Atrial Tachycardias Encountered during and after Catheter Ablation for Atrial Fibrillation: Part I: Classification, Incidence, Management

In the last decade, catheter ablation of paroxysmal, persistent, and long-standing persistent atrial fibrillation (AF) has become a realistic therapeutic option for symptomatic AF. As longer lasting forms of AF are tackled, two things have become clear: (1) more ablation targets are required for success, and (2) more atrial tachycardias (ATs) are encountered along the way. Indeed, sequential ablation (pulmonary vein isolation, electrogram-based ablation, linear lesions) leads to termination of what had previously been considered “permanent” AF in approximately 85% of cases, most often via a series of intermediate ATs.1 The incidence of AT during follow-up is also significant in this population, and successful management of these ATs is the final step to long-lasting maintenance of sinus rhythm. While three-dimensional (3D) mapping systems have a role in the ablation of these complex arrhythmias, their use can be time consuming and potentially misleading in the presence of interacting tachycardia circuits and multiple zones of bystander slow conduction found in the previously ablated atrium. Using conventional mapping tools, a logical electrophysiological analysis of atrial activation and electrogram morphology facilitates a rapid and reliable diagnosis in a majority of ATs. This article reviews ATs that arise during or after catheter ablation for AF. In Part I, ATs will be classified, contextualized according to ablation strategy and mechanism, and early management will be discussed. Part II will describe a practical approach to catheter ablation of these challenging arrhythmias including a simple algorithm employing conventional mapping principles that will rapidly address over 95% of ATs. The last consensus for the classification of AT was established by a joint expert working group in 2001.2 This consensus emphasized the importance of distinguishing ATs as macroreentrant or focal. Macroreentry is due to activation encircling a large central obstacle (fixed anatomic, functional, or both) that is several centimeters in diameter. There is no single point of origin of activation, and atrial myocardium surrounding the circuit is activated from various parts of the circuit. Thus, reentrant activation can be recorded continuously throughout the atrial cycle length and a point of earliest activity does not exist. Entrainment from at least three separate segments of the chamber of interest reveals a postpacing interval (PPI) within 20 ms of the tachycardia cycle length. Macroreentry is facilitated by a zone of slow conduction within the circuit. Important boundaries that confine and stabilize these circuits include the tricuspid annulus and crista terminalis (in the right atrium [RA]) and the mitral annulus, and pulmonary veins (PVs) in the left atrium (LA), while common zones of slow conduction can be contributed to atrial pathology and ablation lesions (particularly incomplete linear lesions). Common circuits encountered in the context of AF ablation include reentry around the tricuspid annulus in the right atrium and reentry around the mitral annulus or PVs (roof dependant) in the left atrium.1, 3, 4 Focal AT is defined as atrial activity originating from a single focus and spreading out centrifugally. The electrophysiologic mechanisms of focal ATs have traditionally included increased automaticity and triggered activity. Differentiating among these mechanisms in the electrophysiology lab, which can be impossible and has little or no practical value, is reviewed elsewhere.2, 5 Distinguishing focal from macroreentrant ATs is of immense practical value as their mapping approaches differ dramatically. Focal ATs are progressively mapped to earlier and earlier sites until the “focus” is identified. The reward after carefully mapping the site of origin is that focal ATs are usually very sensitive to radiofrequency energy and easy to ablate. On the other hand, the goal of mapping a macroreentrant AT is to identify regions of the circuit that can be interrupted (with bidirectional linear block best suited to prevent recurrence). As described above, perimitral, roof-dependant, and peritricuspid reentry account for a vast majority of macroreentrant ATs arising in the context of AF ablation. Awareness of these circuits permits simple and rapid mapping with conventional catheters (Fig. 1). Unfortunately, they can often be difficult to ablate. Part II of this review will expand on practical strategies to map and ablate these ATs. The three most common macroreentrant circuits encountered in the context of catheter ablation of atrial fibrillation. (A) Perimitral reentry can be clockwise or counterclockwise. In either case, activation along the inferior mitral annulus (MA) (medial to lateral or lateral to medial) is opposite to that along the superior MA and accounts for the entire cycle length. Activation along the anterior and posterior left atrium (LA) are both ascending. (B) In roof-dependant reentry, activation along the anterior and posterior LA (ascending or descending) are opposite, while activation along the MA is variable. (C) In peritricuspid reentry, activation is almost always counterclockwise around the tricuspid annulus (not shown) and accounts for the entire cycle length. Activation of the inferior LA is almost invariably medial to lateral. More recently, some studies have emphasized the existence of a third intermediate AT category variably called “microreentry,”2“small reentrant circuits,”6 or “localized reentry.”8 Various features of these ATs, which occur very commonly in the context of AF ablation,8 suggest reentry as their mechanism, including: (1) they are often induced by programmed stimulation, (2) their response to overdrive pacing is consistent with entrainment, (3) they are insensitive to adenosine, and (4) at least 50% of the AT cycle length (and often the entire cycle length) can be accounted for by local electrograms. Very low amplitude signals (<0.05 mV) are common for localized reentry and electrical noise or lack of amplification can make mapping difficult (Fig. 2). While the electrophysiologic mechanism of localized reentry is different from true focal point ATs, both localized reentry and focal AT involve centrifugal activation of both atria. Practically speaking, mapping these small sites, which consists of tracking the earliest atrial region of activation, is similar. Therefore, localized reentry is generally included in the broad definition of “focal” AT. Table I summarizes this practical approach to classifying ATs that arise in the context of AF ablation. A localized reentry circuit is approached by a multielectrode catheter with five splines (high resolution) in the upper panel (A and B), and by an ablation catheter (lower resolution) in the lower panel (C and D). At position (A), recordings from all splines of the catheter account for only a small portion of the atrial tachycardia (AT) cycle length. The activation sequence on the multispline catheter allows localization of the catheter to the source (B) where the entire tachycardia cycle length is accounted for by low-amplitude fractionated recordings consistent with a small reentrant circuit. The ablation catheter at position (C) records distal to proximal activation so the catheter is advanced in the direction of the distal pole to position (D), where alternating fractionated electrograms on the proximal and distal bipoles accounts for nearly the entire AT cycle length. This “activation gradient” between the distal and proximal bipoles is consistent with localized reentry rotating under the ablation catheter. In our experience, the most common sites where localized reentries are discovered include areas previously targeted by sequential ablation for long-lasting persistent AF, namely, the PV-LA junctions, left interatrial septum, and the entrance of the LA appendage. Other sites include the anterior LA, inferior LA/coronary sinus, and the right atrium. This raises the possibility that localized reentry may be caused by prior ablation. Circuits as small as these would almost certainly require local zones of slow conduction to prevent short circuiting, so it should be no surprise that ablation lesions may be contributory, nor that these circuits tend to occur in patients who have AF and/or areas of slow conduction and scar.6-9 Occasionally, two different localized reentries may coexist in the same region. The incidence of ATs after catheter ablation for AF varies widely with estimates ranging from <5% to 50%.1, 9 Factors that influence the likelihood of developing AT (and the type of AT that may develop) include the duration of AF episodes and the lesion set employed at the index procedure. After ostial isolation of PVs for paroxysmal AF, Gerstenfeld and colleagues found that <5% of patients went on to develop ATs that were mostly due to resumption of PV conduction.9 Ouyang and colleagues also found that most recurrent ATs after circumferential PV isolation for paroxysmal AF were related to resumption of PV conduction.10 The underlying mechanisms of these ATs include focal PV tachycardias conducting through gaps,10 large iatrogenic macroreentrant circuits employing at least two gaps in continuous circular ablation lines,11 as well as evidence for localized reentry circuits involving areas of slow conduction related to previous ablation lesions.9, 12 On the other hand, left atrial circumferential ablation (LACA) without PV isolation has been associated with a much higher risk of developing AT13 ranging from 10% to 30%. A majority of these ATs have been due to roof-dependant or perimitral macroreentry.3, 14 Accordingly, a prospective randomized trial confirmed the hypothesis that prophylactic linear ablation at the LA roof and mitral isthmus added to LACA would reduce the incidence of AT.15 An important and consistent observation in both the surgical and catheter ablation literature is the frequency with which left atrial macroreentry is related to gaps in linear lesions.3, 16 Achieving bidirectional linear block halves the risk of subsequently developing macroreentrant AT.17 Accordingly, current guidelines recommend that the goal of linear and PV-based ablation ought to be bidirectional conduction block.18 Because the incidence of AT seems correlated with the amount of ablation performed, strategies that limit the ultimate amount of ablation must be investigated. At least for the time being, however, there appear to be no alternatives. Linear lesions clearly add to the success of PV isolation19, 20 and even when a strategy of avoiding linear lesions is employed, they almost always end up being required, most often because of the development of macroreentry that occurs anyways.17 Electrogram-based ablation, which avoids coalescent lesions around the PVs and linear lesions—a strategy that should theoretically be less apt to promote macroreentry—is also associated with a significant incidence of AT (26–36%) that is, in fact, most commonly due to mitral isthmus and roof-dependent flutters.21, 22 While circumferential PV isolation, electrogram-based ablation, and linear lesions are all associated with the development of AT, they are also clearly associated with greater procedural success.1 Accordingly, not all AT in the context of AF ablation can or should be attributed to proarrhythmia. Conversion of AF to one or more intermediate ATs is an important step in the maintenance of lasting sinus rhythm. Recurrent AF is rarely seen after this conversion occurs, while it is the most common recurrent atrial arrhythmia when it does not.23 Mapping and ablation of these intermediate ATs could be considered the final step in the cure of long-lasting AF, suggesting (along with other lines of evidence) that the underlying mechanism of AF is multiple ATs including both focal mechanisms and large wavelets traversing the common atrial isthmuses. The development of AT should probably be thought of as a beneficial distillation of the fibrillatory process to its slowest and most mappable components. As with the management of atrial fibrillation, the most important components in the management of ATs that arise in the context of AF ablation include managing the risk of thromboembolism, prevention of tachycardia-induced cardiomyopathy, and control of symptoms. Current guidelines recommend managing long-term and pericardioversion anticoagulation for atrial flutter exactly as for atrial fibrillation.23 It seems prudent to apply the recommendations in these guidelines to patients with ATs that arise after AF ablation as well.24 ATs that develop after AF ablation are often associated with a faster ventricular response than the AF that preceded ablation, and may be longer lasting (especially in the case of a reentrant mechanism) and require cardioversion more often.25 It is noteworthy that these ATs may also be asymptomatic, particularly when they are associated with a slower or controlled ventricular response.26 Anecdotal evidence points to the inefficacy of proarrhythmia or antiarrhythmic drugs contributing to the persistence of ATs that disappear when the drug is withdrawn in some cases.27 It has been commonly observed that one-third to one-half of patients who develop ATs in the first few weeks after AF ablation may not develop recurrent atrial arrhythmias during follow-up.28-30 ATs that are inducible at the index procedure do not necessarily become clinical ATs during follow-up.25 In contrast, Lellouche and colleagues found that a vast majority of patients with early ATs do develop ATs in follow-up and often require catheter ablation because they are poorly tolerated despite drug therapy.31 Nevertheless, a strategy involving repeat catheter ablation within 1 month of the index procedure was associated with a higher total number of procedures overall. This could be because some ATs that were the focus of early repeat ablation procedures may never have manifested had a longer blanking period been observed. An initial conservative management strategy including rate control and cardioversion seems reasonable. Symptomatic patients with ATs that persist beyond 2–3 months should be offered catheter ablation, the results of which are gratifying, often leading to lasting maintenance of sinus rhythm.1 Mapping and ablation of these ATs will be the focus of the second part of this article. As longer lasting forms of AF are being successfully treated with more extensive catheter ablation targets, more atrial tachycardias are being encountered. These arrhythmias are often more symptomatic than the AF they replace. Conservative management is prudent for ATs that develop early after ablation as some may disappear, though repeat catheter ablation is often required for those that persist. Focal ATs commonly include PV tachycardias and localized reentry, while macroreentrant ATs commonly involve the mitral isthmus and left atrial roof, even when prior linear ablation in those areas has not been performed. When circumferential PV and linear lesions are deployed, the goal should be to produce bidirectional conduction block. While some ATs encountered in the context of AF ablation are undoubtedly iatrogenic, the AT mechanisms described above are also likely to represent important components of the underlying mechanisms of AF. A practical approach to successful ablation of these slower and mappable arrhythmias will be the subject of the second part of this article.

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