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RF ablation of AF was developed in 1997. The discovery of the PVs as the main driving sources of paroxysmal AF1 led to the global development of current ablation strategies that aim the electrical isolation of the PVs at their antral portion (proximal PV-LA junction).² Ablation strategies depend on clinical types of AF, but especially in persistent and long-standing persistent AF, the volume of atrial tissue ablated to treat AF is high (including PVI, ablation of rapid fractionated atrial sites, and linear lesions in both LA and RA). Paroxysmal AF can be treated by catheter ablation with a limited amount of atrial tissue destruction, because electrical isolation of PVs is sufficient for curing this type of AF.² Persistent and long-standing persistent (patients remaining for more than one year in AF) forms of AF may necessitate more extensive ablation to restore sinus rhythm.^3–7 These include, in addition to PVI, EGM-guided ablation at sites with continuous EGM fractionation/activity during AF until local “regularization” of EGMs has been achieved. Additional linear lesions at the LA roof (between LSPV and RSPV) and at the lateral mitral isthmus (linear ablation between LIPV or LSPV and the mitral annulus) may be necessary to restore sinus rhythm in patients with persisting AF.

The incidence of ATs occurring after PVI is low in young patients with paroxysmal AF. ATs occur frequently in the presence of structural heart disease and also when extensive ablation is undertaken. Therefore, their global incidence varies from 5% to 75% in patients undergoing AF ablation. In persistent AF, and more so in the long-standing persistent AF, atrial tachycardias are almost always observed during AF ablation as an intermediate rhythm prior to the restoration of sinus rhythm.

Incidence of Atrial Tachycardia After AF Ablation

Presence of structural heart disease, the LA size, the baseline AF CL, the type of AF (longer-lasting AF episodes), the type of AF-ablation procedure, and its endpoint impact the incidence of AT. Incidence of AT after PVI has been variably reported from 2.9% to 10%.^10–14 As the number and extent of ablative lesions are higher in the circumferential PVI technique, it may lead to a higher incidence of AT than segmental PVI.^12,13 In patients undergoing circumferential PVI and linear ablation, incidence of AT has been reported to be as high as > 10% to 30%.^15–18 Though < 20% of patients develop AT after isolated ablation of complex fractionated signals, the incidence rises to 40% to 57% in patients wherein EGM-based atrial ablation accompanies PVI and linear ablation.^3,7,19 In a multicenter study on the effectiveness of ablation of complex fractionated signals without PVI and linear ablation in persistent AF, up to 40% patients were found to develop intraprocedural AT (unpublished European data from Bad Krozingen, Munich, and Bordeaux).

Classification of Atrial Tachycardia

AFL/AT are classified by the working group into the clinically relevant macroreentrant and focal categories.20 Macroreentrant ATs are due to large reentrant circuits (> 3 cm diameter), but the EP mechanism of focal AT could be automaticity, triggered activity, or localized reentry.²² Importantly, in the era of AF ablation, the majority of focal ATs seem to be due to localized reentry with the circuit comprising < 2 cm in diameter (see also Figure 22.1).²² Among all forms of ATs, 46% to 70% represent the macroreentrant ATs and 30% to 53% represent the focal forms. Among the focal ATs, 26% to 50% are due to discrete focal source and 50% to 74% represent the localized reentrant variety.^21,22

Mechanisms of Atrial Tachycardia

To simplify and facilitate the diagnostic approach, we consider atrial tachycardia as being due either to a macro-reentrant circuit or a focal source. The latter forms are characterized by centrifugal atrial activation and are due to localized reentrant circuit (diameter < 2 cm) in most of the cases; however, a true focal origin may also be the underlying origin.

Drug Therapy

Usually, AF ablation is undertaken in patients who fail to respond to drug therapy. Patients with AF recurrence may show improved responsiveness to antiarrhythmic drug therapy after AF ablation. But ATs are less responsive to drugs than AF. In addition, ventricular rate is usually faster during AT than during AF, reducing the patient’s level of arrhythmia tolerance. Hence, the risk of developing congestive heart failure due to tachymyopathy is higher under AT than AF. Both recurrence of AF or AT may be transient and limited to the blanking period, but in our experience, they tend to recur in most of the patients over a period of several months postblanking. As a consequence, our strategy is to ablate these ATs if they persist or recur after the first month following AF ablation. ATs are always targeted for ablation when they occur during an AF ablation procedure.

ATs Occurring During AF Ablation

Using the stepwise approach toward the ablation of longstanding AF, PVI is followed by EGM-based ablation of continuous activity/complex fractionated EGMs and sites with activation gradient. The final step involves linear lesions at the LA roof and at the left mitral isthmus. If AF is converted to sinus rhythm, no further lesion is delivered. If the intermediate rhythm is AT, it is mapped and ablated. Additional lesions, if required, are applied and complete isolation of the PVs and bidirectional block across prior linear lesions are ensured. Most of the time, AF ablation is associated with a progressive increase in AF CL until about 200 ms, when AF gets converted into AT. Thus, AT is often observed as a transitional rhythm from AF to sinus rhythm.¹⁹ Such intraprocedural AT is suggestive of hidden organization in the disorganized-appearing AF. When AF organizes into slow, sustained AT, it is a sign of impending restoration of sinus rhythm, which can be achieved following accurate diagnosis and ablation of the critical isthmus/source maintaining the AT. In other words, the AT could be due to a mechanism that was present and active during AF and participated in the maintenance of the latter. Spectral analysis of AF CL in animals and humans has shown a relationship between the AF dominant frequency and the CL of the subsequently occurring AT.^23,24

AT Occurring After AF Ablation

After AF ablation, a variable degree of inflammatory state exists in the atria. The tissue takes about 6 to 12 weeks to organize and form a fibrous scar at the sites of ablation. After AF ablation, this period is usually observed as a blanking period, marked by transient but recurrent and possibly nonclinical atrial arrhythmias. As inflammation heals, inhomogeneous areas of nonuniform scar interspersed with healthy and/or partially damaged atrial tissue remain.²⁵ Thus, the atrium gets transformed into an electrophysiologically heterogeneous chamber with unevenly distributed scar tissue. Areas of low voltage and slow conduction properties coexist as gaps amid the nonconducting scar tissue, generating a substrate highly favorable for reentrant arrhythmias. The likelihood of gaps (slowly conducting, incompletely scarred tissue) increases with increase in the extent of ablation. Arrhythmias observed beyond the blanking period may be attributed to a proarrhythmic effect of ablation. Alternatively, they may also be the consequence of the arrhythmia revealed by AF ablation (see above).²²

Locations of Atrial Tachycardia Circuits

In paroxysmal AF, PVI is enough to treat AF in the vast majority of patients. Very few ATs are observed in this context. They consist of the localized reentry circuits at the PV ostia associated with the formation of gap in the previous PVI lesion. In the era of circumferential PVI involving higher volume of ablated tissue, few patients also develop roof-dependent and/or perimitral circuits.

In persistent AF, wherein more extensive ablation is required to terminate AF, all types of AT may be observed. Notably, patients with AT after previous linear ablations (roof and mitral isthmus lines) for AF/AT show most frequently macroreentrant circuits involving the LA. Perimitral flutters are the most common, followed by roof-dependent ATs. CTI-dependent AT is another likely macroreentrant RA tachycardia, although it is the least common type. These are the only macroreentrant circuits observed post–AF ablation. Importantly, the typical flutter wave morphology is not commonly observed on 12-lead ECG of CTI-dependent flutter in the context of extensive atrial ablation and spontaneous scarring. Although ablation of macroreentrant AT circuits could be challenging, it takes less than 10 minutes to rule them in or out.

Localized ATs with centrifugal activation of the atria may be due either to a localized reentrant circuit or a true focal mechanism. Localized reentry gets established in small areas most commonly at the venous ostia (PV ostia, ostium of SVC, and CS), the left septum, the base of the LAA, the junction of the LAA and the roof, the posterior LA, and the posterolateral mitral isthmus. Such localized, small circuits give rise to centrifugal atrial activation from these sites (Figure 22.1). Most of the time, but not necessarily always, they are located at LA sites with regional slow conduction at areas of prior ablation. However, the anterior wall of the LA can host them spontaneously, and they may have participated in AF maintenance, suggesting that this arrhythmia mechanism is not exclusively created by ablation.^32,21,22 Unlike the point sources of typical focal AT, these sites involve small regions of slowly conducting tissue harboring the entire or almost the entire tachycardia circuit locally within a diameter of 2 cm (Figure 22.1).

Diagnosis

However, when the AT occurs after lone (segmental or wide circumferential) PVI (without previous linear ablation of the LA), the 12-lead ECG can provide more guidance into the mechanism of AT. Under these circumstances, the presence of an isoelectric interval > 90 to 100 ms occurring simultaneously on all of the 12 ECG leads is a diagnostic marker of a localized reentry circuit.28 This probably applies to all centrifugal arrhythmias.

The 12-lead ECG has also been used to predict perimitral circuits, but again, this has been validated in the context of lone PVI³⁰ and doesn’t apply, in our experience, to more extensive AF ablation procedures.

Atrial Tachycardia Diagnosis in the EP Laboratory

In the EP laboratory, it is important to diagnose the mechanism underlying AT to achieve clinical success. As a preliminary step, it is important to acquire the information on previously ablated sites and determine if clear end-point (bidirectional block at previous linear lesions) had been achieved.

If the patient is in sinus rhythm at the beginning of the repeat procedure, the evaluation for completeness of previously performed PVI should be the first step. If there is any evidence of PV reconnection, PVI should be completed before targeting other areas. This is important, as PVs are not just associated with AF but can also host AT, particularly in cases of incomplete isolation or reconduction. If linear ablation involving CTI, roof line, or mitral isthmus line was performed previously, bidirectional block should be reconfirmed. Reablation should be performed, wherever needed, to establish complete bidirectional block.

During ongoing tachycardia, we apply a 3-step approach (Figure 22.2) to diagnose the type of AT based on the classification (macroreentrant vs. focal) cited above.²² We use a quadripolar irrigated-tip mapping/ablation catheter in the atrial chamber and a decapolar catheter in the CS and implement the diagnostic approach during ongoing AT as follows.

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