when only end points of AF Ͼ24 hours, arrhythmia-related hospitalization, or electrical cardioversion were compared. Conclusions-AAD treatment during the first 6 weeks after AF ablation is well tolerated and reduces the incidence of clinically significant atrial arrhythmias and need for cardioversion/hospitalization for arrhythmia management.

During persistent AF, most CFE regions are found in the vicinity of the PVs. There is a significant correlation between two CFE maps constructed 31 minutes apart, with 78% concordance of CFE sites.

No abstract

No abstract

Reproducible spontaneous and provoked PV triggers initiating AF can be observed in most patients undergoing AF ablation. These triggers most commonly originate from the carina region of both right and left PVs. Noncarina PV triggers more commonly require provocation with isoproterenol infusion.