EDITORIAL COMMENT
Atrial Fibrillation Catheter AblationLearning by Burning Continues*
Francis E. Marchlinski, MD, FACC*
Cardiovascular Division, Department of Medicine, Section of Cardiac Electrophysiology, Hospital of the University of Pennsylvania, Philadelphia, Pennsylvania.
* Reprint requests and correspondence: Dr. Francis E. Marchlinski, 9 Founders Pavilion, Hospital of University of Pennsylvania, 3400 Spruce Street, Philadelphia, Pennsylvania 19104. (Email: francis.marchlinski{at}uphs.upenn.edu).
With the widespread use of catheter ablation directed at eliminating atrial fibrillation (AF), there has been concern that there would be little additional attention paid to a further understanding of the physiological basis of this important arrhythmia. Reports on new catheter and energy delivery designs and techniques for improving outcome on the basis of catheter-based empiric placement of lines or "debulking the atria" would mimic the 20 years of experience with the surgical maze procedure. Reports on the "the best" empiric lesion set would rule the day, and efforts to understand and clarify physiological observations would become a rarity.
The expression of concern, although important, may be overstated, as exemplified by the important observations reported in this issue of the Journal by Takahashi et al. (1). Destruction of atrial anatomy with catheter-tip-based radiofrequency energy is relatively discrete. Attention to the details of the intracardiac electrogram recordings at the time of a dramatic ablation effect such as AF termination, coupled with localizing the anatomical location of the catheter tip, provides us with a unique learning opportunity that is somewhat reminiscent of the large body of new physiological information acquired during catheter ablation of other atrial arrhythmias (2).
This specific group of investigators has done much to establish physiological end points and electrogram-based targets for pulmonary vein (PV) isolation and techniques for confirming lines of block when creating linear left atrial lesions (3–5). In the current report, they extend their efforts and define electrogram signal characteristics associated with a defined ablation effect manifest by slowing of the rate of fibrillation, as indexed by recordings in the left and right atrial appendices and/or transition of chronic AF to unimorphic atrial tachycardia or sinus rhythm (1). In a carefully designed prospective study, the authors initially performed PV isolation and created a roof line with confirmed block. They then selected specific anatomical sites outside the PVs for recording and ablation and randomized the initial and subsequent recording and ablation of these anatomical targets so that they could be equally weighted. The authors observed that electrogram characteristics associated with the defined "ablation effect" were characterized as being more continuous over a 4-s recording window. If discrete noncontinuous electrograms were present, they were more likely to demonstrate a consistent gradient of repetitive activation from the distal to proximal recording of the 2 pairs of recording electrodes from the ablation catheter tip.
Importantly, these electrogram observations were consistent both for slowing and/or termination of AF with radiofrequency energy application, suggesting a common link. Also of note was the fact that these electrograms with the dramatic ablation response seemed to be more commonly recorded from the left atrial septum and orifice of the left atrial appendage sites. However, just as remarkable was that these types of electrograms and the desired ablation effect were seen in all sampled areas of the left atrium. Furthermore, they had a relatively low predictive value for identifying a site likely to produce a desired ablation effect.
As with many scientific observations of interest, more questions are frequently raised than are answered. Is AF termination uniformly preceded by slowing? Is it the sum of ablation of sites with the specified electrogram characteristics rather than ablation at a single specific site that produces the desired ablation response? Were PV isolation and the formation of roof line essential components of the observed electrophysiological effect when ablating the specified electrogram targets? Because nearly two-thirds of the ablation sites did not create an "ablation effect," was their ablation truly unnecessary and potentially detrimental, or did their ablation contribute somehow to the ultimate observation of acute AF termination? Did the ablation of the sites not associated with the observed ablation effect contribute to the long-term elimination of AF? Can the sites with the described electrogram characteristics demonstrate a more specific and relevant response to ablation if stable electrogram recordings are noted for a longer duration? How stable are these electrogram observations? Do the changes in cycle length in the left and right atrial appendage always parallel each other? Can the slowing of the rate in these structures be related to amputating access with the ablation from higher frequency areas rather than a direct effect that uniformly predicts termination? Ablation of the left atrial septum may decrease access via Bachmann’s bundle to the right atrial appendage, and ablation anywhere in proximity to the left atrial appendage surely might decrease wave front access to the left atrial appendage and influence the rate. These are some obvious considerations that must be thoroughly investigated to further unravel the physiological links suggested by the reported observations.
Undisputedly, the termination of chronic AF observed nearly uniformly in the study population is of fundamental importance. Even more remarkable was the fact that outcome was marked by the frequent recurrence of atrial tachycardias, many focal, but not fibrillation. This outcome in patients with chronic forms of AF is truly important given the fact that the investigators targeted a very limited and specific number of left atrial anatomical sites for recording and ablation in the protocol as described. The results suggest an imminent deciphering not only of signal characteristics associated with AF termination with ablation but, even more importantly, a further understanding of the electrophysiological and possibly anatomical basis for the maintenance of AF.
Importantly, the success of the described procedure does not yet eliminate the potential for successful AF control, even in the most persistent forms of AF with the permanent isolation of PVs. Persistent PV isolation has been a daunting challenge that has been met with the requirement of repeated isolation procedures in many patients (6). Admittedly, adjunctive, non-PV ablation seems to be required in many patients, but the selection of the appropriate patient remains a challenge, and the exact target still needs to be elucidated. Provocable non-PV triggers initiating AF, autonomic ganglia, and unique electrogram targets have all been suggested (2,7–9). It is interesting to speculate, given the similarity of the anatomical distribution of these targets, whether, at least in some patients, these suggested targets could represent different manifestations of a very localized and physiologically-based system responsible for the initiation and/or maintenance of AF.
Clearly, the debate must continue, and the search for reliable and reproducible targets and end points must continue. Of note, it was only recently (10) that a consensus was established regarding the importance of PV isolation as the backbone to the vast majority of AF ablation procedures. But even with PV isolation, there remains a general disagreement on the need to check for exit block with pacing from a multipolar catheter and the requirement to revisit the PVs to check for acute reconnection before withdrawing the catheters from the left atrium (11,12). Any technique that helps to confirm isolation and enhance persistent isolation of the PVs must be advocated, but proof of the technique’s value should be demonstrated with rigorous confirmatory studies (13).
Finally, the role of provocative maneuvers in the ablation of all forms of AF clearly needs to be established. Both burst atrial pacing and the infusion of high doses of isoproterenol have been used to help establish when more ablating is required beyond PV isolation (6,14). Do these techniques truly mimic physiological events as suggested, or do they create the apparent need for additional lesions but in actuality bear no relevance to clinical arrhythmia episodes? In the study population with chronic AF described by Takahashi et al. (1) with acute AF termination and rare AF during follow-up, it would have been of interest to see whether AF was still inducible. The absence of inducibility would have been another strong piece of evidence that, even acutely, the maintenance of AF had been prevented by the ablation. In addition, it is also possible that some of the focal tachycardias observed in follow-up in that study could have been provoked with isoproterenol and acutely targeted.
Takahashi et al. (1) appear to be leading the charge in the quest to transition from empiric lesions to physiologically based ablation. But our understanding still remains primitive, and fundamental observations regarding electrogram characteristics and their role in the maintenance of AF and the observed clinical response remain speculative. Clearly, some of the first steps in "learning by burning" during AF ablation have been taken. We have to push forward and remain diligent in the quest for reproducibility and detail, create studies to answer questions raised by initial seminal observations, respect prospective and randomized study design more than a report on good outcome with an empiric technique, and, most importantly, remain dedicated to defining the physiology (1,15–17). It is, after all, why we entered the field and enjoy the designation of electrophysiologist. Ultimately, this quest will lead to what is best for our patients and allow for AF ablation techniques that have reliable and predictable targets and reproducible end points based on fundamental electrophysiological principles and a real understanding of AF initiation and maintenance.
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Footnotes
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* Editorials published in the Journal of the American College of Cardiology reflect the views of the authors and do not necessarily represent the views of JACC or the American College of Cardiology. 
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References
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1. Takahashi Y, O’Neill, MD, Hocini M, et al. Characterization of electrograms associated with termination of chronic atrial fibrillation by catheter ablation J Am Coll Cardiol 2008;51:1003-1010.[Abstract/Free Full Text]2. Callans DJ, Schwartzman D, Gottlieb CD, Marchlinski FE. Insights into the electrophysiology of atrial arrhythmias gained by the catheter ablation experience: "learning while burning, part II." J Cardiovasc Electrophysiol 1995;6:229-243.[Medline] 3. Haissaguerre M, Jais P, Shah DC, et al. Electrophysiological end point for catheter ablation of atrial fibrillation initiated from multiple pulmonary venous foci Circulation 2000;28:1011409–17. 4. Jais P, Hocini M, Hsu LF, et al. Technique and results of linear ablation at the mitral isthmus Circulation 2004;110:2996-3002.[Abstract/Free Full Text] 5. Hocini M, Jais P, Sanders P, et al. Techniques, evaluation, and consequences of linear block at the left atrial roof in paroxysmal atrial fibrillation: a prospective randomized study Circulation 2005;112:3688-3696.[Abstract/Free Full Text] 6. Callans DJ, Gerstenfeld EP, Dixit S, et al. Efficacy of repeat pulmonary vein isolation procedures in patients with recurrent atrial fibrillation J Cardiovasc Electrophysiol 2004;15:1050-1055.[CrossRef][Web of Science][Medline] 7. Lee SH, Tai CT, Hsieh MH, et al. Predictors of non-pulmonary vein ectopic beats initiating paroxysmal atrial fibrillation: implication for catheter ablation J Am Coll Cardiol 2005;46:1054-1059.[Abstract/Free Full Text] 8. 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;43:2044-2053.[Abstract/Free Full Text] 9. Scherlag BJ, Nakagawa H, Jackman WM, et al. Electrical stimulation to identify neural elements on the heart: their role in atrial fibrillation J Interv CardiolElectrophysiol 2005;13(Suppl 1):37-42. 10. Calkins H, Brugada J, Packer DL, et al. Consensus statement on catheter and surgical ablation of atrial fibrillation: recommendations for personnel, policy, procedures and follow-up Heart Rhythm 2007;4:816-861.[CrossRef][Web of Science][Medline] 11. Gerstenfeld EP, Callans D, Dixit S, et al. Utility of exit block for identifying electrical isolation of the pulmonary veins J Cardiovasc Electrophysiol 2002;13:971-979.[CrossRef][Web of Science][Medline] 12. Sauer WH, McKernan ML, Lin D, et al. Clinical predictors and outcomes associated with acute return of pulmonary vein conduction during pulmonary vein isolation for treatment of atrial fibrillation Heart Rhythm 2006;3:1024-1028.[CrossRef][Medline] 13. Essebag V, Baldessin F, Reynolds MR, et al. Noninducibility post-pulmonary vein isolation achieving exit block predicts freedom from atrial fibrillation Eur Heart J 2005;26:2550-2555.[Abstract/Free Full Text] 14. Jais P, Hocini M, Sanders P, et al. Long-term evaluation of atrial fibrillation ablation guided by noninducibility Heart Rhythm 2006;3:140-145.[CrossRef][Web of Science][Medline] 15. Jais P, Hocini M, MacLe L, et al. Distinctive electrophysiological properties of pulmonary veins in patients with atrial fibrillation Circulation 2002;106:2479-2485.[Abstract/Free Full Text] 16. Dixit S, Gerstenfeld EG, Callans DJ, Marchlinski FE. Mechanisms underlying sustained firing from pulmonary veins Pacing Clin Electrophysiol 2004;27:1120-1129.[CrossRef][Medline] 17. Gerstenfeld EP, Callans DJ, Sauer W, Jacobson J, Marchlinski FE. Reentrant and nonreentrant focal left atrial tachycardias after pulmonary vein isolation Heart Rhythm 2005;2:1195-2002.[CrossRef][Web of Science][Medline]
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