Editorial Atrial Tachycardia After Ablation of Persistent Atrial Fibrillation Is It Us or Them? Aman Chugh, MD

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rrhythmia recurrence after catheter ablation of persistent atrial fibrillation (AF) is not uncommon and frequently requires repeat ablation procedures.1–3 However, the precise arrhythmia that recurs depends on the strategy that was used at the original session. Patients who undergo sole pulmonary vein (PV) isolation usually manifest recurrent AF. Patients who undergo substrate modification, in the form of electrogram based4 or linear ablation,5 frequently develop atrial tachycardia (AT) either during or after the procedure. Whether these organized arrhythmias represent underlying driver tachycardias that were responsible for maintaining AF or occur as a result of our intervention (that is, proarrhythmia) remains unresolved.

Article see p 1059 If we are truly unmasking underlying drivers, then our ablation strategy may be validated because it allows us to map and potentially eliminate sources of AF, which otherwise could not be identified during fibrillatory conduction. Alternatively, it is possible that substrate ablation, especially linear left atrial ablation, may result in macroreentrant ATs that were not present during or responsible for maintaining AF. In this case, either the original source(s) has been eliminated or simply grazed and is now supplanted by organized reentry related to zones of slow conduction created by ablation. The existing literature provides evidence for both hypotheses. A study using spectral analysis showed that the frequency (ie, the cycle length) of the AT that resulted after AF termination matched that of a spectral component that was already present in the baseline periodogram during AF.6 A follow-up study revealed that when linear ablation resulted in complete conduction block, it was accompanied by a decrease in the prevalence of these spectral components.7 These findings suggest that site-specific ATs may be present during ongoing AF, despite the fact that their frequency is lower than the dominant frequency during AF. These studies then support the contention that organized tachycardias are bound to be encountered after elimination of fibrillatory conduction and, therefore, are The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association. From the Division of Cardiology, Section of Electrophysiology, University of Michigan Hospital, Ann Arbor. Correspondence to Aman Chugh, MD, University of Michigan Hospital, 1500 East Medical Center Dr, Cardiovascular Center, SPC 5853, Ann Arbor, MI 48109. E-mail [email protected] (Circ Arrhythm Electrophysiol. 2013;6:1047-1049.) © 2013 American Heart Association, Inc. Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org DOI: 10.1161/CIRCEP.113.001168

not brought on by ablation-related slowed conduction. They also imply that these underlying tachycardias may be responsible for maintaining AF in a hierarchical manner. However, there is also significant support for the competing argument that the ablation strategy determines whether organized reentrant arrhythmias will be encountered during or after ablation. For example, macroreentrant ATs using the mitral isthmus or the roof are frequently encountered when patients with paroxysmal AF undergo linear ablation, with8 or without PV isolation.5 However, these tachycardias are rarely seen after simple antral PV isolation. If these ATs were truly responsible for maintaining AF, why is it possible to eliminate the arrhythmia in 90% of patients with paroxysmal AF9 without ablation of the left atrial isthmi? An earlier study also showed that virtually all reentrant ATs originated from prior ablation lines.10 A more recent study found that the slowest conduction velocity along a macroreentrant circuit localized to the area that was targeted during the initial ablation procedure for persistent AF.11 If a patient is destined to develop perimitral reentry, for example, after elimination of AF, why should the area of slow conduction be found at the lateral mitral annulus, where linear ablation was performed, and not at other sites around the mitral valve? These studies provide strong evidence supporting the assertion that the ablation strategy does affect the prevalence and type of arrhythmias encountered during ablation of persistent AF. Amid this uncertainty, we receive a timely contribution from Rostock et al12 in the current issue of the journal. The authors strived to determine the mechanistic and prognostic significance of ATs that were encountered during an ablation procedure for persistent AF. Patients in whom AF terminated to AT were randomized to further ablation until sinus rhythm was achieved or transthoracic cardioversion. A total of 110 patients with persistent AF were recruited, and 102 patients (8 patients converted to sinus rhythm with PV isolation alone) underwent PV isolation followed by electrogram-guided ablation. AF terminated to AT during ablation in 69 patients (AF terminated to sinus rhythm in 11 and could not be terminated in 22 patients), who were then randomized to further ablation (n=34) or transthoracic cardioversion (n=35). Among the former, sinus rhythm was achieved with sequential elimination of multiple ATs in 27 patients (79%). After a single procedure, there was a trend toward a better outcome (P=0.075) in patients randomized to ablation of ATs when compared with those to cardioversion. After repeat procedures, during which the end point was elimination of AF and all ATs irrespective of the original group assignment, sinus rhythm was achieved in 85% of patients who were originally randomized

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1048  Circ Arrhythm Electrophysiol  December 2013 to AT ablation and 72% who were randomized to cardioversion (P=ns). Again, the former were more likely to be free of AF (but not AT) at long-term follow-up. The authors concluded that the ATs that were encountered after elimination of AF may have been responsible for maintaining AF, and hence, it is worthwhile to map and ablate these ATs as opposed to simply performing transthoracic cardioversion. The authors are to be commended for having the courage to conduct a randomized study to examine this important issue. In doing so, they also showed remarkable restraint in overcoming the urge to pursue ATs (in the control group) after investing so much time and effort in terminating persistent AF. Let us examine the results a bit more closely. The authors were not able to show a statistically significant difference between the AT ablation and cardioversion groups after the first procedure. This likely has to do with the small sample size (≈35 in each group). In addition, the lack of demonstrable difference in the final outcome (after redo procedures) may be due to the possibility that differences between the groups may have been diluted by the requirement of termination of all arrhythmias during the repeat procedure(s) in all patients, irrespective of the original randomization. This should not take away from the take-home message that ATs encountered during the AF procedure are likely to recur and should be mapped and ablated during the initial procedure. This stance is also supported by the literature. A prior study found that the only predictor of occurrence of AT after ablation was acute AT noted during the initial AF procedure.5 Although it is true that some of these ATs may spontaneously remit perhaps with lesion maturation, the majority of patients who develop postablation AT will require a repeat procedure. Elimination of acute AT not only prevents early recurrence during hospitalization or shortly after discharge (which is quite disruptive and stressful from a patient standpoint) but also probably prevents some patients from requiring a redo procedure. It should be noted that a recent study suggested that inducible AT after stepwise ablation that terminated longstanding persistent AF was not found to be predictive of recurrence.13 However, a tachycardia that spontaneously emerges after elimination of AF is likely to carry more clinical import than one that is induced after extensive substrate ablation. A contrarian would also point out that despite an end point of not only AT but also AF termination during the second procedure, 25% of patients still required either a third or fourth procedure. In other words, why not defer mapping of acute ATs to the repeat session, which is frequently required despite an end point of AF/AT termination? These data are consistent with our experience. In a recent study, despite AT termination in all patients, attainment of linear block across the roof and mitral isthmus in ≈90% of patients, and noninducibility during isoproterenol infusion, 22% of patients required yet another ablation procedure for AT.11 Recurrence in these patients was because of either resumption of conduction along linear lesions or emergence of small circuits, which could not be brought out by the induction protocol. Multiple linear lesions, even when complete, may not be protective, and may favor reentry by acting as lateral barriers. It is thus probably best to avoid empiric linear lesions, especially at the mitral isthmus, during the initial AF procedure. Postablation AT may be eliminated in >90% of patients, and despite recurrence, long-term freedom from atrial arrhythmia may

be achieved in 80% to 90% of patients without the use of antiarrhythmic medications.11,14 However, the circuitry can be complex in some patients, making for long procedures. Furthermore, linear block may be challenging to achieve in some patients,15 which may be met with arrhythmia recurrence. Whether it is possible to eliminate persistent AF without these intervening ATs remains unknown. Preliminary studies in which ablation was guided by mapping of AF sources, as opposed to ablation of empirically chosen targets as is conventionally done, seem to suggest that sinus rhythm may be achieved without AT.16 If the initial results are reproducible and durable, it would not only confirm that these AT are frequently our creation but also more importantly greatly simplify the ablation procedure and improve clinical outcomes. For the time being, the study by Rostock et al12 should reinforce our commitment to prevent the occurrence of AT and also to tackle these tachycardias whenever they are encountered, even though it remains unclear whether the arrhythmias are due to the ablation strategy (us) or the patient’s underlying substrate (them).

Acknowledgments Dr Chugh is supported in part by a grant from the Leducq Transatlantic Network.

Disclosures None.

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Chugh  Post-Ablation AT  1049 10. Chae S, Oral H, Good E, Dey S, Wimmer A, Crawford T, Wells D, Sarrazin JF, Chalfoun N, Kuhne M, Fortino J, Huether E, Lemerand T, Pelosi F, Bogun F, Morady F, Chugh A. Atrial tachycardia after circumferential pulmonary vein ablation of atrial fibrillation: mechanistic insights, results of catheter ablation, and risk factors for recurrence. J Am Coll Cardiol. 2007;50:1781–1787. 11. Yokokawa M, Latchamsetty R, Ghanbari H, Belardi D, Makkar A, Roberts B, Saint-Phard W, Sinno M, Carrigan T, Kennedy R, Suwanagool A, Good E, Crawford T, Jongnarangsin K, Pelosi F Jr, Bogun F, Oral H, Morady F, Chugh A. Characteristics of atrial tachycardia due to small vs large reentrant circuits after ablation of persistent atrial fibrillation. Heart Rhythm. 2013;10:469–476. 12. Rostock T, Salukhe TV, Hoffmann BA, Steven D, Berner I, Mullerleile K, Theis C, Bock K, Servatius H, Sultan A, Willems S. The prognostic role of subsequent atrial tachycardias occurring during ablation of persistent atrial fibrillation: a prospective randomized trial. Circ Arrhythm Electrophysiol. 2013;6:1059–1065. 13. Nagamoto Y, Park JS, Tanubudi D, Ko YK, Ban JE, Kwak JJ, Choi JI, Lim HE, Park SW, Kim YH. Clinical significance of induced atrial tachycardia

after termination of longstanding persistent atrial fibrillation using a stepwise approach. J Cardiovasc Electrophysiol. 2012;23:1171–1178. 14. Jaïs P, Matsuo S, Knecht S, Weerasooriya R, Hocini M, Sacher F, Wright M, Nault I, Lellouche N, Klein G, Clémenty J, Haïssaguerre M. A deductive mapping strategy for atrial tachycardia following atrial fibrillation ablation: importance of localized reentry. J Cardiovasc Electrophysiol. 2009;20:480–491. 15. Yokokawa M, Sundaram B, Garg A, Stojanovska J, Oral H, Morady F, Chugh A. Impact of mitral isthmus anatomy on the likelihood of achieving linear block in patients undergoing catheter ablation of persistent atrial fibrillation. Heart Rhythm. 2011;8:1404–1410. 16. Narayan SM, Krummen DE, Shivkumar K, Clopton P, Rappel WJ, Miller JM. Treatment of atrial fibrillation by the ablation of localized sources: CONFIRM (Conventional Ablation for Atrial Fibrillation With or Without Focal Impulse and Rotor Modulation) trial. J Am Coll Cardiol. 2012;60:628–636. Key Words: Editorials ◼ atrial fibrillation ◼ atrial flutter ◼ atrial tachycardia ◼ catheter ablation

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Atrial Tachycardia After Ablation of Persistent Atrial Fibrillation: Is It Us or Them? Aman Chugh Circ Arrhythm Electrophysiol. 2013;6:1047-1049 doi: 10.1161/CIRCEP.113.001168 Circulation: Arrhythmia and Electrophysiology is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2013 American Heart Association, Inc. All rights reserved. Print ISSN: 1941-3149. Online ISSN: 1941-3084

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Atrial tachycardia after ablation of persistent atrial fibrillation: is it us or them?

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