Top Ten Take-Home Messages from the Atrial Fibrillation Ablation Guidelines

Editor's Note: This Hot Topic is based on Calkins H, Kuck KH, Cappato R, et al. 2012 HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for patient selection, procedural techniques, patient management and follow-up, definitions, endpoints, and research trial design. Heart Rhythm 2012; 9:632-696. e21.

  1. Repeat procedures should be delayed for at least three months following initial ablation, if the patient’s symptoms can be controlled with medical therapy.

    Multiple studies have demonstrated that 30-50% of early recurrences of atrial fibrillation and atypical flutter do resolve on their own, particularly after ablation in patients with persistent AF.1 While early AF recurrence is one of the strongest predictors of late recurrence, the additional risks of a second ablation within 3 months of the first, including groin complications, additional radiation, the possibility that late pulmonary vein reconnection has not yet occurred and the additional cost argue that watchful waiting in the months after ablation is the most prudent strategy. In a study by Haissaguerre and colleagues,2 early redo ablation led to an increase in procedures with no reduction in freedom from AF at approximately 1 year. Of course, rare patients with severe symptoms from recurrent atypical flutter refractory to antiarrhythmic drugs and cardioversion may require repeat ablation earlier than 3 months.

  2. Patients being evaluated as part of a clinical trial or in whom warfarin may be discontinued should have some type of continuous ECG monitoring performed to screen for asymptomatic AF/flutter/tachycardia.

    Multiple studies have demonstrated that symptoms of palpitations from AF are reduced after ablation.3 The mechanism for this is not clearly understood, but likely relates to some denervation of the atrium with ablation. Therefore, both to determine the outcome after ablation and to guide decisions about anticoagulation (see #7), some prolonged monitoring to detect asymptomatic AF after ablation should be performed at any center performing AF ablations. There are multiple types of transtelephonic monitors available, including those that perform continuous monitoring for up to 30 days and those that have an autotrigger feature to detect asymptomatic arrhythmias. Our practice is to perform continuous 2-week monitoring at 6 months and 1 year after AF ablation in all patients.

  3. Freedom from AF/flutter/tachycardia off antiarrhythmic therapy after a single ablation procedure is the primary endpoint of AF ablation.

    When reading the literature, an endpoint of freedom from AF after multiple procedures including patients on antiarrhythmic therapy is often provided as the primary endpoint, and teasing out the single procedure success rate may be difficult. Clinically, it is well recognized that many patients do well with the combination of antiarrhythmic drugs and catheter ablation, and that a second ablation procedure may be required. However, if we are going to be able to gauge improvements in outcome across different centers and techniques then we need a clear comparator, and single procedure success rate off antiarrhythmic medications should remain that barometer for AF ablation outcome. The guidelines based outcome of > 30 seconds of AF indicating a failure of ablation is too strict in my opinion, but this has not changed in the recent guideline update.

  4. Discontinuation of warfarin therapy post ablation is generally not recommended in patients who have a (CHADS) score ≥ 2.

    The guidelines recommend that anticoagulation should be based in CHADS score and not AF recurrence after AF ablation. There is growing data that the stoke risk is low in patients with no detectable AF after ablation.4 Clinically, at some point after ablation, if there is no detectable AF, the cost and risk/benefit of continued anticoagulation will need to be discussed with the patient. For patients with CHADS=0 or 1, anticoagulation can be stopped after ablation in the absence of AF, since systemic anticoagulation is not definitively indicated. Our practice has been that in patients with a CHADS score of 2 who have no symptoms and two continuous transtelephonic monitors without detectable AF, we discuss the risk benefit of continued anticoagulation with the patient and make an informed decision. For patients with a prior stroke or TIA or those with CHADS score ≥3, anticoagulation is typically continued indefinitely.

  5. If patients with longstanding persistent AF are approached, operators should consider more extensive ablation based on linear lesions or complex fractionated electrograms.

    This is one guideline with which I do not completely agree. We all know the outcome after ablation in longlasting persistent AF patients is lower than in those with paroxysmal AF. The single procedure success rate off antiarrhythmic drugs with PV isolation alone is approximately 40%.5 However, the success rate in persistent AF patients, if one includes repeat ablation and antiarrhythmic therapy, is >70%.6 Linear ablation has improved outcome in some studies, however linear ablation without block is more likely to result in atypical flutters after ablation.7 Complex atrial fractionated electrograms (CAFÉ) have multiple etiologies and are not specific enough indicators of AF drivers to warrant widespread ablation, in my opinion. In a recent randomized study, PVI plus ablation of left atrial CAFÉ alone did not improve outcome compared to PVI alone.8 Until an approach that clearly leads to an improvement in single procedure efficacy beyond PVI becomes available, I would argue that antral PV isolation has clear endpoints and reasonable success on longlasting AF patients. These patients should be informed that a second procedure may be required 50% of the time and that antiarrhythmic drugs to maintain sinus rhythm may also be required.

  6. If additional linear lesions are applied, line completeness should be demonstrated by mapping or pacing maneuvers.

    Some of the earliest models of reentry were created by delivering linear lesions in the atrium leaving an intentional “gap”. It is therefore not surprising that delivery of linear lesions without block will create the substrate for atypical flutters in an already diseased atrium. It is imperative that linear ablation be minimized in the atrium, and when performed the endpoint should be bidirectional block across the line. Because linear ablation to achieve block often requires extensive ablation, both endocardially and epicardially, one should reserve linear ablation for treating a reentrant flutter rather than for empiric ablation. There are some circumstances in which multiple flutters exist that cannot be entrained where empiric linear ablation may be required.

  7. If the PVs are targeted, complete electrical isolation should be the goal.

    Earlier studies where purely anatomic lesions were delivered around the pulmonary veins led to an unacceptably high incidence of left atrial flutters after ablation. The purely anatomic approach to AF ablation has largely been abandoned as a strategy for treating AF. The current problem is not with achieving acute PV isolation, but assuring permanent PV isolation. Because entry block can be achieved without exit block, pacing to ensure exit block should be performed after ablation. Use of catheters and sheaths to assure maximum stability, waiting at least 20 minutes after PV isolation to exclude acute reconnection, pace and ablate along the isolation lines, and use of adenosine to detect partially damaged PV tissue all may contribute to achieving durable PV isolation.

  8. For surgical PV isolation, entrance and/or exit block should be demonstrated.

    PV isolation may be more challenging in the surgical suite where surgeons may not be as familiar with electrical endpoints. Tools for measuring entry and exit block after surgical PV isolation have been developed, and should be the endpoint after surgical PV isolation. The delivery of lesions across the PVs using a bipolar RF clamp, as with catheter ablation, is not a sufficient endpoint.

  9. Ablation strategies which target the PVs and/or PV antrum are the cornerstone for most AF ablation procedures.

    There is certainly some interesting data regarding other ablation strategies for AF, including CAFÉ ablation,9 ablation targeting the ganglionic plexi,10 and ablation targeting atrial rotors.11 However, the vast majority of data currently supports antral PVI as the best strategy for treating AF with nonpharmacologic therapy. The procedure has evolved with clear procedural and safety endpoints and will likely remain the mainstay of AF ablation therapy.

  10. The primary indication for catheter ablation is symptomatic AF refractory or intolerant to at least one Class 1 or 3 antiarrhythmic medications.

    It is often debated whether antiarrhythmic therapy is always required prior to ablation in patients with symptomatic paroxysmal AF. This guideline makes sense for several reasons. First, some patients may require antiarrhythmic therapy after ablation, and knowledge about drug tolerability is always helpful. Second, although we realize the efficacy of side effect profile of antiarrhythmic therapy is not ideal, there is little to lose with a trial of antiarrhythmic therapy. Patients who do not tolerate or who have recurrent AF on antiarrhythmics will often feel better about undergoing an invasive procedure for a non life-threatening disorder. This is particularly true if a complication occurs after ablation. There are some patients, typically athletes, who have side effects from even AV nodal blockers and request primary ablation therapy. The guidelines do state that in rare clinical situations, AF ablation may be performed as first line therapy in experienced centers.


  1. Themistoclakis S, Schweikert RA, Saliba WI, et al. Clinical predictors and relationship between early and late atrial tachyarrhythmias after pulmonary vein antrum isolation. Heart Rhythm 2008;5:679-85.
  2. Lellouche N, Jaïs P, Nault I, et al. Early recurrences after atrial fibrillation ablation: prognostic value and effect of early reablation. J Cardiovasc Electrophysiol 2008;19:599-605.
  3. Piorkowski C, Kottkamp H, Tanner H, et al. Value of different follow-up strategies to assess the efficacy of circumferential pulmonary vein ablation for the curative treatment of atrial fibrillation. J Cardiovasc Electrophysiol 2005;16:1286-92.
  4. Themistoclakis S, Corrado A, Marchlinski FE, et al. The risk of thromboembolism and need for oral anticoagulation after successful atrial fibrillation ablation. J Am Coll Cardiol 2010;55:735-43.
  5. Brooks AG, Stiles MK, Laborderie J, et al. Outcomes of long-standing persistent atrial fibrillation ablation: a systematic review. Heart Rhythm 2010;7:835.
  6. Lin D, Frankel DS, Zado ES, et al. Pulmonary Vein Antral Isolation and Nonpulmonary Vein Trigger Ablation without Additional Substrate Modification for Treating Longstanding Persistent Atrial Fibrillation. J Cardiovasc Electrophysiol 2012; doi: 10.1111/j.1540-8167.2012.02307.x. [Epub ahead of print].
  7. Sawhney N, Anousheh R, Chen W, Feld GK. Circumferential pulmonary vein ablation with additional linear ablation results in an increased incidence of left atrial flutter compared with segmental pulmonary vein isolation as an initial approach to ablation of paroxysmal atrial fibrillation. Circ Arrhythm Electrophysiol 2010;3:24
  8. Dixit S, Marchlinski FE, Lin D, et al. Randomized ablation strategies for the treatment of persistent atrial fibrillation: RASTA study. Circ Arrhythm Electrophysiol 2012;5:287-94.
  9. Nademanee K, McKenzie J, Kosar E, et al. A new approach for catheter ablation of atrial fibrillation: mapping of the electrophysiologic substrate. J Am Coll Cardiol 2004;43:2044-53.
  10. Po SS, Nakagawa H, Jackman WM. Localization of left atrial ganglionated plexi in patients with atrial fibrillation. J Cardiovasc Electrophysiol 2009;20:1186-9.
  11. Narayan SM, Krummen DE, Rappel WJ. Clinical mapping approach to diagnose electrical rotors and focal impulse sources for human atrial fibrillation. J Cardiovasc Electrophysiol 2012;23:447-54.

Clinical Topics: Anticoagulation Management, Arrhythmias and Clinical EP, Sports and Exercise Cardiology, Anticoagulation Management and Atrial Fibrillation, SCD/Ventricular Arrhythmias, Atrial Fibrillation/Supraventricular Arrhythmias

Keywords: Adenosine, Athletes, Atrial Fibrillation, Atrial Flutter, Catheter Ablation, Denervation, Pulmonary Veins, Recurrence, Stroke, Tachycardia, Warfarin

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