Europace

Europace 2007 9(6):335-379; doi:10.1093/europace/eum120

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Copyright [2007] by the Heart Rhythm Society and the European Heart Rhythm Association, registered branch of the European Society of Cardiology

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CONSENSUS STATEMENT

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 Developed in partnership with the European Heart Rhythm Association (EHRA) and the European Cardiac Arrhythmia Society (ECAS); in collaboration with the American College of Cardiology (ACC), American Heart Association (AHA), and the Society of Thoracic Surgeons (STS). Endorsed and Approved by the governing bodies of the American College of Cardiology, the American Heart Association, the European Cardiac Arrhythmia Society, the European Heart Rhythm Association, the Society of Thoracic Surgeons, and the Heart Rhythm Society.

Hugh Calkins, MD, FHRS, Josep Brugada, MD, FESC, Douglas L. Packer, MD, FHRS, Riccardo Cappato, MD, FESC, Shih-Ann Chen, MD, FHRS, Harry J.G. Crijns, MD, FESC, Ralph J. Damiano, Jr, MD, D. Wyn Davies, MD, FHRS, David E. Haines, MD, FHRS, Michel Haissaguerre, MD, Yoshito Iesaka, MD, Warren Jackman, MD, FHRS, Pierre Jais, MD, Hans Kottkamp, MD, Karl Heinz Kuck, MD, FESC, Bruce D. Lindsay, MD FHRS, Francis E. Marchlinski, MD, Patrick M. McCarthy, MD, J. Lluis Mont, MD, FESC, Fred Morady, MD, Koonlawee Nademanee, MD, Andrea Natale, MD, FHRS, Carlo Pappone, MD, PhD, Eric Prystowsky, MD, FHRS, Antonio Raviele, MD, FESC, Jeremy N. Ruskin, MD and Richard J. Shemin, MD

TASK FORCE MEMBERS, Hugh Calkins, MD, FHRS, Chair, Josep Brugada, MD, FESC, Co-Chair, EHRA representative, Section Chairs, Atrial Fibrillation: Definitions, Mechanisms, and Rationale for Ablation, Shih-Ann Chen, MD, FHRS, Indications for Ablation and Patient Selection, Eric N. Prystowsky, MD, FHRS, Techniques and Endpoints for Atrial Fibrillation, Karl Heinz Kuck, MD, FESC, Technologies and Tools, Andrea Natale, MD, FHRS, ACC representative, Other Technical Aspects, David E. Haines, MD, FHRS, Chair, Follow-up Considerations, Francis E. Marchlinski, MD, Outcomes and Efficacy of Catheter Ablation of Atrial Fibrillation, Hugh Calkins, MD, FHRS, Complications of Atrial Fibrillation Ablation, D. Wyn Davies, MD, FHRS, Training Requirements and Competencies, Bruce D. Lindsay, MD, FHRS, AHA representative, Surgical Ablation of Atrial Fibrillation, Patrick M. McCarthy, MD, STS representative, Clinical Trial Considerations and Douglas L. Packer, MD, FHRS

Johns Hopkins Hospital, Maryland, USA; Hospital Clinic, University of Barcelona, SPAIN; Taipei Veterans General Hospital, TAIWAN; The Care Group, LLC, Indiana, USA; Allgemeines Krankenhaus St. Georg, Hamburg, GERMANY; Cleveland Clinic Foundation, Ohio, USA; William Beaumont Hospital, Michigan, USA; Hospital of the University of Pennsylvania, USA; Johns Hopkins Hospital, Maryland, USA; St. Mary's Hospital, London, ENGLAND; Washington University School of Medicine Missouri, USA; Feinberg School of Medicine, Illinois, USA; Mayo Foundation, Minnesota, USA

Co-Authors, Riccardo Cappato, MD, FESC, ECAS representative, Harry J.G. Crijns, MD, PhD, FESC, Ralph J. Damiano, Jr, MD, Michel Haissaguerre, MD, Warren M. Jackman, MD, FHRS, Pierre Jais, MD, Yoshito Iesaka, MD, Hans Kottkamp, MD, Lluis Mont, MD, Fred Morady, MD, Koonlawee Nademanee, MD, Carlo Pappone, MD, PhD, Antonio Raviele, MD, FESC, Jeremy N. Ruskin, MD and Richard J. Shemin, MD

Arrhythmia and EP Center, Milan, ITALY; University Hospital Maastricht, THE NETHERLANDS; Washington University School of Medicine, Missouri, USA; Université De Bordeaux, Hôpital Cardiologique, FRANCE; University of Oklahoma Health Science Center, USA; Université De Bordeaux, Hôpital Cardiologique, FRANCE; Tsuchiura Kyodo Hospital, JAPAN; Clinic Hirslanden Zurich, SWITZERLAND; FESC Hospital Clinic, University of Barcelona, SPAIN; University of Michigan Hospital, USA; Pacific Rim EP Research Institute Center, California, USA; Hospital San Raffaele, Milano, ITALY; Umberto I Hospital, Venice, ITALY; Massachusetts General Hospital, USA; David Geffen School of Medicine at UCLA, California, USA

	I. Introduction

Top I. Introduction II. Atrial fibrillation:... III. Indications for catheter... IV. Techniques and endpoints... V. Technologies and tools VI. Other technical aspects VII. Follow-up considerations VIII. Outcomes and efficacy... IX. Complications of atrial... X. Training requirements and... XI. Surgical ablation of... XII. Clinical trial... XIII. Conclusion References

 
During the past decade, catheter ablation of atrial fibrillation (AF) has evolved rapidly from a highly experimental unproven procedure, to its current status as a commonly performed ablation procedure in many major hospitals throughout the world. Surgical ablation of AF, using either standard or minimally invasive techniques, is also performed in many major hospitals throughout the world.

The purpose of this Consensus Statement is to provide a state-of-the-art review of the field of catheter and surgical ablation of AF, and to report the findings of a Task Force, convened by the Heart Rhythm Society and charged with defining the indications, techniques, and outcomes of this procedure. The Heart Rhythm Society was pleased to develop this Consensus Statement in partnership with the European Heart Rhythm Association and the European Cardiac Arrhythmia Society.

This statement summarizes the opinion of the Task Force members based on their own experience in treating patients, as well as a review of the literature, and is directed to all health care professionals who are involved in the care of patients with AF, particularly those who are undergoing or are being considered for catheter or surgical ablation procedures for AF. This statement is not intended to recommend or promote catheter ablation of AF. Rather the ultimate judgment regarding care of a particular patient must be made by the health care provider and patient in light of all the circumstances presented by that patient.

In writing a "consensus" document, it is recognized that consensus does not mean that there was complete agreement among all Task Force members. We attempted to identify those aspects of AF ablation for which a true "consensus" could be identified (Tables 1 and 2). Surveys of the entire Task Force were used to identify these areas of consensus. The main objective of this document is to improve patient care by providing a foundation of knowledge for those involved with catheter ablation of AF. It is recognized that this field continues to evolve rapidly; as this document was being prepared, further clinical trials of catheter and surgical ablation of AF were underway.

View this table: [in this window] [in a new window]   Table 1 Areas of Consensus: Definitions, Indications, Technique, and Laboratory Management

 

View this table: [in this window] [in a new window]   Table 2 Areas of Consensus: Post procedure, Follow-up, and Clinical Trial Considerations

 
The Task Force writing group was composed of experts representing six organizations: the American College of Cardiology (ACC), the American Heart Association (AHA), the European Cardiac Arrhythmia Society (ECAS), the European Heart Rhythm Association (EHRA), the Society of Thoracic Surgeons (STS), and the Heart Rhythm Society (HRS). All members of the Task Force, as well as peer reviewers of the document, were asked to provide disclosure statements of all relationships that might be perceived as real or potential conflicts of interest. These tables are shown at the end of this document.

	II. Atrial fibrillation: definitions, mechanisms, and rationale for ablation

Top I. Introduction II. Atrial fibrillation:... III. Indications for catheter... IV. Techniques and endpoints... V. Technologies and tools VI. Other technical aspects VII. Follow-up considerations VIII. Outcomes and efficacy... IX. Complications of atrial... X. Training requirements and... XI. Surgical ablation of... XII. Clinical trial... XIII. Conclusion References

 
Definitions
AF is a common supraventricular arrhythmia that is characterized by chaotic and uncoordinated contraction of the atrium. The common electrocardiographic (ECG) manifestations of AF include the presence of irregular fibrillatory waves and, in patients with intact atrioventricular conduction, the presence of an irregular ventricular response. Although there are several classification systems for AF, for this consensus document we have adopted the classification system that was developed by the ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation (AF).¹ We recommend that this classification system be used for future studies of catheter and surgical ablation of AF.

Paroxysmal AF is defined as recurrent AF (2 episodes) that terminates spontaneously within seven days (Table 1). Persistent AF is defined as AF which is sustained beyond seven days, or lasting less than seven days but necessitating pharmacologic or electrical cardioversion. Included within the category of persistent AF is "longstanding persistent AF" which is defined as continuous AF of greater than one year duration. The term permanent AF is defined as AF in which cardioversion has either failed or not been attempted. The term permanent AF is not appropriate in the context of patients undergoing catheter and/or surgical ablation of AF as it refers to a group of patients where a decision has been made not to pursue restoration of sinus rhythm by any means, including catheter or surgical ablation. As noted in the ACC/AHA/ESC 2006 Guidelines, it is recognized that a particular patient may have AF episodes that fall into one or more of these categories. It is recommended that patients be categorized by their most frequent pattern of AF. These AF definitions apply only to AF episodes which are of at least 30 seconds' duration and do not have a reversible cause such as acute pulmonary disease and hyperthyroidism.

It is recognized by the consensus Task Force that these definitions of AF are very broad, and that when describing a population of patients undergoing AF ablation, additional detail should be provided. This is especially important when considering the category of persistent AF. In particular, investigators are urged to specify the duration of time patients have spent in continuous AF prior to an ablation procedure, and also to specify whether patients undergoing AF ablation have previously failed pharmacologic therapy, electrical cardioversion, or both.

Mechanisms of atrial fibrillation
For many years, three major schools of thought competed to explain the mechanism(s) of AF: multiple, random propagating wavelets; focal electrical discharges; and localized reentrant activity with fibrillatory conduction.² Considerable progress has been made in defining the mechanisms of initiation and perpetuation of AF.^3–9 Perhaps the most striking breakthrough was the recognition that, in a subset of patients, AF was triggered by a rapidly firing focus and could be "cured" with a catheter ablation procedure.^10–12 This landmark observation compelled the arrhythmia community to refocus its attention on the pulmonary veins (PVs) and the posterior wall of the left atrium (LA), as well as the autonomic innervation in that region (Figure 1). It also reinforced the concept that the development of AF requires a "trigger" and an anatomic substrate capable of both initiation and perpetuation of AF.

View larger version (65K): [in this window] [in a new window] [Download PowerPoint slide]   Figure 1 Structure and mechanisms of atrial fibrillation. (A) Schematic drawing of the left and right atria as viewed from the posterior. The extension of muscular fibers onto the PVs can be appreciated. Shown in yellow are the four major LA autonomic ganglionic plexi and axons (superior left, inferior left, anterior right, and inferior right). Shown in blue is the coronary sinus which is enveloped by muscular fibers which have connections to the atria. Also shown in blue is the vein and ligament of Marshall which travels from the coronary sinus to the region between the left superior PV and the LA appendage. (B) Large and small reentrant wavelets that play a role in initiating and sustaining AF. (C) Common locations of PV (red) and also the common sites of origin of non PV triggers (shown in green). (D) Composite of the anatomic and arrhythmic mechanisms of AF. (Adapted from Circulation,13 Am J Cardiol,336 and Tex Heart Inst J.337)

 
In this section of the document, a contemporary understanding of the mechanisms of AF is summarized. As illustrated in Figure 2, some authors² have proposed that, in the presence of an appropriate heterogeneous AF substrate, a focal trigger can result in sustained high frequency reentrant AF drivers (rotors). The waves that emerge from the rotors undergo spatially distributed fragmentation and give rise to fibrillatory conduction.^13–15 Evidence suggests that when high frequency atrial activation is maintained for relatively long time periods, ion channel remodeling changes the electrophysiologic substrate^6–9 and increases the role of triggers further contributing to AF permanence. Sustained high rates in the atrium and/or the presence of heart disease are associated with structural remodeling of the atria and alter the substrate even further^6,8 and help to perpetuate AF. Although much has been learned about the mechanisms of AF, they remain incompletely understood. Because of this, it is not possible to precisely tailor an ablation strategy to a particular AF mechanism.

View larger version (50K): [in this window] [in a new window] [Download PowerPoint slide]   Figure 2 Focal triggers leading to initiation of reentry, Schematic drawing which illustrates the manner in which focal triggers lead to initiation of reentry (rotors). Eventually, atrial remodeling leads to additional focal triggers and perpetuation of reentry.

 
Multiple wavelet hypothesis
Until the mid to late 1980s, the multiple wavelet hypothesis for AF was widely accepted as the dominant AF mechanism.¹⁶ This hypothesis was developed by Moe and colleagues and subsequently confirmed by experimental work.¹⁷ According to this hypothesis, AF results from the presence of multiple reentrant wavelets occurring simultaneously in the left and right atria. According to this model, the number of wavelets at any point in time depends on the atrial conduction velocity, refractory period, and mass. Perpetuation of AF is favored by slowed conduction, shortened refractory periods, and increased atrial mass. Enhanced spatial dispersion of refractoriness promotes reentry by conduction block and conduction delay. It is notable that the development of the surgical Maze procedure was predicated on this model of AF and the concept that maintenance of AF requires a critical number of circulating reentrant wavelets, each of which requires a critical mass of atrial tissue.¹⁸

Focal triggers
Haissaguerre and colleagues are credited with making the landmark observation that AF is often triggered by a focal source, and that ablation of that focal trigger can eliminate AF.^10–12 This observation was reported in a series of three manuscripts. An initial series of three patients who underwent successful catheter ablation of AF was published in 1994.¹⁰ In each of these patients, AF was determined to arise from a "focal source." The successful treatment of these three patients with catheter ablation suggested that in some patients, AF may result from a focal trigger and that ablation of this trigger could eliminate AF. It is notable that prior research in an animal model had demonstrated that AF could be induced by local administration of aconitine which triggered a rapid focal atrial tachycardia.¹⁹ This type of "focal AF" also was shown to be cured by isolation of the site of the aconitine-induced focal atrial tachycardia from the remainder of the atria. In a subsequent report on 45 patients with frequent drug-refractory episodes of AF, Haissaguerre and colleagues found that a purely right-sided linear ablation approach resulted in an extremely low long-term success rate.²⁰ These investigators also found that linear lesions were often arrhythmogenic due to gaps in the ablative lines, and that many patients were ultimately cured with ablation of a single rapidly firing ectopic focus. These ectopic foci were found at the orifices of the left or right superior PVs or near the superior vena cava. The latter observation led these investigators to systematically attempt cure of paroxysmal AF by mapping and ablating individual foci of ectopic activity.^11,12 Many of these foci were found well into the PVs, outside of the cardiac silhouette, where myocardial sleeves are known to extend.²¹ These observations of the importance of a focal trigger in the development of AF have been confirmed by others. Thus, it is now well established that the PVs appear to be a crucial source of triggers which initiate AF.

Electrophysiology of the pulmonary veins
Nathan and Eliakim are credited with first drawing attention to the presence of sleeves of cardiac tissue that extend onto the PVs (Figure 1).²¹ The electrophysiologic properties of the PVs and also the sleeves of myocardial tissue that extend onto the superior and inferior vena cava were studied in animal models by investigators who noted that AF was recorded from these thoracic veins.²² Despite these very early observations, detailed investigation of the anatomic and electrophysiologic properties of the PVs remained unexplored for many decades, until the importance of PV triggers in the development of AF was appreciated. There is now general agreement that myocardial muscle fibers extend from the LA into all the PVs for a length of one to three centimeters; the thickness of the muscular sleeve is highest at the proximal end of the veins (1–1.5 mm), and then gradually tapers distally.^23,24

It is also recognized that the muscular sleeves of the PVs are an important source of focal firing that may trigger or maintain AF. The mechanisms of this focal firing are incompletely understood. Whereas classical cardiac anatomists do not feel that specialized conduction cells or tissues are present in the PV muscular sleeves, other more recent studies have arrived at different conclusions. It is notable that the location of the precursors of the conduction system are defined, during embryological development of the heart, by the looping process of the heart tube.²⁵ Specialized conduction tissue, which is derived from the heart tube and is destined to have pacemaker activity, has been shown to be located within the myocardial sleeves of the PVs.^25,26 One recent study demonstrated the presence of P cells, transitional cells, and Purkinje cells in the human PVs.²⁷ The presence of these tissues provides an explanation for the observation that electrical activity within the PVs is commonly observed after electrical disconnection of the PVs' musculature from the atrium.^26–28 Further studies identified spontaneous electrical activity with phase 4 depolarization in the PVs of guinea pigs.²⁹ In this model, administration of digitalis induced triggered activity in guinea pig PV tissue preparations with the genesis of atrial tachyarrhythmias. More recent studies have isolated cardiomyocytes from rabbit and canine PVs and identified the abnormal automaticity and triggered activity after isoproterenol infusion.³⁰ Abnormal regulation of calcium current and sodium–calcium exchanger has been identified as the major mechanism of PV focal arrhythmogenicity.

Other studies have provided evidence to suggest that the PVs and the posterior LA are also a preferred site for reentrant arrhythmias.^14,31 One study, for example, examined the electrophysiologic properties of 45 PVs from 33 dogs. Optical mapping techniques were used to study the electrical properties of the veins.³¹ Action potential duration was shown to be longer in the endocardium of these PVs as compared with the epicardium. In addition, these investigators reported that the action potential duration of the PVs was shorter than in the atrium. This study also demonstrated marked slowing of conduction in the proximal portion of the PV as compared with the adjacent atrial tissue. With rapid atrial pacing, 2:1 conduction block into the veins was observed. These findings led the authors to propose that AF resulted from a focal trigger arising from within the PVs and was maintained as a rapid reentrant circuit within the PVs. A somewhat different approach was used by other authors who used a blood perfused heart preparation to examine the electrophysiologic characteristics of the PVs.³² Intracellular and extracellular recordings were obtained. These authors identified zones of conduction delay in all PVs. Fractionated signals were also found in areas of slow conduction. They also examined PV histology and reported that these zones of slow conduction were related to sudden changes in fiber orientation. These changes could facilitate reentry. Yet another study examined the impact of increasing atrial pressure on PV activation.³³ They reported that as LA pressure was increased above 10 cm H₂O, the LA–PV junction became the source of dominant rotors. These observations help explain the clinical link between AF and increased atrial pressure.

Several studies have reported shorter refractory period inside PVs compared to the LA, decremental conduction inside PVs, and easy induction of PV reentry with premature stimulation from the PVs. And other studies have demonstrated the presence of rapid reentrant activities with entrainment phenomenon inside the human PVs after successful PV isolation as well as the important role of PV–LA junction reentry in maintenance of AF.^34,35 However, despite ample evidence to support the understanding that PVs and the PV–LA junction provide the reentrant substrate for AF, the mechanism underlying the very first beat of spontaneous PV firing which initiates AF remains poorly understood. One study investigated the effects of ibutilide on PV firing using a canine model of pacing-induced AF. Ibutilide suppressed reentry at the PV–LA junction but not PV firing, indicating that PV firing is due to a non-reentrant mechanism.³⁶

Left-to-right frequency gradients in atrial fibrillation organization
A number of well conducted experimental and clinical studies have appeared over the last several years demonstrating the importance of the local atrial activation rate (cycle length) in the maintenance of AF,^37–41 the role of atrial remodeling in the perpetuation of AF,^6–9 the importance of wavebreak and reentry in the posterior LA,⁴² and the existence of a hierarchical organization and left-to-right gradients of the electrical excitation frequency both in animals^39,43 and in humans.^37,40,41 Such studies offer mechanistic rationale for the empirical observation by clinical electrophysiologists that the LA is the region that seems to harbor the AF sources in the majority of patients.⁴¹ They also afford an explanation for the need for circumferential and linear ablation, as well as other anatomic approaches that not only include the PVs but also a large portion of the LA. Inclusion of the atrial myocardium in ablation strategies is particularly important in patients with persistent AF, who in fact represent the vast majority of patients presenting the arrhythmia. Recent data in patients provide compelling evidence that the sources are in fact reentrant and are located outside of the PVs.⁴⁴ Other studies in patients have used power spectral analysis and mapping to localize dominant frequency sites of activation.⁴¹ They demonstrated that in paroxysmal AF patients the PV ostial region does harbor the highest frequency sites and AF can be terminated successfully by targeting radiofrequency (RF) ablation to those sites in up to 87% of patients.⁴¹ However, in longstanding persistent AF patients it is rare to find dominant frequency sites at the PV region and this agrees well with the relatively poor success rate of RF ablation in such patients.⁴¹ The data suggest that in patients with longstanding persistent AF, atrial remodeling somehow augments the number of AF drivers and shifts their location away from the PV/ostial region. Therefore, while eliminating focal triggers is sensible, evidence in the clinic and the laboratory demonstrates that focusing on understanding mechanisms of AF initiation, maintenance and perpetuation in the atrial muscle proper is of utmost importance if one wants to increase the success of therapy in the majority of patients.

Cardiac autonomic nervous system and triggered spontaneous pulmonary vein firing
It has been shown that an increase in both sympathetic and parasympathetic tone precedes the onset of paroxysmal AF in many patients.⁴⁵ A subsequent study demonstrated that although both sympathetic and parasympathetic components play a role in AF, the cholinergic component appears to be the main factor for spontaneous AF initiation in an open-chest canine model.⁴⁶ Using a superfused canine PV preparation, other authors described rapid PV triggered firing initiated by delivering high frequency electrical stimulation to the PV preparation during atrial refractory periods. Such triggered firing depends on both the sympathetic and parasympathetic components of the cardiac autonomic nervous system.⁴⁷ Moreover, spontaneous PV firing followed by AF could be induced by electrical stimulation of the ganglionic plexi (GP) or the autonomic nerve endings that retrogradely activate the GP and initiate AF from the PV–LA junction.⁴⁸ These findings provide experimental evidence that the intrinsic cardiac autonomic nervous system facilitates the formation of triggered PV firing that either initiates AF or initiates reentry, which subsequently induces AF.

Electrophysiologic basis for catheter ablation of atrial fibrillation
It is well accepted that the development of AF requires both a trigger and a susceptible substrate. The goals of AF ablation procedures are to prevent AF by either eliminating the trigger that initiates AF or by altering the arrhythmogenic substrate. The most commonly employed ablation strategy today, which involves the electrical isolation of the PVs by creation of circumferential lesions around the right and the left PV ostia, probably impacts both the trigger and substrate of AF (Figure 3).^49–51 In particular, this approach seeks to electrically isolate the PVs, which are the most common site of triggers for AF. Other less common trigger sites for AF, including the vein and ligament of Marshall and the posterior LA wall, are also encompassed by this lesion set. The circumferential lesions may also alter the arrhythmogenic substrate by elimination of tissue located near the atrial–PV junction that provides a substrate for reentrant circuits that may generate or perpetuate AF, and/or by reduction of the mass of atrial tissue needed to sustain reentry.⁵² And finally, the circumferential lesion set may interrupt sympathetic and parasympathetic innervation from the autonomic ganglia, which have been identified as potential triggers for AF (Figure 1).^53,54

View larger version (60K): [in this window] [in a new window] [Download PowerPoint slide]   Figure 3 Schematic of common lesion sets employed in AF ablation. (A) Circumferential ablation lesions, which are created in a circumferential fashion around the right and the left PVs. The primary endpoint of this ablation strategy is the electrical isolation of the PV musculature. (B) Some of the most common sites of linear ablation lesions. These include a "roof line" connecting the lesions encircling the left and and/or right PVs, a "mitral isthmus" line connecting the mitral valve and the lesion encircling the left PVs at the level of the left inferior PV, and an anterior linear lesion connecting either the "roof line" or the left or right circumferential lesion to the mitral annulus anteriorly. Also shown is a linear lesion created at the cavotricuspid isthmus. This lesion is generally placed in patients who have experienced cavotricuspid isthmus dependent atrial flutter clinically or have it induced during EP testing. (C) Similar to B but also shows the addition of additional linear ablation lesions between the superior and inferior PVs resulting in a figure of 8 lesion set. Also shown is an encircling lesion of the superior vena cava directed at electrical isolation of the superior vena cava. SVC isolation is performed if focal firing from the SVC can be demonstrated. A subset of operators empirically isolate the SVC. (D) Some of the most common sites of ablation lesions when complex fractionated electrograms are targeted. (Adapted from Circulation,21 Am J Cardiol,352 and Tex Heart Inst J.353)

 
Rationale for eliminating atrial fibrillation with ablation
There are several hypothetical reasons to perform ablation procedures for treatment of AF. These include improvement in quality of life, decreased stroke risk, decreased heart failure risk, and improved survival. In this section of the document, these issues will be explored in more detail. However, it is important to recognize that the primary justification for an AF ablation procedure at this time is the presence of symptomatic AF, with a goal of improving a patient's quality of life. Although each of the other reasons to perform AF ablation identified above may be correct, they have not been systematically evaluated as part of a large randomized clinical trial and are therefore unproven.

Several epidemiologic studies have shown strong associations between AF and increased risk of cerebral thromboembolism, development of heart failure, and increased mortality.^55–57 It is well known that AF causes hemodynamic abnormalities including a decrease in stroke volume, increased LA pressure and volume, shortened diastolic ventricular filling period, AV valvular regurgitation, and an irregular and often rapid ventricular rate.⁵⁸ Persistence of AF leads to anatomic and electrical remodeling of the LA that may facilitate persistence of AF. Most importantly, many patients, even those with good rate control, experience intolerable symptoms during AF.

There have been multiple randomized clinical trials performed that address the question of whether rhythm control is more beneficial than rate control for AF patients. In all trials, antiarrhythmic drugs were used for rhythm control. The Pharmacological Intervention in Atrial Fibrillation (PIAF) trial first demonstrated that rate control was not inferior to rhythm control in the improvement of symptoms and quality of life.⁵⁹ Similar findings were reported in RACE.⁶⁰ The Strategies of Treatment of Atrial Fibrillation (STAF) trial showed no significant difference in the primary endpoints of death, systemic emboli and cardiopulmonary resuscitation between the two strategies.⁶¹ Another recent study demonstrated an improvement in quality of life and exercise performance at 12 months' follow-up in a series of patients with persistent AF.⁶² In the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) trial, in which 4,060 AF patients with high risk for stroke and death were randomized to either rhythm control or rate control, there were no significant differences in all-cause death between the two strategies.⁶³ However, a new on-treatment analysis of the AFFIRM study revealed that the presence of sinus rhythm was associated with a significant reduction in mortality, whereas the use of antiarrhythmic drugs increased mortality by 49%,⁶⁴ suggesting that the beneficial effect of sinus rhythm restoration on survival might be offset by the adverse effects of antiarrhythmic drugs. Previously, the Danish Investigations of Arrhythmia and Mortality on Dofetilide (DIAMOND) study also showed the presence of sinus rhythm was associated with improved survival.⁶⁵ It must be noted, however, that this was a retrospective analysis, and the improvement in survival may have resulted from factors other than the presence of sinus rhythm.

These clinical trials clearly show that the strategy of using antiarrhythmic drugs to maintain sinus rhythm does not achieve the potential goals of sinus rhythm mentioned above. However, there are signals in these data to suggest that sinus rhythm may be preferred over rate control if it could be achieved by a method other than drug therapy. Pappone et al compared the efficacy and safety of circumferential PV ablation with antiarrhythmic drug treatment in a large number of patients with long-term follow-up, and showed that ablation therapy significantly improved the morbidity and mortality of AF patients.⁵¹ Because this was not a prospective randomized study, these findings must be considered preliminary. Three recent small randomized trials in patients with paroxysmal AF demonstrated that catheter ablation was superior to antiarrhythmic therapy in the prevention of recurrent AF.^66–68 Further, a recent small retrospective study suggests that some patients with successful ablation may not require long-term anticoagulation.⁶⁹ The results of these studies suggest there are benefits to sinus rhythm obtained by ablation techniques over rate control. However, large prospective multicenter randomized clinical trials will be needed to definitively determine whether sinus rhythm achieved with ablation techniques lowers morbidity and mortality as compared with rate control alone or treatment with antiarrhythmic therapy.

	III. Indications for catheter ablation of atrial fibrillation and patient selection

Top I. Introduction II. Atrial fibrillation:... III. Indications for catheter... IV. Techniques and endpoints... V. Technologies and tools VI. Other technical aspects VII. Follow-up considerations VIII. Outcomes and efficacy... IX. Complications of atrial... X. Training requirements and... XI. Surgical ablation of... XII. Clinical trial... XIII. Conclusion References

 
The ACC/AHA/ESC 2006 Guidelines for the Management of Patients with Atrial Fibrillation, written in collaboration with the Heart Rhythm Society, state that "Catheter ablation is a reasonable alternative to pharmacological therapy to prevent recurrent AF in symptomatic patients with little or no LA enlargement" (Class 2A recommendation, level of evidence C).¹ It is noteworthy that the only Class 1 indication in this section of the document states that treatment of precipitating or reversible causes of AF is recommended before initiating antiarrhythmic drug therapy. Further, the maintenance of sinus rhythm treatment algorithm lists catheter ablation as second-line therapy for all categories of patients.¹

The Task Force supports these recommendations. In particular, the Task Force agrees that catheter ablation of AF in general should not be considered as first line therapy. There is a consensus among the Task Force that the primary indication for catheter AF ablation is the presence of symptomatic AF refractory or intolerant to at least one Class 1 or 3 antiarrhythmic medication (Table 1). The Task Force also recognizes that in rare clinical situations, it may be appropriate to perform catheter ablation of AF as first line therapy. Catheter ablation of AF is also appropriate in selected symptomatic patients with heart failure and/or reduced ejection fraction. The presence of a LA thrombus is a contraindication to catheter ablation of AF. It is important to recognize that catheter ablation of AF is a demanding technical procedure that may result in complications. Patients should only undergo AF ablation after carefully weighing the risks and benefits of the procedure.

Patient selection for catheter ablation of atrial fibrillation
As demonstrated in a large number of published studies, the primary clinical benefit from catheter ablation of AF is an improvement in quality of life resulting from elimination of arrhythmia-related symptoms such as palpitations, fatigue, or effort intolerance (see section on Outcomes and Efficacy of Catheter Ablation of Atrial Fibrillation). Thus, the primary selection criterion for catheter ablation should be the presence of symptomatic AF refractory or intolerant to at least one Class 1 or 3 antiarrhythmic medication.

Other considerations in patient selection include age, LA diameter, and duration of AF. The heightened risk of myocardial perforation and thromboembolic complications in very elderly patients, and the lower probability of a successful outcome when the LA is markedly dilated should be taken into account when considering ablation. Furthermore, catheter ablation of AF is less likely to be successful when used in the treatment of patients with longstanding persistent AF (see section on Outcomes and Efficacy of Catheter Ablation of Atrial Fibrillation).

In clinical practice, many patients with AF may be asymptomatic but seek catheter ablation as an alternative to long-term anticoagulation with warfarin. Although one study demonstrated that discontinuation of warfarin therapy after catheter ablation may be safe over medium-term follow-up in some subsets of patients, this has never been confirmed by a large prospective randomized clinical trial and therefore remains unproven.⁶⁹ Furthermore, it is well recognized that symptomatic and/or asymptomatic AF may recur during long-term follow-up after an AF ablation procedure.^70–74 It is for these reasons that this Task Force recommends that discontinuation of warfarin therapy post ablation is generally not recommended in patients who have a congestive heart failure, history of high blood pressure, age (75 years), diabetes, prior stroke or transient ischemic attack (CHADS) score 2.^1,75 Either aspirin or warfarin is appropriate for patients with a CHADS score of 1 following an ablation procedure. A patient's desire to eliminate the need for long-term anticoagulation by itself should not be considered an appropriate selection criterion. In arriving at this recommendation, the Task Force recognizes that patients who have undergone catheter ablation of AF represent a new and previously unstudied population of patients. Clinical trials are therefore needed to define the stroke risk of this patient population and to determine whether the risk factors identified in the CHADS or other scoring systems apply to these patients.

	IV. Techniques and endpoints for atrial fibrillation ablation

Top I. Introduction II. Atrial fibrillation:... III. Indications for catheter... IV. Techniques and endpoints... V. Technologies and tools VI. Other technical aspects VII. Follow-up considerations VIII. Outcomes and efficacy... IX. Complications of atrial... X. Training requirements and... XI. Surgical ablation of... XII. Clinical trial... XIII. Conclusion References

 
Historical considerations
Cox and colleagues are credited with developing and demonstrating the efficacy of surgical ablation of AF.^18,76 Subsequent surgeons evaluated the efficacy of surgical approaches that limit the lesion set to PV isolation.^77,78 The final iteration of the procedure developed by Cox, which is referred to as the Maze-III procedure, was based on a model of AF in which maintenance of the arrhythmia was shown to require maintenance of a critical number of circulating wavelets of reentry. The success of the Maze-III procedure in the early 1990s led some interventional cardiac electrophysiologists to attempt to reproduce the procedure with RF catheter lesions using a transvenous approach. Swartz and colleagues reported recreation of the Maze-I lesion set in a small series of patients using specially designed sheaths and standard RF catheters.⁷⁹ Although the efficacy was modest, the complication rate was high, and the procedure and fluoroscopy times were long in their early experience, this report demonstrated a proof of concept that led others to try to improve the catheter based procedure. Although a large number of investigators attempted to replicate the surgical Maze procedure through the use of either three-dimensional (3D) mapping systems or the use of multipolar ablation electrode catheters, these clinical trials had limited success.^80–86 Based on these observations and the rapid advances in ablation of AF targeting initiating focal triggers, electrophysiologists lost interest in catheter based linear ablation for AF ablation.

Ablation approaches targeting the pulmonary veins
The identification of triggers that initiate AF within the PVs led to prevention of AF recurrence by catheter ablation at the site of origin of the trigger.^10–12,87 Direct catheter ablation of the triggers was limited by the infrequency with which AF initiation could be reproducibly triggered during a catheter ablation procedure. A further limitation of this approach is that multiple sites of triggering foci were commonly observed.

To overcome these limitations, an ablation approach was introduced by Haissaguerre and colleagues⁸⁸ which was designed to electrically isolate the PV myocardium. This segmental PV isolation technique involved the sequential identification and ablation of the PV ostium close to the earliest sites of activation of the PV musculature. This typically involved the delivery of RF energy to 30% to 80% of the circumference of the PVs. The endpoint of this procedure was the electrical isolation of at least three PVs. An anatomically based ablation strategy of encircling the PVs guided by 3D electroanatomical mapping was subsequently developed by Pappone and colleagues.^86,89

The recognition of PV stenosis as a complication of RF delivery within a PV, as well as the recognition that sites of AF initiation and/or maintenance were frequently located within the PV antrum, resulted in a shift in ablation strategies to target the atrial tissue located in the antrum rather than the PV itself.^49,90 Ablation at these sites was either performed segmentally, guided by a circular mapping catheter^88,91 positioned close to the PV ostium, or by a continuous circumferential ablation lesion created to surround the right or left PVs.^86,89 The circumferential ablation line targeted either each ipsilateral PV separately or both ipsilateral PVs together (Figure 3). The circumferential ablation/isolation line was either guided by 3D electroanatomical mapping,^50,89,92 by fluoroscopy,⁹³ or by intracardiac echocardiography (ICE).^49,94 The endpoint for this procedure is either amplitude reduction within the ablated area,^89,92 elimination (or dissociation) of the PV potentials recorded from either one or two circular mapping catheters or a basket catheter within the ipsilateral PVs,^{49,50,93,95–98} and/or exit block from the PV.⁹⁹

Although ablation strategies, which target the PVs, remain the cornerstone of AF ablation procedures for both paroxysmal and persistent AF, continued efforts are underway to identify additive strategies to improve outcome. One of these strategies is to create additional linear lesions in the LA similar to those advocated with the Cox Maze-III, the Swartz approach, and others (Figure 3).^100–103 The most common sites are the LA "roof" connecting the superior aspects of the left and right upper PV isolation lesions, the region of tissue between the mitral valve and the left inferior PV (the mitral isthmus), and anteriorly between the roof line near the left or right circumferential lesion and the mitral annulus (Figure 3).¹⁰⁰ Ablation of the cavotricuspid isthmus is recommended by the Task Force in patients with a history of typical atrial flutter or inducible cavotricuspid isthmus dependent atrial flutter.¹⁰⁴

Ablation approaches not targeting the pulmonary veins
Non-PV triggers initiating AF can be identified in up to one third of unselected patients referred for catheter ablation for paroxysmal AF.^{12,34,105–108} Supraventricular tachycardias such as AV nodal reentry or accessory pathway mediated atrioventricular reciprocating tachycardia may also be identified in up to 4% of unselected patients referred for AF ablation and may serve as a triggering mechanism for AF.¹⁰⁹ Non-PV triggers can be provoked in patients with both paroxysmal and more persistent forms of AF.¹⁰⁷ In selected patients, elimination of only the non-PV triggers has resulted in elimination of AF.^34,109,110 The sites of origin for non-PV atrial triggers include the posterior wall of the LA, the superior vena cava, crista terminalis, the fossa ovalis, the coronary sinus, behind the Eustachian ridge, along the ligament of Marshall, and adjacent to the AV valve annuli (Figure 1).^{34,106,108,110,111} Furthermore, reentrant circuits maintaining AF may be located within the right and left atria.¹¹² Provocative maneuvers such as the administration of isoproterenol in incremental doses of up to 20: µg/min, and/or cardioversion of induced and spontaneous AF, can aid in the identification of PV and non-PV triggers. Linear LA lesions not aiming at PV isolation have been demonstrated to successfully prevent AF recurrences as previously introduced as a surgical approach.¹¹³

Areas with complex fractionated atrial electrograms (CFAE) have been reported to potentially represent AF substrate sites and became target sites for AF ablation.^{52,54,114,115} CFAE are electrograms with highly fractionated potentials or with a very short cycle length (120 ms). CFAEs usually are low-voltage multiple potential signals between 0.06 and 0.25 mV. The primary endpoints during RF ablation of AF using this approach are either complete elimination of the areas with CFAEs, conversion of AF to sinus rhythm (either directly or first to an atrial tachycardia), and/or noninducibility of AF. For patients with paroxysmal AF, the endpoint of the ablation procedure using this approach is noninducibility of AF. For patients with persistent AF, the endpoint of ablation with this approach is AF termination. When the areas with CFAEs are completely eliminated, but the arrhythmias continue as organized atrial flutter or atrial tachycardia, the atrial tachyarrhythmias are mapped and ablated.

A tailored approach to catheter ablation of AF targets specific drivers of AF and seeks to eliminate AF using the least amount of ablation necessary.¹¹⁶ Recognizing that the mechanisms of AF may vary from patient to patient, an individualized, electrogram-based approach is used instead of a standardized, predetermined lesion set. If the most rapid electrical activity is within the PVs, the PVs are isolated. PV isolation is then followed by CFAE ablation or serial creation of linear lesions. In contrast, if the PVs exhibit a slow, well organized rhythm, non-PV sites are targeted including CFAE ablation. The endpoint of these procedures in patients with paroxysmal AF is the inability to induce AF. In patients with longstanding persistent AF, a step-wise approach to ablation has been reported to successfully convert AF to either sinus rhythm or atrial tachycardia in > 80% of patients,^117,118 but an endpoint of noninducibility of AF does not appear to be feasible or even necessary.¹¹⁹

Adding GP to other ablation targets may improve ablation success.^53,54 The four major LA GP (superior left GP, inferior left GP, anterior right GP, and inferior right GP) are located in epicardial fat pads at the border of the PV antrum, and can be localized at the time of ablation using endocardial high frequency stimulation (HFS) (Figure 1). For ablation, RF current can be applied endocardially at each site of positive vagal response to HFS. HFS is repeated and additional RF applications can be applied until the vagal response to HFS is eliminated.

Task Force consensus
Shown in Table 1 are the areas of consensus on ablation techniques that were identified by the Task Force. The Task Force recommends that:

1. Ablation strategies which target the PVs and/or PV antrum are the cornerstone for most AF ablation procedures.
   
2. If the PVs are targeted, complete electrical isolation should be the goal.
   
3. Careful identification of the PV ostia is mandatory to avoid ablation within the PVs.
   
4. If a focal trigger is identified outside a PV at the time of an AF ablation procedure, it should be targeted, if possible.
   
5. If additional linear lesions are applied, line completeness should be demonstrated by mapping or pacing maneuvers.
   
6. Ablation of the cavotricuspid isthmus is recommended only in patients with a history of typical atrial flutter or inducible cavotricuspid isthmus dependent atrial flutter.
   
7. If patients with longstanding persistent AF are approached, ostial PV isolation alone may not be sufficient.
   

	V. Technologies and tools

Top I. Introduction II. Atrial fibrillation:... III. Indications for catheter... IV. Techniques and endpoints... V. Technologies and tools VI. Other technical aspects VII. Follow-up considerations VIII. Outcomes and efficacy... IX. Complications of atrial... X. Training requirements and... XI. Surgical ablation of... XII. Clinical trial... XIII. Conclusion References

 
Energy sources—radiofrequency energy
The presumed basis of successful AF ablation is production of myocardial lesions that block the propagation of AF wave fronts from a rapidly firing triggering source, or modification of the arrhythmogenic substrate responsible for reentry. Successful ablation depends upon achieving lesions that are reliably transmural.^120,121 The conventional approach employed by cardiac electrophysiologists to reach the goal of AF ablation is RF energy delivery by way of a transvenous electrode catheter.

RF energy achieves myocardial ablation by the conduction of alternating electrical current through myocardial tissue, a resistive medium. The tissue resistivity results in dissipation of RF energy as heat, and the heat then conducts passively to deeper tissue layers. Most tissues exposed to temperatures of 50°C or higher for more than several seconds will show irreversible coagulation necrosis, and evolve into non-conducting myocardial scar.¹²² High power delivery and good electrode–tissue contact promote the formation of larger lesions and improve procedure efficacy. High power delivery can be achieved with large-tip or cooled-tip catheters.^123,124 Optimal catheter–tissue contact is achieved by a combination of steerable catheter selection, guide sheath manipulation, and skill of the operator. Significant complications can occur during AF ablation if high RF power is administered in an uncontrolled fashion. The increased risk of AF ablation compared to ablation of other arrhythmias may be attributable to the great surface area of tissue ablated, the large cumulative energy delivery, the risk of systemic thrombo-embolism, and the close location of structures susceptible to collateral injury, such as phrenic nerve,¹²⁵ PVs,¹²⁶ and esophagus.¹²⁷ Thrombus and char can be minimized by limiting power and/or target temperature,¹²⁸ by monitoring the production of steam microbubbles at the catheter tip with ICE,^129–131 and by cooling the electrode–tissue interface with saline irrigated tips.¹³² Intramural steam pops can be reduced by limiting power and the electrode–tissue contact pressure, which is greater when the catheter is oriented perpendicular to the atrial wall.

Early reports of catheter ablation of AF employed conventional 4-mm or 5-mm tip ablation catheters. Lesions were created with point-to-point application of RF energy or with continuous RF energy application while the catheter was dragged across the myocardium. It was observed clinically and experimentally that this approach resulted in multiple sites of non-transmural lesion formation. The majority of the members of the Task Force now employ irrigated tip catheters. Although comparative trials of irrigated tip and large tip RF technologies versus conventional RF electrodes have demonstrated increased efficacy and decreased procedure duration in the ablation of atrial flutter,^133–135 comparative trials of large tip and open irrigation catheters have not been performed in patients undergoing AF ablation. Therefore, we are unable to make a firm recommendation regarding the optimal RF energy delivery system and catheter.

Various techniques have been proposed to minimize collateral injury. Temperature sensors at the electrode catheter tip can provide gross feedback of surface temperature, but because of passive convective cooling from circulating blood flow, or active cooling in a cooled tip catheter, the peak tissue temperatures are sometimes millimeters below the endocardial surface. Depending upon the ablation technology employed many operators limit RF power to 25–35 watts. Limiting power will limit collateral injury but at the expense of reliably transmural lesions. ICE has been employed to monitor lesion formation. If the tissue shows evidence of increased echogenicity, or if small gas bubbles are observed, then power should be reduced or terminated.^129–131 The time to steady-state tissue temperatures during RF catheter ablation is approximately 60–90 seconds.¹²² Therefore, limiting lesion duration may result in smaller ablative lesions. Monitoring unipolar electrogram amplitude has been p