Periprocedural dabigatran anticoagulation for atrial fibrillation ablation: do we have enough information to make a rational decision.

Atrial fibrillation (AF) ablation has become an established therapy for treating patients with drug-resistant symptomatic arrhythmia. Initial enthusiasm has been tempered by modest efficacy, frequent recurrences, and uncommon but significant periprocedural complications, including bleeding and systemic thromboembolization [1]. Additionally, AF ablation is a quality-of-life improving treatment with no demonstrated direct survival benefit. As a result, an exceptionally high value on procedural safety is critical to justify its continued utilization. Substantial advances have been made in reducing embolic complications [1–4]. These include intracardiac echocardiography (ICE) and heparinization with full anticoagulation prior to transseptal puncture [2, 3]. A major advance has been the acceptance of uninterrupted therapeutic warfarin instead of routine periprocedural bridging with low-molecular weight heparin (LMWH). This has been associated with a significant reduction in embolic events without increasing the rate of vascular and bleeding complications [5]. The anticoagulation landscape for patients with nonvalvular AF has changed in the last 3–4 years with the adoption of direct thrombin inhibitor dabigatran and anti-factor Xa agents rivaroxaban and apixaban. Patients on dabigatran considered for AF ablation pose a dilemma for periprocedural management with three potential options. First, continue uninterrupted dabigatran with increased risk of bleeding on concomitant unfractionated heparin (UFH) during the procedure. Second, hold dabigatran for one to two doses before the procedure and restart postprocedure, a strategy enabled by the short half-life and a rapid onset of action. And third is the transition from dabigatran to warfarin as the periprocedural anticoagulant with the inherent logistical challenges in accomplishing a therapeutic INR. A substudy of the RE-LY trial showed that dabigatran could be safely continued periprocedurally for direct current cardioversion with the risk of systemic embolism being similar to warfarin [6]. However, there are no randomized trial data to support use of dabigatran as the periprocedural anticoagulant for ablation. There is some concern in using dabigatran with AF ablation because of the possibility of inadequate anticoagulation due to the short half-life, variable clearance, and the absence of a good test to monitor therapeutic effect. On the other hand, dabigatran is susceptible to drug–drug interactions and it intensifies the effect of UFH on activated partial thromboplastin time in vitro even when compared to factor Xa inhibitors [7]. Concomitant use of dabigatran with intraprocedural UFH may thus increase risk of bleeding unless it is held 1–2 days in advance [8]. Despite these challenges, many operators have adopted the strategy of performing AF ablation with brief interruption of dabigatran and resumption of dosing soon afterwards. In this issue, Steinberg et al. report a meta-analysis of 10 observational studies, and thus summarize the hitherto published experience on periprocedural anticoagulation with dabigatran versus warfarin for AF ablation [9]. They show an overall safe profile of dabigatran similar to the published rates of complications in general [10]—10 of 1,501 patients (0.7 %) reportedly had any neurological event, and 24 (1.6 %) had major bleeding. Compared to warfarin, bleeding with dabigatran was similar but there was an absolute increase in neurological events by 0.47 % (95 % confidence interval 0.07 and 0.99 %). The authors deserve praise for compiling this metaanalysis. As the number of adverse events reported from individual studies is extremely small, a meta-analysis is a justifiable and valid way to obtain statistical power for any comparative assessments. Historically, meta-analyses have had the greatest impact on clinical practice when rare adverse A. Noheria : S. J. Asirvatham (*) Division of Cardiovascular Diseases, Mayo Clinic College of Medicine, 200 First Street SW, Rochester, MN 55905, USA e-mail: asirvatham.samuel@mayo.edu