Atrial Fibrillation–Atrial Flutter Interactions
Clinical Implications for Ablation
An appreciation of the article by Moreira et al in the current issue of Circulation1 requires an understanding of the close interrelationship between atrial fibrillation (AF) and atrial flutter (AFL). These authors have understood this interrelationship and applied it to their data to advance the approach to both AF and AFL ablation. Key to this understanding is the recognition that cavotricuspid isthmus (CTI)–dependent AFL almost always develops from antecedent AF of variable duration.2–5 This is because in almost all instances, it is during the AF that a functional line of block (LoB) necessary for the development of AFL forms between the superior and inferior vena cavae. This LoB acts as a critical lateral boundary that prevents short-circuiting of the AFL reentrant circuit. Thus, in the vast majority of instances, without preceding AF, there can be no AFL. The most recent additional support of this concept comes from the report by Ellis et al,6 which found that of 363 patients who presented with only CTI-dependent AFL and who underwent CTI ablation, long-term follow-up (mean of 39±11 months) demonstrated newly recognized AF in 82%. It also should be noted that, as Moreira et al1 recognize, in some patients, a LoB between the vena cavae may be fixed (ie, anatomic) rather than functional. In such patients, AF may not be required for AFL to develop.
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As Moreira et al1 further recognize, their report does not answer all the questions about the interrelationships of AF and AFL as they relate to AF ablation, but they do raise and consider relevant questions. The most fundamental question is a logical extension of understanding the development of classic, CTI-dependent AFL: ie, “Can the successful elimination of AF prevent the development of AFL?” If eliminating AF by ablation means successfully isolating pulmonary vein triggers that precipitate AF, the pathophysiology of AFL would lead one to expect that AFL would no longer occur. But because triggers may be at places other than the pulmonary veins, successful isolation of only the pulmonary veins may not be enough. Then, too, isolation of all the pulmonary veins may not always be possible or even be attempted. In fact, in the study by Moreira et al,1 the mean number of pulmonary veins isolated was 3.06 in patients with AFL and AF (group I) and 2.89 in patients with AF only (group II). Even in the most experienced hands, after catheter ablation of AF, there is at least a 10% to 20% AF recurrence rate, and a still higher rate during the early postablation 2- to 3-month blanking period.7 Thus, if AFL was present before AF ablation, one should expect AFL recurrence after ablation, too, unless CTI ablation was performed. This is what occurred in the study by Moreira et al1 and was the experience in 108 patients with both AF and AFL reported by Wazni et al.8 Interestingly, after the early postablation period, the AFL recurrence rate was only 8% during long-term follow-up in patients treated only with AF ablation in the study by Wazni et al,8 reflecting the much lower incidence of AF recurrence during late follow-up. Then, too, in the occasional patient with a fixed intercaval LoB, even a premature atrial beat that results from ventriculoatrial conduction of a premature ventricular beat could be enough to precipitate AFL. Lastly, if our knowledge of AF mechanisms improves such that ablation of a targeted atrial substrate alone, eg, of a driver causing fibrillatory conduction, is all that may be needed for some, if not most, to prevent sustained AF, the triggers, which would still be present, may precipitate brief episodes of AF (eg, due to multiple reentrant wavelets). This might be sufficient to generate a LoB between the vena cavae and, thereby, result in the development of AFL.
But it is quite striking that the same ablation team (ie, Moreira et al),1 using the same techniques to ablate paroxysmal AF (PAF) in all their patients, found a remarkable difference in success rates between group I (AF/AFL patients) and group II (only-AF patients). Although the authors did not restudy all of the patients with AF recurrence, one would not expect that the enormous difference in success rates for preventing AF (33% in group I versus 89% in group II) would be explained simply by a greater failure rate of pulmonary vein isolation in group I. So, the authors asked another important, relevant question: “Is common-type AFL a sign of an arrhythmogenic substrate in [patients with] PAF?” They suggest the answer is “yes,” and they well may be right. But it should be noted that Wazni et al8 had a far greater success rate (86%) of AF ablation in patients who also presented with AFL and in whom CTI ablation was performed in addition to pulmonary vein isolation.
In the context of considering the interrelationship of AF and AFL, one should ask, “Why don’t all patients who get AF also develop AFL?” It may be because they do not have that more extensive arrhythmogenic substrate. But, in the same context, why don’t patients who present with both AF and AFL only get AFL? And why don’t all patients who initially present with only AFL subsequently develop sustained AF after CTI ablation? Or do they all develop AF if they are followed up long enough? Citing again the recent study by Ellis et al,6 perhaps they mostly do. Ah, questions, questions, questions. Clearly, there is much more to understand.
Another question relates to the need to do a “prophylactic” CTI ablation in patients with PAF who present without any history of AFL. Although 5 (8%) of such patients in group II later presented with a new onset of CTI-dependent AFL, Moreira et al1 concluded that “preventive CTI ablation should not be included in the strategy for treatment of PAF.” All 5 of those patients underwent successful CTI ablation, but then, not surprisingly, manifested problematic recurrence of PAF. So, this really gets us back to the first question, because if the AF had been prevented, it is fair to assert that the AFL would not have developed. It seems to make sense that if the expected efficacy rate of AF ablation is ≥80% for PAF patients without AFL, prophylactic CTI ablation would mostly be unnecessary. Thus, most such patients would not needlessly be exposed to the small, but not zero, risk of CTI ablation without much likelihood of benefit, and an already long procedure would not needlessly be prolonged further. In fact, the recently issued consensus statement from the Heart Rhythm Society recommends that prophylactic CTI ablation not be performed in this group of patients.7
Finally, the present report also nicely serves to reemphasize the need to think mechanistically and to understand better the relationships of triggers and substrate in AF, and AFL as well. When we have understood these relationships, as with atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia, and, per the latter, Wolff-Parkinson-White syndrome, we have been exquisite in applying ablation techniques to the vulnerable substrate.
Sources of Funding
Dr Waldo is supported in part by grant R01 HL38408 from the United States Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, Bethesda, Md, by grant BRTT/WCI TECH 05-066 from the Ohio Wright Center of Innovations, a Third Frontier program from the State of Ohio, Columbus, Ohio, and by grants from the Jennie Zoline, Blue Dot, and Glenstone Foundations, Washington, DC.
Dr Waldo serves as a consultant for Biosense Webster and is on the scientific advisory board of Cryocor.
The opinions expressed in this editorial are not necessarily those of the editors or of the American Heart Association.
Moreira W, Timmermans C, Wellens HJJ, Mizusawa Y, Philippens S, Perez D, Rodriguez L-M. Can common-type atrial flutter be a sign of an arrhythmogenic substrate in paroxysmal atrial fibrillation? Clinical and ablative consequences in patients with coexistent paroxysmal atrial fibrillation/atrial flutter. Circulation. 2007; 116: 2786–2792.
Waldo AL. Mechanisms of atrial flutter and atrial fibrillation: distinct entities or two sides of a coin? Cardiovasc Res. 2002; 54: 216–229.
Ellis K, Wazni O, Marrouche N, Martin D, Gillinov M, McCarthy P, Saad EB, Bhargava M, Schweikert R, Saliba W, Bash D, Rossillo A, Erciyes D, Tchou P, Natale A. Incidence of atrial fibrillation post-cavotricuspid isthmus ablation in patients with typical atrial flutter: left-atrial size as an independent predictor of atrial fibrillation recurrence. J Cardiovasc Electrophysiol. 2007; 18: 799–802.
European Heart Rhythm Association (EHRA); European Cardiac Arrhythmia Society (ECAS); American College of Cardiology (ACC); American Heart Association (AHA); Society of Thoracic Surgeons (STS); Calkins H, Brugada J, Packer DL, Cappato R, Chen SA, Crijns HJ, Damiano RJ Jr, Davies DW, Haines DE, Haissaguerre M, Iesaka Y, Jackman W, Jais P, Kottkamp H, Kuck KH, Lindsay BD, Marchlinksi FE, McCarthy PM, Mont JL, Morady F, Nademanee K, Natale A, Pappone C, Prystowsky E, Raviele A, Ruskin JN, Shemin RL. HRS/EHRA/ECAS expert consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for personnel, policy, procedures and follow-up: a report of the Heart Rhythm Society (HRS) Task Force on catheter and surgical ablation of atrial fibrillation. Heart Rhythm. 2007; 4: 816–861.
Wazni O, Marrouche NF, Martin DO, Gillinov AM, Saliba W, Saad E, Klein A, Bhargava M, Bash D, Schweikert R, Erciyes D, Abdul-Karin A, Brachman J, Gunther J, Pisano E, Potenza D, Fanelli R, Natale A. Randomized study comparing combined pulmonary vein–left atrial junction disconnection and cavotricuspid isthmus ablation versus pulmonary vein–left atrial junction disconnection alone in patients presenting with typical atrial flutter and atrial fibrillation. Circulation. 2003; 108: 2479–2483.