Antiarrhythmic Therapy Following Ablation of Atrial Fibrillation

Giuseppe Stabile; Assunta Iuliano; Alessia Agresta; Vincenzo La Rocca; Salvatore D'Ascia; Antonio De Simone


Expert Rev Cardiovasc Ther. 2013;11(7):837-842. 

In This Article

Rationale of AAD Use After Catheter Ablation

The use of AADs in the early period after AF aims to reduce early recurrence of atrial arrhythmia or the occurrence of macroreentrant LA tachycardia, during the 'blanking period'. Early recurrence of atrial arrhythmias can be disappointing to the patients and are often associated with adverse symptoms, hospitalizations or cardioversion, pharmacological or electrical. Moreover, the use of AADs could theoretically, by reducing early atrial tachyarrhythmia recurrences, promote reverse electrical remodeling, thus favoring long-term success.

AADs are usually used soon after ablation for a period lasting approximately 3–6 months. In fact, it is speculated that the mechanism of AF in this period may be different from that of the patient's clinical arrhythmia and may resolve completely upon resolution of the transient factors promoting early AF recurrences.[9] AAD therapy may either decrease the number or the duration of arrhythmia recurrence or increase the incidence of asymptomatic AF recurrences by providing rate control during recurrence.[10]

The drugs employed for this purpose vary, but most common are the drugs that were unsuccessful prior to ablation, which include flecainide, propafenone, sotalol, dofetilide, dronedarone and amiodarone, since it seems that the efficacy of AADs might substantially increase after catheter ablation of AF. Verma et al. examined pulmonary vein (PV) conduction in patients who had previously undergone PV antrum isolation.[11] They found that patients who were able to maintain sinus rhythm on antiarrhythmic medication demonstrated a significant conduction delay between recurrent PVs and the LA, whereas patients who did not respond to AADs had only minimal conduction delay. Because of the already delayed conduction, AADs may slow conduction even further, potentially causing an exit block of the triggering impulses and preventing the development of AF. Another possible explanation is that arrhythmias recurring after AF catheter ablation are often more organized compared with preablation and, therefore, could have a different response to AADs.[12]