2025 EHRA／HRS／APHRS／LAHRS／AEPC临床共识声明：房性心动过速患者的管理

Graphical abstract

 SMART-AT 10-Point Plan. The graphical abstract summarizes the 10-Point SMART-AT framework guiding the management of patients with atrial tachycardia. Points 1–3 (blue) emphasize standardized patient evaluation and procedural safety; points 4–8 (green) outline mechanism-based mapping and ablation strategies for focal, localized, and macro-reentrant AT of de novo and consecutive (x2) arrhythmias; points 9–10 (purple) highlight institutional quality and future innovation through collaborative research.

Keywords

Atrial fibrillation $\cdot$ Atrial flutter $\cdot$ Atrial tachycardia $\cdot$ Consensus statement $\cdot$ Electroanatomical mapping $\cdot$ Electrocardiogram $\cdot$ Focal atrial tachycardia $\cdot$ Localized reentrant atrial tachycardia $\cdot$ Macro-reentrant atrial tachycardia $\cdot$ Pulsed-field ablation $\cdot$ Radiofrequency ablation

Table of contents

|1. Introduction and background|4| |---|---| |1. Document aims and scope|4| |1.2 Methods|5| |2. Clinical evaluation and procedural planning|6| |2.1 AT definition|6| |2.2 Differentiating clinical and subclinical device-detected AT from AF|7| |2.3 Clinical manifestation|7| |2.4 Diagnostics|8| |2.5 Electrocardiogram|9| |2.6 Antiarrhythmic drug treatment|11| |2.7 Cardioversion|12| |2.8 Ablation indication|13| |2.9 Preprocedural management|13| |2.10 Relevance of structural heart disease and comorbidities|15| |2.10.1 Aetiology|15| |2.10.2 Comorbidities|17| |2.11 AT in older patients|17| |2.12 AT in pregnancy|17| |2.13 Neural control of AT|18| |3. Intra- and postprocedural patient care|18| |3.1 Anaesthesia and ventilation|18| |3.2 Safety|19| |3.3 Intraprocedural care|19| |3.4 Anticoagulation after catheter ablation|20| |3.5 Recurrence and heart rate monitoring|20| |3.6 Repeat ablation|20|

|4. Mapping and ablation: conceptual considerations|21| |---|---| |4.1 Catheter setting|21| |4.1.1 Less is more: dynamic conventional (activation)|| |mapping|21| |4.1.2 Pattern and timing of activation|21| |4.2 Diagnostic electrophysiological manoeuvres|21| |4.2.1 Manoeuvres to verify AT|21| |4.2.2 Distinguishing mon-reentrant from reentrant AT|21| |4.3 Entrainment mapping for AT localization|21| |4.3.1 When, where and how|22| |4.32 Interpretation and potential pitfalls|23| |4.4 Electroanatomical mapping|23| |4.5 Potential value and standards of high-resolution mapping|23| |4.6 Power sources and techniques|24| |4.61 Radiofrequency ablation: power settings and lesion creation monitoring|25| |4.6.2 Pulsed-field ablation|25| |4.63 Ethanol injection/ablation|25| |4.6.4 Cryoablation|26| |4.6.5 Combined ablation forms and other|26| |4.6.6 Robotic ablation|26| |4.7 Ablation strategies|27| |4.7.1 Targeted critical area ablation|27| |4.7.2 Anatomically guided linear ablation|27| |4.7.3 Substrate modulation and other strategies|27| |4.7.4 Procedural endpoints and validation of ablation|28| |strategy|28| |5. Focal AT|28| |5.1 Definition|28|

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|5.2 Mechanism|29| |---|---| |5.3 Localization|31| |5.4 Mapping and ablation strategy|31| |5.4.1 General|31| |5.4.2 Challenging anatomical areas|31| |6. Localized reentrant AT|32| |6.1 Definition|32| |6.2 Mechanism|32| |6.3 Localization|32| |6.4 Mapping and ablation strategy|32| |6.4.1 General|32| |6.4.2 Challenging anatomical areas|32| |7. Macro-reentrant AT|33| |7.1 Peritricuspid macro-reentrant AT|34| |Treatment|34| |7.2 Peritrimal macro-reentrant AT|34| |Treatment|34| |7.3 LA roof-dependent macro-reentrant AT|34| |Treatment|36| |7.4 Figure-of-eight and complex dual-loop circuits|36| |7.5 Multiple-loop AT|36| |Treatment|36| |7.6 Biatrial AT|36| |7.7 Epicardial components|36| |8. AT following previous cardiac interventions|37| |8.1 AT after catheter ablation of AF|37| |8.1.1 AT after pulmonary vein isolation|37| |8.1.2 AT after electrogram-guided ablation|37| |8.1.3 AT after additional linear ablation|38| |8.2. AT after cardiac surgery|38| |8.2.1 Anatomical and surgical considerations|38| |8.2.2 Hybrid ablation|38| |8.2.3 Mechanisms and other specifics|38| |8.3. AT in ACHD|38| |8.3.1 Anatomical and surgical considerations|38| |Evolution of surgical approaches in CHD and potential impact on AT substrates|39| |8.3.2 Common substrates and mechanisms|40| |Common AT mechanisms|40| |Special aspects|40| |Fontan|40| |Dextro-transposition of the great arteries with atrial switch|40| |8.3.3 Mapping and ablation strategy|40| |Access to the pulmonary venous atrium|40| |Endpoints of ablation|40| |8.4 Specifics in the paediatric population|41| |8.4.1 Ablation indication in the paediatric population|41| |8.4.2 Interdisciplinary management|41| |9. Efficacy, safety, and institutional requirements|41| |9.1 Acute procedural success|41| |9.2 Recognition and management of complications|41| |9.3 AF and AT during follow-up|42| |9.4 Training and institutional requirements|42| |10. Gaps of knowledge and future directions|42| |Supplementary material|44| |Acknowledgements|44| |Conflict of interest|44| |Data availability|44|

Abbreviations

AAD

antiarrhythmic drug

ACHD

adults with congenital heart disease

AF

atrial fibrillation

AiCMP

atrihythmia-induced cardiomyopathy

AT

atrial tachycardia

AV

atrioventricular

CA

catheter ablation

CHD

congenital heart disease

CL

cycle length

CS

coronary sinus

CTI

cavotricuspid isthmus

DDAF

device-detected atrial fibrillation

DDAT

device-detected atrial tachycardia

EAM

electroanatomical mapping

ECG

electrocardiogram

EP lab

electrophysiology laboratory

FAT

focal atrial tachycardia

IART

intera-atrial reentrant tachycardia

LA

left atrium

LAA

left atrial appendage

LRAT

localized reentrant atrial tachycardia

LVEF

left ventricular ejection fraction

MiRAT

micro-reentrant atrial tachycardia

MRAT

macro-reentrant atrial tachycardia

NRAT

non-reentrant atrial tachycardia

PFA

pulsed-field ablation

PPI

post-pacing interval

PV

pulmonary vein

PVI

pulmonary vein isolation

RA

right atrium

RF

radiofrequency

SMART-AT

Standardized Management and Ablation

Roadmap for Treatment of Patients with Atrial

Tachycardia

Tachycardia

SR

sinus rhythm

SR SRAT

small circuit reentrant atrial tachycardia

TCL

tachycardia cycle length

TOE

transoesophageal echocardiography

VoM

vein of Marshall

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1. Introduction and background

1.1 Document aims and scope

The understanding and treatment of atrial tachycardia (AT) have advanced considerably over the past decade. Recent ESC Guidelines downgraded the pharmacological therapy of focal AT (FAT), while catheter ablation (CA) has become the most effective therapy for maintaining sinus rhythm (SR) in patients with reentrant AT.$^{1}$ Concurrently, mapping and ablation techniques for regular AT have significantly improved. However, despite evidence suggesting that survival in patients with AT is worse than in those with atrial fibrillation (AF),$^{2}$ there are currently no international guidelines regarding the optimal management of AT.

This international clinical consensus statement aims to complement the 2001 classification of atrial flutter and regular AT.$^{3}$ This is necessary as in the past 20 years relevant novel mechanistic studies and therapeutic concepts related to AT have emerged.

The scope of the present document is to provide practical guidance on the management of regular AT with a special focus on indications, timing and technical aspects of CA, and to

(1) update the current mechanistic understanding of stable AT and its clinical implications

(2) propose diagnostic, and therapeutic approaches focusing on CA and perprocedural management

(3) highlight knowledge gaps to guide future collaborative research.

Management of patients with atrial tachycardia

Table 1 SMART-AT 10-Point Plan

|Call for action|Atrial tachycardias (AT) are increasingly encountered in clinical practice, with major impact on patients and healthcare systems, while catheter ablation has emerged as its most effective rhythm-control therapy.| |---|---| |Clinical evaluation and planning|A structured diagnostic approach, including electrocardiogram confirmation, imaging, and assessment of comorbidities, integrated with a mechanistic AT classification, enables patient-specific therapy planning within a standardized, evidence-based management framework (SMART-AT).| |Periprocedural management and safety|A comprehensive periprocedural management strategy, addressing clinical and procedural complexity under standardized institutional protocols for anaesthesia, anticoagulation, and management of adverse events, can ensure procedural safety and optimize patient outcomes.| |Mapping and ablation principles|Mapping and ablation strategies are guided by the underlying arrhythmia mechanism, combining conventional and electroanatomical activation with electrogram analysis and entrainment manoeuvres to achieve targeted or anatomically guided lesion delivery while preserving atrial function.| |Focal AT|In symptomatic focal, non-reentrant AT, catheter ablation targeting the site of earliest activation represents an effective rhythm-control approach with high acute success and favourable long-term outcomes.| |Localized reentrant AT (LRAT)|Localized reentrant AT are associated with atrial fibrosis and confined to a circuit diameter <2 cm. Diagnosis relies on high-resolution activation mapping with detailed electrogram analysis to identify subtypes such as small circuit (SRAT) or micro-reentrant AT (MiRAT). Ablation of the critical isthmus is often complemented by limited linear lesions toward adjacent structures.| |Macro-reentrant AT (MRAT)|Macro-reentrant AT comprises distinct mechanistic categories, including peritricuspid, perimitral, roof-dependent, and complex multi-loop circuits. Despite long-standing recognition, functional and anatomical variability, including epicardial components, continue to challenge arrhythmia management. Integration of high-resolution mapping, entrainment, and mechanistic classification supports accurate identification of the critical isthmus and ablation lesion planning.| |Secondary AT following cardiac intervention|Consecutive AT following cardiac interventions or surgery often result from incomplete lesions or scar formation. Recurrent AT, as well as AT in patients with congenital heart disease or in paediatric populations, should be managed in specialized centres with dedicated expertise.| |Outcomes, training, and institutional standards|AT management demands advanced electrophysiological expertise, structured training, and multidisciplinary infrastructure. Standardized workflows, certified programs, and continuous outcome evaluation support procedural safety, quality, and readiness to manage patients with complex arrhythmias.| |Future directions|Emerging diagnostic and therapeutical concepts evaluated in collaborative multicentre, multiprofessional research and data integration are expected to refine the understanding and treatment of patients with AT, fostering innovation within the SMART-AT framework.|

Abbreviations: SMART-AT, Standardized Management and Ablation Roadmap for Treatment of Patients with Atrial Tachycardia.

Wherever possible, the proposed strategies in this document are evidence-based. The goal is to establish reasonable standards that can be applied globally, while acknowledging variations in resources, disease prevalence, and healthcare delivery logistics across different regions due to demographic changes, comorbidities, and the increasing number of multimorbid patients undergoing various catheter-based and surgical cardiac interventions.

The proposed 'SMART-AT' ('Standardized Management and Ablation Roadmap for Treatment of Patients with AT') 10-Point Plan aims to provide a dedicated framework to guide clinical decision-making while shaping future scientific and institutional standards in a specific, measurable, achievable, relevant, and time-bound manner (Table 1).

1.2 Methods

A panel of AT experts was endorsed by the EHRA to publish this international consensus statement. Members of associated societies, i.e. the US (HRS), the Latin American (LAHRS), the Asian Pacific Heart Rhythm Society (APHRS), and the Association for European Paediatric and Congenital Cardiology (AEPC) additionally designated authors each to complete the collaborative group. A systematic literature review

Table 2 Definition of categories of advice and areas of uncertainty

Definition

Evidence or general agreement that a given measure is clinically useful and appropriate

Evidence or general agreement that a given measure may be clinically useful and appropriate

Evidence or general agreement that a given measure is not appropriate or harmful

No advice can be given because of lack of data or inconsistency of data. The topic is important to be addressed.

Category of advice

Advice TO DO

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and meta-analysis were performed based on Cochrane standards. The preprint servers medRxiv, bioRxiv, Research Square and arXiv were additionally searched (search 'trial tachycardia' (n): 471; 386; 1739; 10, respectively). All authors were asked to perform a detailed literature review, including case reports, observational studies, and randomized trials published (publications included until 08/05/2025), and to weigh the strength of evidence for or against a particular advice based on these published studies and/or on expert opinions. In controversial areas, a consensus was achieved by agreement of the expert panel (Tables 2 and 3).

|Type of supporting evidence|Criteria of evidence|Strength of evidence| |---|---|---| |Published data|>1 High-quality RCT Meta-analysis or high-quality RCT High-quality RCT 1 moderate quality RCT Meta-analysis or moderate quality RCT High-quality, large observational studies|META RCT OBS OPN LOPS| |Expert opinion|Strong consensus >90% of WG supports advice Consensus >70% of WG supports advice||

2. Clinical evaluation and procedural planning

2.1 AT definition

Historically, rapid, regular atrial arrhythmias were classified as either AT or atrial flutter. The differences between these nomenclatures were somewhat arbitrary and based on rate (slower for AT, faster for atrial flutter), P wave appearance (isolated wave with isoelectric segment for AT vs. continuous activation for flutter (previously termed F waves)), and the implication that a rhythm was focal (AT) or macro-reentrant (flower). However, using high-resolution mapping, it has become apparent that such distinguishing features are oversimplified. In the setting of a significant scar, a macro-reentrant tachycardia can be relatively slow and may have clear isoelectric intervals between P waves, making such distinguishing features less useful.$^{4,5}$

Thus, for this document, all regular tachycardias with an atrial origin >100 bpm are classified as AT, either specified as

$\bullet$ non-reentrant AT (NRAT) or

$\bullet$ reentrant AT

NRAT, previously also termed 'true' focal AT,$^{6,7}$ mechanistically include enhanced automaticity and triggered activity. Reentrant AT includes localized reentrant AT (LRAT) and macro-reentrant AT (MRAT). The writing group recommends using LRAT as an umbrella classification for reentrant AT with spatially restricted circuits.$^{1}$ Within this framework, small circuit reentrant AT (SRAT) and micro-reentrant AT (MiRAT) are considered mechanistic subtypes of LRAT. Especially, MiRAT may present with features of both focal (radial spread) and reentrant mechanisms. For additional details see Figure 1, Table 4 (electrophysiological characteristics) and Table 5 (definitions). The term 'flutter' is historically synonymous with MRAT. The writing group advises that 'atrial flutter' is a term which, today, should be restricted to circuits around the tricuspid annulus (counter-clockwise ['typical'] and clockwise ['reverse typical']) atrial flutter), especially since

![graph TD\n A1[Non-reentrant AT] --> A2[Automatic]\n A1 --> A3[Triggered]\n A4[Reentrant AT] --> A5[Localized reentry]\n A4 --> A6[Macro-reentry]\n A5 --> A7[Micro-reentry]\n A5 --> A8[Small circuit reentry]\n](1/parseimages/figure1cff76cee8a34805a712e24a9039cafb_0_12.png) Management of patients with atrial tachycardia

|EP characteristics|Non-reentrant (NRAT)|Reentrant AT|Reentrant AT|Reentrant AT| |---|---|---|---|---| |EP characteristics|Non-reentrant (NRAT)|Automatic/triggered|Localized (LRAT)|Localized (LRAT)| |EP characteristics|Non-reentrant (NRAT)|Automatic/triggered|Micro (MiRAT)|Macro (MRAT)| |Atrial substrate/prior iatrogenic intervention|Not required|Not required|Yes|Yes| |Induction with programmed stimulation|Usually not|Yes|Yes|Yes| |Activation pattern|Radial spread|(Very) small loop/Radial spread|Small loop/(radial spread)|Loop diameter > 2 cm| |Local electrogram characteristics|Non-fractionated, discrete potential|Local fractionation|Prolonged (diastolic) potential|Multi-fractionated, prolonged potential| |Record from >75% of CL|No|No|Yes (on single catheter)|Yes| |Entrain with intracardiac fusion|No|No|Yes|Yes| |Overdrive with PPI~TCL (entrained)|No|Yes|Yes|Yes| |Entrain PPI~TCL, 2 sites > 2 cm apart|No|No|No|Yes|

*PPI may equal the TCL in NRAT depending on the characteristics of automatic/triggered activity if the mapping catheter is placed close to the focal origin during overdrive pacing (reset without entrainment).

other arrhythmias have been found to be misclassified based on surface electrocardiograms (ECGs) only. A non-sustained AT is defined as ≥3 consecutive premature atrial contractions with a rate > 100 bpm lasting <30 s.$^{8}$

2.2 Differentiating clinical and subclinical device-detected AT from AF

Although the distinction between AT and 'coarse' AF can generally be discerned from the (12-lead) ECG, there can be diagnostic challenges, especially due to slight changes of activation patterns related to atrial scarring. While a monomorphic regular P wave is typically present during AT, at least subtle variations in P wave morphology and tachycardia cycle length (TCL) are characteristic of 'organized' AF (Figure 2).$^{9}$ Reentrant AT with alternating CL might challenge the correct diagnosis. If in doubt, a prolonged ECG rhythm strip can be useful for carefully comparing P wave morphology and CL over time across different ECG leads (Figure 3).$^{12,13}$ Vagal manoeuvres or pharmacological interventions such as adenosine might improve diagnostic accuracy due to better P wave discrimination by slowing atrioventricular (AV) nodal conduction. These manoeuvres can also be helpful for the determination of the type of supraventricular tachycardia in some cases. This is often performed in the electrophysiology laboratory (EP lab). Noteworthy, adenosine might challenge AT and patient management by resulting in degeneration of AT into AF.$^{12,14}$

Of note, in AF, one may often see quite organized P waves in V1 representing relatively organized activity of the right atrium (RA), so that V1 should not be used to differentiate AT from AF. However, if a pseudo-regular CL is observed in V1, an atrial CL <200 ms is rare in AT and therefore suggests AF. Albeit rarely indicated as a stand-alone diagnostic manoeuvre, catheters (e.g. (at least) in the coronary sinus

(CS) ± sequential conventional mapping) can help to differentiate between these arrhythmias in the EP lab.$^{15-19}$ Organized AF can be defined by beat-to-beat variability in CL (≥20 ms) and intracardiac electrogram morphology, whereas AT mostly behaves as a consistent organized atrial rhythm (beat-to-beat variability in CL commonly <20 ms) and a stable activation sequence in both atria that depends on the type and number of catheters used.$^{15}$ Mapping system-specific automated electrogram analyses can be useful to objectify the local stability of activation. A gradient of CL from discrete sites of high-frequency activity to the surrounding atrium can be found in AF.$^{15,20}$

In patients with cardiac implantable electronic devices, detected AF (DDAF) should be carefully reviewed to rule out device-detected stable AT (DDAT).$^{21}$,$^{22}$ Interestingly, in a recent hallmark trial, a small but relevant number of patients were diagnosed with AT during follow-up.$^{23}$ This observation, combined with mechanistic, epidemiological, and long-term data emphasizes the importance of individual differentiation of detected atrial high-rate episodes between DDAF and DDAT (Figure 4).$^{24}$

2.3 Clinical manifestation

Symptoms of AT commonly include palpitations and/or 'a racing heart',$^{12}$ but can, e.g. also be manifest as shortness of breath, chest pain, or reduced exercise capacity (Figure 5).$^{25,26}$ Symptoms emerge earlier at higher tachycardia rates, especially in patients with persistent AT with 2:1 AV conduction and rates exceeding 150 bpm.$^{27,28}$ Arrhythmia-induced cardiomyopathy (AiCMP)$^{28}$ may occur in 8–25% of patients with sustained AT.$^{29–32}$ While especially a non-sustained AT can also be asymptomatic, a relationship with unspecific symptoms or signs including, e.g. fatigue (or vomiting in children (along with feeding difficulties)), should be evaluated.$^{26}$ If cognitive decline is present, evaluation of AF should be performed.$^{33}$

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Table 5 Definitions related to mechanisms and mapping patterns of AT

Definition

|Reentrant AT|Circuit typically exhibiting activation throughout the entire tachycardia cycle length (CL), involving fixed anatomical or morphological obstacles and/or functional lines of block. The reentrant mechanism of AT encompasses both macro-reentrant and localized reentrant forms, the latter including small circuit (SRAT) and micro-reentrant (MiRAT) subtypes.| |---|---| |Macro-reentrant AT (MRAT)|Circuit around an anatomical obstacle (valve annulus, venous structure, surgical incision) where the CL is determined by the obstacle and regions of slowed conduction. May be initiated or terminated either by programmed stimulation or atrial burst pacing.| |Localized reentrant AT (LRAT)|A subform of reentry not typically around a fixed anatomical obstacle but associated with atrial disease or fibrosis and confined to a circuit diameter of approximately <2 cm. The path length is determined by local electrophysology with a small/no excitable gap. LRAT represents an umbrella term encompassing small circuit reentrant AT (SRAT) and micro-reentrant AT (MiRAT), which share similar mechanisms but can differ in circuit size and electrogram characteristics. LRAT can usually be initiated and terminated by programmed stimulation or atrial burst pacing.| |Small circuit reentrant AT (SRAT)|Subtype of LRAT with circumferential local activation that may spread away centrifugally to the periphery, with initiation and termination by programmed stimulation/burst pacing. Electrograms at origin are typically characterized by fractionated (diastolic) potentials which encompass >50% of the CL over a small diameter.| |Micro-reentrant AT (MiRAT)|Subtype of LRAT with centrifugal atrial spread radiating from a (very) small circuit that can be readily initiated by programmed electrical stimulation as the marker of reentry. Electrograms at the site of origin are typically long-duration, fractionated, and localized to a very small diameter.| |Non-reentrant AT (NRAT)|Atrial activation originating from a discrete region separate to the sinus node which radiates centrifugally. The mechanism of non-reentrant AT involves enhanced automaticity and triggered activity, resulting in a focal activation pattern without evidence of reentry.| |Enhanced automaticity|Acceleration or burst of activity from an automatic focus due to an increase in the slope of phase 4 depolarization, shortening of the refractory period or decrease in the threshold for excitation, with transient termination and then reinitiation with adenosine.| |Triggered activity|The result of afterdepolarizations which are focal electrical events that result in repeat depolarization at phase 2, 3, or 4 of the action potential and accordingly may be referred to as early or late, with abrupt termination with adenosine.| |Critical isthmus|Area of atrial myocardium that is essential for the maintenance of a reentrant AT, resulting from scars and/or anatomical obstacles, often containing fractionated electrograms indicating slow conduction.| |Anatomical isthmus|The portion of the reentrant circuit bounded by anatomical obstacles (alone or in combination with scar).| |Practical isthmus|The narrowest pathway between scars and/or anatomical obstacles which is anticipated to be the most appropriate site for ablation, based on anatomical length, local activation/electrogram characteristics indicating slow conduction, entrainment and tissue thickness.|

Two major forms of AT (non-reentrant and reentrant AT) can now be classified based on recent mechanistic insights and findings from high-resolution mapping.

2.4 Diagnostics

Diagnostics

Advised TO DO

It is advised to perform a 12-lead ECG, whenever possible, to identify a monomorphic regular P wave and potential AT localization.

For detailed AT characterization it is advised to assess only P waves, which are not superimposed by QRS complexes or T waves.

It is advised to perform a transthoracic echocardiogram in patients with AT.

It is advised to use vagal manoeuvres or adenosine in selected cases to improve diagnostic ECG accuracy due to better P wave discrimination by slowing AV nodal conduction.

Strength of evidence

    With the emerging use of mobile ECGs,$^{34}$ smart devices have become an integral part of patient care and can support the diagnosis of regular, mostly narrow-complex tachycardia with a P wave morphology distinct from SR, as AT,$^{25,35}$ particularly in patients with non-sustained, only intermittent, or asymptomatic episodes.$^{36}$ However, atrial activity may be difficult to discern and affected by the positioning of the smart device, resulting in a lower diagnostic accuracy compared to AF.$^{37}$ Therefore, the writing group members recommend the usage of mobile ECGs with more than 1 lead, followed by verification with a 12-lead ECG, whenever available.$^{10,38}$

If an incessant AT with a P wave morphology that only subtly differs from SR is suspected, exercise testing can help to confirm the diagnosis by demonstrating a lack of relevant atrial rate increase.$^{39}$ Since in some AT, the degree of AV conduction may vary with exercise, an increase in heart rate may occur.$^{40}$ This increase may, in rare cases, lead to a 1:1 AV response and even presyncope or syncope, underscoring the need for cautious use of exercise testing for diagnostic purposes. Inappropriate sinus tachycardia might be differentiated from AT by its PR shortening and increased P wave amplitude during tachycardia, whereas AT from the crista terminalis has been found to commonly show PR lengthening, indicating a distinct activation pattern.$^{41}$

Management of patients with atrial tachycardia

 In patients with cardiac implantable electronic devices, interrogation and reprogramming should be performed (Table 6), as appropriate. Considering the growing importance of AiCMP, an echocardiogram is needed in patients with AT to guide additional diagnostic, prognostic, and therapeutic decision-making; including the evaluation of potential structural/valvular heart diseases, systolic and diastolic left ventricular function, and atrial size at baseline and over time.$^{28,63}$

2.5 Electrocardiogram

The diagnosis of AT can generally be established from a 12-lead ECG. The determination of the AT mechanism (Table 4, Figure 1) and localization from a 12-lead ECG may be difficult as P waves may be masked by the QRS complex or T waves, depending on AV conduction and CL.

A NRAT and LRAT typically present with a discrete P wave and an intervening isoelectric line,$^{64}$ which, however, can also be missing when the atrial activation duration exceeds the CL.$^{65}$ In these patients with mostly abnormal substrates characterized by markedly altered

atrial activation, prolongation of atrial activation manifests as continuous atrial activity without an isoelectric line between two P waves.$^{65}$ Different algorithms based on the morphology of the P wave have been developed for the prediction of a FAT origin (Figure 6, see also chapter 5).$^{64,66-68}$ Lead V1 and I/aVL have been found to be the best leads to differentiate between left and right atrial foci. A positive P wave in V1 favors an AT in the left atrium (LA) aside from the crista terminalis, whereas a negative P wave in V1 suggests an origin in the RA. However, this does not hold true for counter-clockwise peritricuspid MRAT, where commonly a positive P wave is recorded.$^{5,69}$ In contrast, in lead V1, a biphasic P wave (positive, then negative) favours the crista terminalis and a negative, then positive P wave suggests a paraseptal focus.$^{70}$ Of note, the interpretation of V1 depends on individual anatomy as well as correct positioning of the electrode. Leads I and aVL may be more robust in clinical practice: A negative deflection in these leads quite reliably points to a LA origin.

Counter-clockwise pertricuspid MRAT remains the most common MRAT, with opposite appearance of P waves in the inferior leads

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 compared to V1. It is defined as continuous regular electrical activity with negative saw-tooth waves with predominately negative P waves and terminal positivity in the inferior leads and positive waves in V1 transitioning to negative by V6. During the much less common clockwise pertricuspid MRAT, waves in the inferior leads are positive and broad, and often bimodal negative in V1.$^{71}$,$^{72}$ The surface ECG can assist in distinguishing pertricuspid from non-pertricuspid MRAT in patients with otherwise normal atrial myocardium. In other settings, however, it does not provide reliable guidance for the mechanism or localization.$^{73}$⁻$^{75}$ Noteworthy, despite established diagnostic and therapeutic concepts, novel mechanistic insights include areas of slow conduction beyond the cavotricuspid isthmus (CTI) favouring the term pertricuspid as more accurate than CTI-dependent atrial flutter (see also 2.1).$^{76}$,$^{77}$

The presence of an isoelectric line has not only been illustrated in NRAT ('true' FAT)$^{6}$ and LRAT,$^{78}$ but also in MRAT, e.g. in the presence of a slow-conducting isthmus,$^{78}$ small activated atrial areas, and/or large

low voltage areas.$^{65,79}$ In patients without prior cardiac surgery, a non-pertricuspid MRAT mostly presents with P waves not indicative of typical circuits.$^{80-82}$ Importantly, scarred tissue after previous ablation or surgery or due to an underlying structural heart disease resulting in alteration of atrial activation sequences and reduction of activation voltage as well as antiarrhythmic drugs (AADs) may change typical ECG patterns.$^{65,73}$ In these cases, an atypical ECG does not exclude the diagnosis of pertricuspid MRAT (with an activation pattern along the tricuspid annulus).$^{73,75,83,84}$ Especially pertricuspid MRAT occurring after AF ablation often has atypical ECG characteristics due to altered activation.$^{73-75}$ Roof-dependent, perimitral, and other types of MRAT may exhibit similar ECG patterns, especially if the frontal plane axis is dictated by septal activation.$^{85}$ A non-pertricuspid MRAT can therefore only reliably be diagnosed in the EP lab. Consequently, since the underlying AT mechanisms cannot be reliably differentiated from a 12-lead ECG, assessment of intracardiac electrograms and response to pacing or pharmacologic intervention is required.

Management of patients with atrial tachycardia


2.6 Antiarrhythmic drug treatment

Considering currently available evidence, AAD treatment is of limited efficacy for most patients with AT.$^{1,86}$ Beta-receptor blockers and calcium channel blockers may be used especially for rate control with a low risk of side effects. While beta-receptor blockers should be avoided in AT with a vagal pattern, selected arrhythmias, like left septal AT, have been reported to terminate with verapamil.$^{87}$ For in-hospital conversion of MRAT to SR,$^{1}$ ibutilide or, alternatively, dofetilide may be appropriate.$^{88}$ However, the availability of both agents is limited in many countries. If ablation is not desirable or feasible, class IC drugs may be used with caution for rhythm control in selected patients. Even

though their use in the 2019 ESC Guidelines is only recommended for acute treatment of FAT,$^{89}$ they can be effective as maintenance therapy in some patients. Ivabradine may also be effective as a bailout strategy in some patients with NRAT due to enhanced automatity.$^{90,91}$ whereas in multifocal AT, AADs are generally not very effective.$^{92}$ Dronedarone and sotalol may be used for chronic AAD therapy in patients without structural heart disease or with LVEF > 40%.$^{88}$ Amiodarone and dofetide may also be suitable in some patients with structural heart disease and a left ventricular ejection fraction ≤40%, although long-term use is limited by their modest efficacy and well-known adverse effects.$^{88}$

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2.7 Cardioversion

Cardioversion

Advised TO DO

In haemodynamically stable patients with sustained symptomatic AT, pharmacological rhythm or rate control is advised, especially if electrical cardioversion or ablation is not part of the initial treatment strategy.

 In patients presenting with sustained, symptomatic AT with suspected AiCMP, it is advised to perform cardioversion and/or ablation.

In haemodynamically compromised patients with sustained AT, emergency electrical cardioversion is advised.

In high-risk patients (considering frailty and/or comorbidities) for hypotension, bradycardia, apnoea, airway obstruction, and/or oxygen desaturation, intensified and/or prolonged

  Continued

Continued

Cardioversion

monitoring is advised during and after cardioversion.

May be appropriate TO DO

Cardioversion with restoration and maintenance of SR prior to AT ablation may be appropriate depending on patient status.

In low-risk patients with haemodynamically well-tolerated arrhythmia, allowing an ongoing AT to continue by avoiding its termination via overdrive pacing/cardioversion may be appropriate to ensure that the clinical AT can be mapped.

In symptomatic patients with normal left ventricular function and rate control, clinical observation may be appropriate if the patient prefers a pharmacological approach.

Strength of evidence

   Management of patients with atrial tachycardia

Table 6 Device interrogation and programming for SMART-AT care

|Aim|CIED interrogation/programming| |---|---| |Optimal interpretation of atrial high-rate episodes to distinguish between DDAF and DDAT|Cardiac implantable electronic device-reordered atrial high-rate episode tracings need visual inspection and adjudication to avoid false positive DDAF$^{42}$| |Optimized device-based detection of AT and rejection of far-field R wave signal|Assess the (variability of) CL and the local electrogram (activation pattern and amplitude) to distinguish DDAF vs. $DDAT^{43}$| |Symptom improvement and heart failure prevention|Evaluate atrial lead (choice, positioning)$^{44}$ Optimized programming (sensitivity, PVAB, mode switch etc.)$^{45-50}$ Adopt maximum tracking rate$^{46,51}$ Evaluate mode switch (to VVI vs. $DDI^{52,53}$ Minimize ventricular pacing$^{54}$ Explore heart rate optimization$^{55-58}$ Adjust programming of short PVAB and AV intervals potentially preventing decompensation, especially in heart failure patients with cardiac resynchronization therapy devices$^{45,59,60}$ Apply atrial overdrive pacing in presumed MRAT (especially (with Ramp) in case of AT CL > 240 ms)$^{61}$ if cardioversion of AT is planned$^{62}$|

Abbreviations: CIED, cardiac implantable electronic device; DDAF, device-detected atrial fibrillation; DDAT, device-detected atrial tachycardia; and PVAB, post-ventricular atrial blanking period.

A preprocedural risk assessment—particularly considering frailty and comorbidities as well as the depth and choice of sedation—is essential to minimize the risk of hypotension, bradycardia, apnoea, airway obstruction, and/or oxygen desaturation.$^{93}$ In patients presenting with sustained, symptom at T加强 to cardiac compensation with AiCMP,$^{28}$ rate control$^{94}$,$^{95}$ and/or (electrical) cardioversion or ablation can be acutely performed. Observational data suggest that patients in SR at the start of AT ablation experience fewer recurrences than those presenting with ongoing AT, indicating potential benefits of reverse remodelling before ablation.$^{96}$

2.8 Ablation indication

|Ablation indication|Strength of evidence| |---|---| |Advised TO DO|| |Catheter ablation is advised for recurrent, symptomatic AT.|| |Catheter ablation should be considered after the first episode of pertricuspid MRAT, except when occurring within 30 days after cardiac surgery.|| |Catheter ablation is advised in patients with pertricuspid MRAT or incessant AT in the presence of AiCMP.|| |Ablation of pertricuspid MRAT is safe and efficient and is advised with no age limitation.||

CA has become the preferred treatment for most patients with AT, while the pharmacological therapy of NRAT has been downgraded.$^{1}$ Especially in patients with incessant or recurrent symptomatic AT, CA is recommended.$^{1,32,97,98}$

CA is highly effective in maintaining SR and is clearly superior to AADs for MRAT.$^{99}$ For both right and left-sided AT, targeted CA is

often the most effective treatment for long-term AT control.$^{100-102}$ When pertricuspid MRAT occurs during AAD therapy (class IC or amiodarone) for AF, in selected patients, CTI ablation can be a reasonable option to facilitate continued use of AADs for AF control$^{103,104}$ or as additive therapy in patients undergoing pulmonary vein isolation (PVI). Non-pertricuspid MRAT are also observed following AF ablation, particularly after extensive ablation in patients with persistent AF. The ablation technique may have an impact on the occurrence of post-PVI AT.$^{105,106}$ Although clinical and procedural complexity can result in challenges associated with AT ablation post-AF ablation, several studies have demonstrated promising outcomes in acute termination of AT and long-term maintenance of SR.$^{107-109}$

2.9 Preprocedural management

Preprocedural management for reentrant AT

Strength of evidence

Advised TO DO

In patients not presenting in SR and <3 weeks of therapeutic oral anticagulation, it is advised to perform an imaging study (preferentially TOE).

   For baseline assessment, transthoracic echocardiography is utilized, while variation in ejection fraction between AT and SR, irrespective

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![graph TD\n A1[Lead V1] --> A2[neg]\n A1 --> A3[ pos/neg]\n A1 --> A4[neg/pos iso/pos iso]\n A1 --> A5[ pos]\n A2 --> A6[V2-4 pos]\n A3 --> A7[Crista]\n A4 --> A8[Para-septal]\n A5 --> A9[bifid in II &/or V1]\n A6 -->|Yes| A10[Crista]\n A6 -->|No| A11[neg. in all inf. leads]\n A7 -->|Yes| A12[TA]\n A7 -->|No| A13[TA RAA]\n A8 -->|Yes| A14[Lead l iso or neg]\n A9 -->|Yes| A15[Lead l]\n A9 -->|No| A16[sinus P wave]\n A11 -->|Yes| A12\n A11 -->|No| A13\n A14 -->|Yes| A17[LPV LAA]\n A14 -->|No| A18[RPV]\n A15 -->|+/-| A18\n A16 -->|Pos| A19[Crista RPV]\n](1/parseimages/figurebb5e2876294742aabf072a4273b85c2c_0_2.png) of structural heart disease, should be evaluated.$^{110}$ Transoesophageal echocardiography (TOE) currently serves as the gold standard for detecting left atrial appendage (LAA) thrombi (Figure 7), particularly in those patients at high risk.$^{115-118}$ However, TOE is semi-invasive and

not universally available. Current guidelines are also limited regarding the precise role of LA imaging for thrombus detection before CA, as no randomized clinical trials have been conducted on this specific topic.$^{1,94}$ However, clinical decision-making is of importance, especially

Management of patients with atrial tachycardia

15

![graph TD\n A1[Need of TOE prior to CA?] -->|Yes| A2[Sinus rhythm]\n A1 -->|No| A3[>3 weeks of therapeutic OAC]\n A2 -->|Yes| A3\n A2 -->|No| A4[CHA2DS2-VAScore ≤2]\n A3 -->|Yes| A4\n A3 -->|No| A5[Thromboembolic risk factors*]\n A4 -->|Yes| A6[TOE not advised prior to CA*]\n A4 -->|No| A7[TOE advised prior to CA]\n A5 -->|Yes| A7\n A5 -->|No| A6\n A6 --> A8[CA performed]\n A7 --> A9[LAA thrombus]\n A8 --> A8\n A9 -->|Yes| A10[CA cancelled]\n A9 -->|No| A6\n A10 --> A10\n](1/parseimages/figure1c5034f9b28d462abccc0f8f42a279c5_0_2.png) for patients with a history of AF and/or suspected reentrant AT. An analysis from a single-centre registry indicated that patients compliant with oral anticoagulation and presenting for ablation in AF or MRAT without TOE may have a relatively low risk of thromboembolic complications.$^{119}$ By contrast, another study in adequately anticoagulated patients with AF/AT undergoing TOE before cardioversion or CA found a prevalence of LA thrombus of 6.3% in patients with CHA₂DS₂-VASc scores ≥3 vs. still 1.1% in those with scores ≤2.$^{114}$ Moreover, risk scores such as the CHA₂DS₂-VA alone may also underestimate the individual risk.$^{94,95}$ In consequence, the writing group members recommend an imaging study, predominantly TOE, in patients not presenting in SR prior to suspected reentrant AT ablation, depending on the individual risk-benefit ratio (including thromboembolic risk vs. potential TOE complications, including bleeding/relative contraindications).$^{120,121}$

In patients presenting in SR with >3 weeks of therapeutic oral anticoagulation, a TOE is not generally advised prior to AT ablation. In patients presenting in SR with <3 weeks of therapeutic oral anticoagulation and a CHA2DS2-VA score <2, TOE is not advised prior to AT ablation in the absence of other risk factors. In patients presenting in SR for CTI ablation without >3 weeks of therapeutic oral anticoagulation; TOE may not be necessary irrespective of the CHA2DS2-VA score, but systematic data are missing. A TOE is not indicated in patients with suspected FAT/NRAT in the absence of a history of AF.

Non-invasive, multimodal imaging can provide comprehensive information.$^{122}$ Compared to TOE, computed tomography imaging exhibits an excellent negative predictive value but lower specificity and positive predictive value, although specificity can significantly improve to 99% with delayed computed tomography, particularly using contrast-enhanced imaging protocols.$^{123,124}$ Cardiac magnetic resonance imaging has also been evaluated for identifying LAA thrombi, with some studies indicating a comparable performance to TOE, especially when employing delayed enhancement sequences, which can be of additional usefulness.$^{125}$ A recent meta-analysis comparing computed tomography and cardiac magnetic resonance imaging to TOE head-to-head found no difference in their sensitivity and specificity, indicating both modalities can be reasonable alternatives for identifying LAA thrombi.$^{126}$

In addition to detecting LAA thrombi, preprocedural and/or intraprocedural imaging can provide crucial anatomical and structural information, including the heart axis, landmark structures, septum anatomy, and the degree of (atrial) cardiomyopathy to aid in the procedure.$^{127,128}$

2.10 Relevance of structural heart disease and comorbidities

|Relevance of structural heart disease and comorbidities|Strength of evidence| |---|---| |May be appropriate TO DO|| |It is advised to consider AT ablation in patients with complex structural heart disease to reduce heart failure hospitalization and mortality.|| |AT ablation may be preferred over AAD in patients with pulmonary hypertension due to their potential negative inotropic properties and interaction with specific therapy for pulmonary hypertension.|| |AT ablation may be reasonable in patients with pulmonary hypertension to improve clinical outcomes.||

2.1.0 Aetiology

Therapeutic success of AT ablation differs widely across various populations (see Supplementary material online, Figure S1), which is partly explained by the underlying aetiologies and related comorbidities. This is particularly important for risk-benefit analysis in scenarios of advanced clinical complexity (Figure 8). The aetiology of AT is often

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 multifactorial and involves a combination of structural and functional changes. NRAT (especially in younger patients without relevant comorbidities) is often idiopathic. However, atrial structural remodelling may occur in the presence of ageing, arterial hypertension, valular disease, heart failure, and atrial fibrosis.$^{129}$ Systemic arterial hypertension is the most common risk factor promoting atrial cardiomyopathy,$^{130}$ but is understudied in the context of AT. Depending on the underlying aetiology, procedural complexity (Figure 9) can also increase, especially in repeat ablation procedures.$^{131}$

Various structural heart diseases may also contribute to the aetiology of AT through disease-specific substrate formation. Patients with hypertrophic cardiomyopathy frequently present with a complex arrhythmogenic substrate, which is determined by atrial fibrosis, dilatation, or intrinsic atrial myopathy, and predisposes to the occurrence of AT.$^{132-135}$ Here, the lack of standardized voltage cut-off values for atrial substrate mapping remains a challenge. Careful procedural planning, including adjustment of mapping settings and clinical AT definition, is essential and 34 usually allows effective rhythm control without the need for AADs.$^{13,136}$ Similarly, in patients with amyloid cardiomyopathy, AT ablation has been reported to reduce all-cause mortality, cardiovascular mortality, and heart failure

hospitalization compared to those without ablation and is especially effective for peritricuspid MRAT and NRAT.$^{137}$ Consequently, CA may be a reasonable treatment option in these patients depending on the patient's condition to improve prognosis.$^{137,138}$ Finally, the aetiology of LRAT and MRAT in patients without previous iatrogenic interventions,$^{139,140}$ which is suspicious for atrial cardiomyopathy, needs to be determined.$^{141,142}$ An increased incidence of AT has been found in several electrical and structural cardiac diseases with relevant therapeutic and prognostic implications (see Supplementary material online, Table S1): Patients with arrhythmogenic (ventricular) cardiomyopathy mainly present with (peritricuspid) MRAT and left-sided NRAT. CA has high success rates, which are comparable to the general population. Optimized implantable cardioverder-defibrillator programming (and/or system choice) is needed as AT are associated with shocks.$^{143-147}$ In patients with sarcoidosis, atrial 18F-fluorodeoxy-glucose uptake is associated with AT occurrence, which mostly presents as peritricuspid MRAT and left-sided reentrant AT, among others, located at the septum due to atrial-septal conduction disturbances. Glucocorticoid treatment may decrease AT burden, which is usually very low even before ablation, rendering the AT non-inducible during an electrophysiological study. Diffuse LA thickening may raise suspicion of sarcoidosis.$^{148-158}$

Management of patients with atrial tachycardia

 In patients with inherited arrhythmia syndromes and arrhythmias, AT occur in up to 20% of patients. Atrial arrhythmias are the first clinical manifestation in about half of the cases and their occurrence earlier in life may be associated with a higher risk of ventricular arrhythmias. Despite the young age and lack of risk factors, the risk of stroke and sinus node dysfunction in this population is substantial.$^{159}$ Furthermore, some patients with neuromuscular disorders are at high risk of developing AT. Since atrial standstill is characteristic for some populations and is associated with a highly thrombogenic substrate, these patients have an increased risk of stroke underlining the need of initiation of oral anticoagulation.$^{160}$

2.10.2 Comorbidities

Multiple comorbidities not only impact periprocedural management but also AT management strategies. In general, risk factor management in line with recent guidelines is mandatory.$^{94}$ In detail, considering the high likelihood of co-existing or future development of AF,$^{161}$ modification of risk factors like arterial hypertension, diabetes mellitus, obesity, metabolic syndrome, physical inactivity, obstructive sleep apnoea, alcohol consumption, and smoking is recommended as an integral part of arrhythmia care.$^{94}$,$^{130}$,$^{162}$⁻$^{167}$

AT also frequently occurs in patients with pulmonary hypertension, often leading to haemodynamic deterioration and worse prognosis.$^{168}$ Maintenance of SR appears to improve clinical outcome,$^{169}$ ADDAs may not be a feasible option because of their negative inotropic properties and interaction with specific therapy for pulmonary hypertension.$^{170}$ Whereas peritricuspid MRAT is frequently found as the first manifestation of supraventricular tachycardia in this population, ablation has been shown to be associated with a longer procedure duration and a greater amount of cumulative tissue ablation needed to achieve bidirectional block compared to patients without pulmonary hypertension.$^{171}$

In patients with pulmonary hypertension, additional substrate-based ablation does not seem to reduce arrhythmia recurrences compared with a limited approach.$^{172}$

2.11 AT in older patients

Despite its growing clinical relevance there are only limited data on elderly patients with AT.^173,174 Both the number of MRAT in general as well as peritricuspid MRAT increase with ageing, the latter from 5/100 000 in patients aged <50 years to 587/100 000 in those aged ≥80 years.^175,176 Ablation of AT has been demonstrated to be safe and efficient.^{2,109,177,178} Considering recent advances in techniques and technologies, ablation should not be avoided in elderly patients due to chronological age alone.¹⁷⁹ Available data from tertiary arrhythmia centres indicate the safety and efficacy of AT ablation independent of the underlying mechanism in patients ≥75 years compared to those <75 years, without an increasing rate of procedure-related complications in those ≥80 years.¹⁷⁴.

2.12 AT in pregnancy

Atrial arrhythmias in some patients manifest for the first time or become more frequent during pregnancy, with a peak at the end of the second trimester, as well as with concomitant structural heart disease and increasing age.$^{180-183}$ Although rare, the management of AF/AT in pregnancy can pose a unique challenge. In the prospective ROPAC (Registry of Pregnancy and Cardiac Disease), an increase in maternal mortality in patients with AF/AT during pregnancy and low birth weight has been observed.$^{182}$ Considering these findings and the overall limited evidence, in the case of already previously diagnosed AT, a dedicated plan for arrhythmia treatment should be created by an interdisciplinary team, including shared decision-making prior to pregnancy. In line with

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 current guidelines, rhythm control is the preferred therapeutic approach in pregnant women with AT. Beta-receptor blockers are commonly the first medical option; in case of inefficacy, flecinide and sotalol may be considered.$^{183,184}$ Electrical cardioversion is advised whenever AT is haemodynamically unstable or in the case of inefficacy of AADs and can generally be safely performed.$^{183,185}$ In case of a sustained AT refractory to AADs, ablation with minimal/zero fluoroscopy is a treatment option, whereas deferring ablation to postpartum is preferred.$^{183,186,187}$ If an intervention is deemed necessary, the timing of pregnancy should be carefully assessed.$^{188,189}$ Digoxin and verapamil may be appropriate for rate control of AT if beta-blockers fail. Anticoagulation is recommended for reentrant AT or if a history of AF is present.$^{94,184}$ Low molecular weight heparin (that might be switched to unfractionated heparin) is the therapy of choice for most scenarios, while non-vitamin K oral anticoagulation drugs are contrain-dicated during pregnancy.$^{183,184}$ The route of delivery should usually be determined by obstetrical factors rather than maternal arrhythmia,$^{183}$ without any differences in outcomes between vaginal or caesarean delivery in patients with atrial arrhythmia.$^{190}$

2.13 Neural control of AT

The extrinsic and intrinsic cardiac autonomic nervous system are well known to be related to the induction, maintenance, and termination of AT.$^{191}$⁻$^{193}$ Common arrhythmias like pulmonary vein (PV) ectopy$^{194}$ and AT$^{195}$,$^{196}$ as well as rather rare arrhythmias like speech-,$^{197}$⁻$^{199}$ breathing-, $^{196}$ and deglutition-induced$^{200}$ AT have been mechanistically linked with changes of cardiac neural control.$^{201}$,$^{202}$

Transient autonomic perturbations, exemplified by acute alcohol intake, may promote AT through sympathetic activation.$^{203}$

Autonomic influences have also been found to promote spontaneous automaticity and triggered activity in superior caval vein sleeves.$^{204}$ In parallel, AT itself may induce remodelling of muscarinergic receptors and their coupled potassium currents.$^{205}$ For some scenarios, individualized management concepts have been proposed but supporting evidence is mostly limited to preclinical data$^{206}$ and case reports.$^{207}$

Intraprocedural modulation of cardiac neural control by targeted changes in sedation and/or pharmacological interventions to induce and maintain AT in challenging situations are well established (Figure 10).$^{208}$ Related changes in AT CL as well as induction of junctional rhythms and AF might additionally challenge AT mapping and ablation, warranting time, advanced technical and patient support as well as careful standardization and titration of these interventions.

In recent years, electrical stimulation of extra- and intracardiac parasympathetic/sympathetic neural control is of growing interest in this context.$^{209-211}$ Ectopy-triggering ganglionated plexus can also be identified by endocardial delivery of bursts of high-frequency stimulation within the local atrial refractory period.$^{212}$ However, the usefulness of these techniques to gain mechanistic insights and finally improve patient outcome needs to be explored in more detail before routine use.$^{213-216}$

3. Intra- and postprocedural patient care

3.1 Anaesthesia and ventilation

Similar to AF ablation,$^{162}$ an AT ablation procedure can be safely performed under conscious sedation, deep sedation, or general anaesthesia, considering patient risk factors and anaesthesia availability.$^{217}$ Core principles have been well defined in the 2024 EHRA/HRS/APHRS/LAHRS expert consensus statement on AF ablation and can be adopted for most patients with AT. Importantly, deep sedation or general anaesthesia may limit the inducibility of AT, depending on the agents used.$^{218}$ Conversely, general anaesthesia with or without high-frequency jet ventilation$^{219}$,$^{220}$ may improve catheter stability, which may contribute to better outcomes in selected patients. Using the least sedation required for patient comfort is advised as well as using agents with a short half-life that can be titrated rather than longer acting agents that are difficult to reverse. Sedation and analgesia requirements may depend on patient characteristics and the energy source of ablation.$^{221}$

Management of patients with atrial tachycardia

3.2 Safety

 The overall risk of major adverse events is relatively low and comparable to AF ablation.$^{178,222,223}$ Intravenous heparin administration with a targeted activated clotting time >300 s is the recommended cornerstone for prevention of thromboembolic events during LA procedures (as well as selected RA procedures depending on the used multipolar catheter).$^{224,225}$ In patients with a history of AF and/or MRAT taking the morning dose as usual before the procedure ensures uninterrupted oral anticoagulation. For some patients it might be reasonable to hold one dose prior to CA with early reinitiation post-ablation. A loading dose of heparin is well established during RA procedures not using a multipolar catheter in most EP labs.$^{226}$ Intraprocedural safety, including respiratory and haemodynamic stability, requires standardized care that incorporates procedural factors (especially procedure time and fluid load) as well as patient-specific characteristics.

3.3 Intraprocedural care

 Compared to PVI, procedure durations of AT ablation are commonly longer due to complex substrate characteristics and/or multiple co-existing tachycardias, often with more extensive mapping and ablation, and patient-related factors increasing clinical complexity (Figure 8) and sometimes procedural complexity (Figure 9). These patient-related factors need to be considered to optimize patient safety and procedural success (Figure 11). First, ultrasound-guided vascular access might minimize the risk of vascular complications.$^{227,228}$ Second, managing fluid balance and regulating blood pressure are of particular importance especially in patients with heart failure. In contrast to PVI and other straightforward procedures, avoidance of fluid overload due to flushing of sheaths, catheters and volume administered through medication is of special importance.

 Figure 11 Risk stratification for the prediction of AT/AF recurrences after AT ablation. Classification of patients into a high and low risk group predicting AT/AF recurrences after AT ablation. Abbreviations: AF, atrial fibrillation; AT, atrial tachycardia; CV, conduction velocity; FAT, focal AT; LA, left atrial; LVEF, left ventricular ejection fraction; MRAT, macro-reentrant AT; and SR, sinus rhythm.

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In elderly patients and those with cerebrovascular disease, avoidance of hypotension is of particular importance to minimize the risk of cerebral ischaemia due to a decrease in cerebral perfusion pressure. Third, in patients with diabetes mellitus, repeated glucose monitoring is of importance especially during prolonged procedures to reduce the risk of hyper- or hypoglycaemic episodes, with a targeted periprocedural glucose level of 5.6-10.0 mmol/L$^{93}$ Finally, particularly in patients with chronic renal insufficiency, prevention of acute kidney injury should be strived for by minimizing the volume of contrast medium administered. The application of high-voltage pulsed-field energy can cause haemolysis, with the number of pulsed-field applications and post-ablation hydration as independent predictors; fluid infusion before the procedure has been found to mitigate acute kidney injury, though this is rarely needed given the number of lesions typically delivered for isolated AT.$^{229}$

3.4 Anticoagulation after catheter ablation

Anticoagulation after catheter ablation

Strength of evidence

Advised TO DO

Systemic anticoagulation is advised for at least 2 months (and thereafter depending on the CHA₂DS₂-VA score) following left-sided AT ablation in patients with a history of AF.

May be appropriate TO DO

In patients with isolated peritricuspid MRAT,

continuation of anticagulation may be appropriate depending on the CHA₂DS₂-VA score, considering

the high incidence of concomitant AF in these patients.

Advised NOT TO DO

  Oral anticoagulation is not generally advised following

CA of NRAT in the absence of a history of AF.

 Anticoagulation is recommended for at least 2 months after CA of left-sided reentrant AT, especially in patients with a history of AF.$^{162,230-233}$ In line with AF ablation,$^{234}$ the writing group advises that continuation of anticoagulation afterwards should be based on individual risk stratification including the CHA₂DS₂-VA score.$^{235}$ In patients with isolated perentricuspid MRAT, systemic anticoagulation may be applied depending on the CHA₂DS₂-VA score, considering the high incidence of up to 77% of AF during a median follow-up of 24 months after CTI ablation.$^{161}$ In patients with primary NRAT or right-sided AT excluding perricuspid MRAT, in the absence of a history of AF systemic anticoagulation following CA is not generally recommended. However, in the case of extensive LA ablation, this recommendation might be individualized after shared decision-making, depending on patient risk factors. In an analysis of 12 566 patients undergoing CA for supraventricular tachycardia, the highest mortality and non-fatal stroke rates during follow-up were observed in patients with MRAT, underlining the need for intensified monitoring and strict evaluation of long-term anticagulation.$^{2}$ Especially in patients without a history of AF and with a low risk of developing future AF, the duration of anticoagulation as well as the threshold for the initiation of permanent anticoagulation is unknown, as conflicting data exists.$^{8,236-238}$ Considering a differentiation between the underlying AT mechanisms, non-pertricuspid MRAT has been shown to have an increased thromboembolic risk compared to pertricuspid MRAT.$^{236}$ Pertricuspid MRAT is associated

In patients with a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminated after a period of non-terminat

with a reduced incidence of ischaemic stroke in comparison to AF at $CHA_2DS_2-VASc scores \ge 1$ and an increased risk compared to controls only at $CHA_2DS_2-VASc scores \ge 5.$^{237}$ Still, in two studies analysing a total of 681 and 5342 patients with Holter monitoring, respectively, even non-sustained AT without concomitant AF and independent of structural heart disease or previous atrial interventions have been suggested as a potential source of cerebral embolism$^{8}$,$^{238}$ proposing the initiation of systemic anticoagulation in selected patients with non-sustained AT depending on the $CHA_2DS_2$-VA score and other risk factors.

3.5 Recurrence and heart rate monitoring

ECG monitoring after AT ablation is recommended to identify patients at higher risk of needing ongoing AAD therapy or repeat ablation procedures. Individualized follow-ups, including scheduled visits at least 2 months post-ablation, can help optimize patient management within the SMART-AT framework.

Whereas negative drotropic agents are commonly continued temporarily after ablation, the impact of AAD initiation or discontinuation on long-term outcomes has not been investigated yet. AAD treatment is therefore widely individualized among centres depending on clinical needs weighing AT/AF burden, symptom severity and possible extracardiac side effects, with amiodarone as the most frequent approach used in up to 22% of patients, especially in those with concomitant AF.$^{28,139,239,240}$ AAD treatment following AT ablation is therefore reasonable in selected patients, particularly in the case of early recurrence.$^{240}$ Besides, attaining SR may have impact on the overall prognosis in AT patients with concomitant AF.$^{241,242}$

Clinical characteristics predicting recurrent AT after previous ablation include the presence of structural heart disease, LA diameter/volume, left ventricular ejection fraction, previous atrial surgery and duration of arrhythmia history.$^{239,240,243,244}$ Procedural characteristics predictive of recurrent AT are additionally summarized in Figure 11.$^{77,96,239,243,245}$

3.6 Repeat ablation

Repeat ablation

Advised TO DO

During repeat ablation of a left-sided AT and previously performed PVI, check for PV reconnection and bidirectional block of any additional linear lesions is recommended.

During repeat ablation, it is advised that pacing manoeuvres and activation mapping are used for linear block validation.

In patients with extensive low atrial voltage, it is advised to consider high-resolution activation mapping combined with entrainment.

During repeat ablation, previous bidirectional CTI block is advised to be ensured. Area of uncertainty

During repeat ablation of a right-sided AT in patients with previously performed PVI, check for PV reconnection and bidirectional block of any additional linear lesions is reasonable.

Strength of evidence

     Management of patients with atrial tachycardia

Repeat ablation is typically avoided for early AT recurrences which are usually treated by cardioversion, with possible AAD optimization.$^{109,240,246-249}$ Repeat ablation is advised on an individual basis, considering AT burden, symptom severity, and clinical risk factors for recurrence after reintervention. During repeat ablation of a left-sided AT, endpoints of previously performed procedures such as PVI or conduction block of linear lesions should be verified by pacing manoeuvres and/or activation mapping and completed, if appropriate. In patients with extensive low atrial voltage, consideration of high-resolution activation mapping combined with entrainment is advised to improve procedural success$^{250}$ and minimize the need for a second repeat ablation. During repeat ablation of a right-sided, non-pertricuspid AT, a previous bidirectional CTI block should be ensured.$^{109,131}$ During repeat ablation of a right-sided AT in patients with previously performed PVI, checking for PV reconnection and bidirectional block of any additional linear lesions is reasonable.

4. Mapping and ablation: conceptual considerations

4.1 Catheter setting

4.1.1 Less is more: dynamic conventional (activation) mapping

In most cases, activation mapping can be performed with a small number of diagnostic catheters. A multipolar catheter is typically inserted into the CS and serves as a fiducial reference. The CS activation pattern during AT can be used to rapidly guide AT localization (see below). A second (typically multipolar high-resolution mapping) catheter can then be used to rapidly map the atria.$^{251-253}$ Single-tip ablation catheters can offer a straightforward alternative or adjunct for activation and entrainment mapping, e.g. in suspected common AT forms of NRAT or MRAT. There are rare scenarios in which the relative timing of RA and LA activation is not fixed due to diffuse disease or prior ablation. In these cases, mapping of a right-sided AT using a CS reference may yield erroneous results and a RA reference catheter should be considered.$^{254}$ A right ventricular catheter may be used in rare cases for diagnosis (A-A-V pattern, see below) and/or unblocking P waves in some patients with a rapid AT or masked P waves.$^{255}$ Consequently, the concept of simple mapping is fundamental, highlighting the importance of using a stable reference catheter (such as a CS catheter) alongside a mapping catheter to identify the critical site of cardiac activation. In contemporary practice using three-dimensional (3D) mapping, this approach typically involves an ablation catheter and/or a high-resolution multipolar catheter.$^{109}$

4.1.2 Pattern and timing of activation

The pattern and timing of CS activation can be used to narrow the differential diagnosis of AT.$^{16}$ While a distal to proximal CS activation indicates a left-sided AT, a proximal to distal CS activation is the most non-specific pattern and could be secondary to a right-sided AT or a left-sided AT with septal to lateral activation of the inferior LA. In the latter scenario the timing of the mid-CS activation referenced to the P wave peak in V1 can be helpful. Whenever the mid-CS activation occurs at 50-70% of the P-P interval, pertricuspid MRAT will be identified with good specificity.$^{16}$

A chevron/reverse chevron CS activation is most commonly seen in roof-dependent MRAT, but can also be found, e.g. in LRAT or NRAT located at the anterior or posterior LA.

Noteworthy, double potentials along the whole CS can challenge mapping. Low-amplitude and broad potentials might represent far-field LA endocardial activity, while sharper potentials may represent the local activation of the CS musculature; sometimes with propagation in opposite directions.$^{19}$ Careful interpretation of the pattern and timing

of CS activation should therefore be performed in a stepwise approach, including targeted entrainment mapping manoeuvres for subsequent AT diagnosis and characterization.$^{16}$

4.2 Diagnostic electrophysiological manoeuvres

Diagnostic electrophysiological manoeuvres

Strength of evidence

Advised TO DO

It is advised to perform ventricular overdrive pacing demonstrating an A-V response if confirmation of AT is needed.

 It is advised to use atrial overdrive pacing in conjunction with common supraventricular tachycardia features if ventricular overdrive pacing does not accelerate the atria to the pacing CL.


4.2.1 Manoeuvres to verify AT

In patients with supraventricular tachycardia and predominant 1:1 AV conduction, manoeuvres to verify AT are critical. Right ventricular overdrive pacing 10-40 ms faster than the TCL provides a rapid tool to diagnose AT.$^{256-259}$ If the atrial CL accelerates to the ventricular paling CL and the tachycardia persists after pacing cessation, an A-A-V response is diagnostic of AT, whereas termination without atrial depolarization excludes it. An A-V response suggests AV reentrant or AV nodal reentrant tachycardia. Care must be taken to ensure that the atria are accelerated to the ventricular pacing CL, as AT cannot be definitively differentiated from AV nodal reentrant tachycardia in the setting of VA dissociation with this manoeuvre.$^{258}$ During atrial overdrive pacing, a post-pacing interval (PPI)-TCL <30 ms together with concealed fusion can be helpful to diagnose AT. Fixed V-A intervals on return to the CL suggest V-A linking, consistent with AV nodal reentrant tachycardia rather than AT.$^{260,261}$

4.2.2 Distinguishing non-reentrant from reentrant AT

Activation and entrainment mapping can be used together to distinguish non-reentry from reentry mechanisms, especially in difficult mapping situations (Figure 12). If two anatomically disparate sites within the atrium demonstrate a PPI-TCL of <30 ms after atrial entrainment, a re-entrant mechanism is established. Variability in the PPI when pacing from the same atrial site at different CLs can help differentiate the mechanism: relative stability of the PPI suggests reentry, whereas marked variability indicates a non-reentrant mechanism.$^{262}$ Atrial over-drive pacing is helpful not only for identifying the underlying AT mechanism but also for locating the optimal ablation site.$^{62,263,264}$ When entrainment cannot be demonstrated based on fusion assessment, concealed entrainment may still occur and may not be readily distinguishable from overdrive suppression of an automatic tachycardia.

4.3 Entrainment mapping for AT localization

Atrial overdrive pacing at a CL slightly shorter than the tachycardia can serve as a key diagnostic element. Entrainment is confirmed by acceleration of atrial activation to the pacing rate, constant fusion, and

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 resumption of the tachycardia after pacing cessation. As atrial activation is often small, fusion of intracardiac electrograms can provide a useful alternative to the surface electrocardiogram. If there is fusion or progressive fusion of intracardiac electrograms: (1) it supports reentry as the mechanism of sustained AT, (2) facilitates delineation of the re-entrant circuit, and (3) aids in identifying potential critical isthmuses (Figure 12).$^{257,265}$

Entrainment mapping for AT localization

Strength of evidence

Advised TO DO Entrainment mapping is useful for the diagnosis of reentrant AT and its localization.

May be appropriate TO DO

Entrainment mapping may be appropriate for the localization of AT even with a centrifugal activation in the activation map.


4.3.1 When, where and how

Advances in mapping technology have reduced the reliance on entrainment mapping. Nevertheless, it is still of importance, especially if an AT mechanism and/or optimal ablation site is not obvious. It is reasonable to guide entrainment by prior activation mapping to minimize unnecessary pacing. In complex cases with true multiple-loop circuits$^{266}$ or multiple-loop-like circuits$^{267}$ entrainment can unmask visual reentries as passive.$^{268}$ Additionally, reentrant circuits may present as centrifugal activation, potentially involving deep intramural myocardium or epicardial structures.$^{252,269}$ In such cases, entrainment serves as a valuable tool to identify the active circuit$^{76,270}$ and distinguish pseudo-focal from NRAT.$^{269}$ Entrainment mapping can also serve as a rapid tool to obtain initial insights into the reentrant circuit of AT before engaging in more detailed mapping. For instance, a PPI-TCL of >50 ms at the lateral RA, usually indicates that the circuit is in the LA. Entrainment can also clarify whether the same AT persists or has transitioned to a different AT, allowing adjustment of the ablation strategy.

Technically, it is helpful to consider both: Overdrive pacing, which is a manoeuvre, and the response to pacing with fusion, which reflects entrainment. Depending on a given intraprocedural situation, targeted vs. systematic entrainment (different LA sites including roof, septum, inferior, lateral, posterior, and anterior followed by RA (septal, lateral), appendage, and CS (proximal, distal)) can be appropriate.$^{247}$ The number of pacing stimuli needed to entrain is a simple and reliable criterion,

Management of patients with atrial tachycardia

which facilitates mapping intra-atrial reentrant tachycardia (IART).$^{271}$ Entrainment from two opposite regions, such as the septal and lateral or the anterior and posterior LA, with a return CL within 30 ms of the TCL, indicates a reentrant circuit involving both sites at which the over-drive pacing manoeuvre was performed.$^{6}$ Additionally, entrainment can offer valuable insights into the proximity of a pacing site to the reentrant circuit or origin of NRAT. Specifically, shorter PPIs indicate closer proximity, which can aid in the AT localization. Termination of MRAT by pacing stimuli without global propagation can be helpful to identify a narrow critical isthmus at which CA is highly effective.$^{272}$

4.3.2 Interpretation and potential pitfalls

To ensure effective use of entrainment,$^{273}$ several limitations or pitfalls must be acknowledged: (1) rate-dependent conduction slowing may occur, potentially leading to a PPI exceeding the TCL; (2) failure to capture may happen in critical regions of some reentreintracultis and; (3) pacing may alter (to e.g. another (non-clinical) AT or AF) or terminate the AT. AT with greater CL variability is more likely to be altered or terminated with overdrive pacing.$^{274}$ Pacing performed only for a short period at intervals no more than 20 ms shorter than the TCL can minimize the risk of unintentional alteration or termination.$^{274}$

Sometimes, the PPI may be shorter than the TCL. Causes of pseudo-short PPIs include intermittent capture, high output or and oral capture of parts of the circuit at a distance from the pacing electrode, spontaneous TCL variability, transient acceleration of the tachycardia, and incorrect annotation of the return cycle.$^{275,276}$ When excluding such artifacts, a PPI shorter than the TCL suggests the pacing site is within a narrow isthmus of slow conduction in the circuit and is critical to perpetuation of the tachycardia.$^{277}$ In case of difficult signal interpretation, it is advised to re-evaluate unipolar and bipolar electrogram morphology and amplitude and, if necessary, adjust filter settings, gain, and catheter contact or position to maintain accurate representation of local activation.

4.4 Electroanatomical mapping

 Three-dimensional electroanatomical mapping (EAM) systems have been in clinical use since the 1990s,$^{278}$,$^{279}$ with continuous improvements, greatly enhancing our understanding of complex arrhythmias. The resolution of these maps depends on catheter platforms,$^{280}$ the system's filtering for noise reduction, and the algorithms for signal processing and annotation.$^{281}$ These advancements have led to better visualization of arrhythmia circuits, improving both diagnosis and treatment (Figure 13). EAM has been found to reduce fluoroscopy time and radiation dose,$^{283-288}$ while procedural and mid-term success are influenced by the underlying arrhythmia and the used mapping approach.$^{289,290}$ Currently, several multielectrode catheter platforms are utilized with widely adopted 3D mapping systems. Mapping resolution is primarily enhanced by catheters equipped with smaller

electrodes and narrower inter-electrode spacing. Improved resolution and annotation is—depending on the given mapping system—additionally supported by advanced algorithms.

The activation map is constructed from the timing of each electrogram relative to a predefined reference to visualize atrial activation in AT. Local activation timing is typically determined by the steepest negative dV/dt of both unipolar and bipolar electrograms. Local electrograms are significantly influenced by the catheter platform used. Smaller electrodes with narrower spacing produce clearer and less fragmented electrograms, resulting in more accurate annotation of the local activation timing.$^{280,291}$ Voltage mapping provides additional valuable information, often revealing that the termination site of AT is located in low voltage areas.$^{292}$ While a threshold of 0.5 mV is commonly used to define low voltage regions,$^{293}$ this threshold may vary depending on the catheter platforms employed as well as the catheter orientation, electrode type, AT aetiology, atrial region, and heart rate.

4.5 Potential value and standards of high-resolution mapping

|Potential value and standards of high-resolution mapping| |---|

|Strength of evidence| |---|

Advised TO DO

For complex AT, combining high-resolution mapping with entrainment mapping and anatomical considerations is advised for accurate diagnosis and determination of the optimal ablation site.

 Conventional point-by-point mapping catheters are typically equipped with a large distal-tip electrode, primarily designed for delivering ablation energy. In contrast, multielectrode catheters collect a higher density of data points with variable orientations to the wavefront.$^{294}$ These catheters are less prone to the cancellation effect caused by different bipolar vectors. Multielectrode catheters can efficiently gather more electrograms within a shorter timeframe. Novel simultaneous mapping techniques can additionally be helpful to guide rapid arrhythmia characterization if more than one AT is present in a given patient.$^{295}$ However, electrogram annotation relies on automated algorithms that may require later editing, particularly in the case of fractionated signals.

Catheters featuring smaller electrodes with narrower inter-electrode spacing, when combined with algorithms specifically engineered to minimize far-field signals while emphasizing near-field activation, enhance the accuracy of near-field signal detection and annotation. This improvement leads to enhanced mapping resolution, as each data point more precisely reflects the electrical activity of a smaller, localized tissue area, providing a more detailed characterization of the substrate.$^{296-298}$

In AT mapping studies using conventional systems, post-AF ablation-related AT were reported to be either NRAT or LRAT in 21-37% of cases, and macro-reentrant in approximately 58-100% of cases.$^{73}$ A recent multicentre, observational cohort study conducted by Derval et al.$^{299}$ demonstrated a notably lower incidence of NRAT (9% of

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![graph TD\n A1[Analysis of 12-lead ECG(SR vs. AT)] --> A2[Targeted activation map during AT]\n A1 --> A3[Full activation map during AT]\n A2 --> A4[Analysis of activation + wavefront propagation]\n A3 --> A4\n A4 --> A5[MRAT]\n A4 --> A6[LRAT]\n A4 --> A7[NRAT]\n A5 --> A8[Suspected mechanism → Perimital → LA roof → Peritricuspid]\n A6 --> A9[Localization of possible target ishmus]\n A7 --> A10[Identification of site of earliest activation]\n A8 --> A11[Evaluate entrainment vs. direct ishms ablation]\n A9 --> A12[Advanced automated EGM analysis → Signal characteristcs → Activation pattern]\n A10 --> A12\n A11 --> A12\n A12 --> A13[Differentiation of active / passive / blind loops]\n A13 --> A14[Targeted entrainment]\n A14 --> A15[Identification of target ishmus]\n A14 -->|Not conclusive| A16[Evaluate additionally → Extensive entrainment → Activation mapping(CS, SVC) → Epicardial structures → Critical boundaries]\n](1/parseimages/figure726c35998ff64175af96c36d4af1f724_0_2.png) cases) by using high-resolution mapping. In contrast, 90% of AT were defined as MRAT (60%) or LRAT (27%), with only 4% of AT remaining undetermined. The discrepancy in diagnosed mechanisms may reflect the higher resolution of high-density mapping, revealing reentrant circuits missed by traditional approaches. Beyond enhancing diagnostic precision, high-resolution mapping systems play a pivotal role in identifying the most effective ablation sites. Since AT circuits have been found to be more intricate than previously thought (Figure 13),$^{300}$ high-resolution mapping systems provide a comprehensive methodology by integrating detailed (electro)physiological and anatomical data. This advanced level of insight not only facilitates more precise localization of ablation targets but also allows revisiting the same site to complete or extend the ablation, and therefore can optimize treatment strategies.$^{301,302}$

Although activation maps sometimes display complex wavefronts, reentry AT is often simplified to an active circuit and additional passive components (partly with wavefront collisions).$^{303}$ A detailed analysis of

the initial high-resolution map—with or without additional entrainment mapping (see 4.3)—can offer valuable predictive insights into how the AT will respond to radiofrequency (RF) ablation.$^{303}$ This includes whether the AT will terminate or convert, and any changes in CL that may follow.$^{274}$

4.6 Power sources and techniques

As our understanding of the optimal techniques and strategies for ab-lation of cardiac arrhythmias has improved, a focus has been placed on optimizing the biophysics of ablation to aid improvements in lesion dur-ability and safety.$^{162}$ The optimal power source and ‘dosing’ can differ depending on arrhythmia aetiology, localization, and patient his-tory.$^{137,304–306}$ For example, the fact that the substrate encountered in repeat procedures consists of a mixture of healthy tissue, diseased tissue, and ablated tissue can impact lesion creation.$^{307,308}$

Management of patients with atrial tachycardia

|Choice of ablation technology|Strength of evidence| |---|---| |Advised TO DO|| |It is advised to use single-tip irrigated catheters, preferably with contact force, for RF ablation.|| |May be appropriate TO DO|| |It may be reasonable to use PFA, especially if a lesion set on the posterior wall or near the phrenic nerve is required.|| |It may be reasonable to consider ethanol ablation in AT involving the VoM.|| |It may be reasonable to consider cryoablation if lesions near the AV node are required or if catheter stability is problematic.||

4.6.1 Radiofrequency ablation: power settings and lesion creation monitoring

The primary mechanism underlying RF-induced injury to myocardium is thermal, with myocardial injury and death occurring when a temperature of approximately 50°C is reached.$^{309}$ Thus, the primary objective of RF ablation should be to attain this critical temperature while avoiding adverse thermal effects such as coagulum formation, steam pops, and heating of adjacent structures. Standard 4 mm tip RF catheters have largely been supplanted by open saline-irrigated catheters, which allow improved power delivery in areas of low blood flow and reduce char/thrombus formation at the expense of losing the utility of catheter tip temperature to guide lesion formation.$^{162}$ Gold tip electrodes have the theoretical advantage of creating bigger lesions than standard platinum-iridium electrodes, as supported by some but not all studies.$^{310}$ Available evidence overall indicates equivalent efficacies of gold and platinum-iridium tip catheters for successful de novo ablation of the CTI.$^{311}$

The integration of contact force sensing in RF ablation represents a significant advancement.$^{312-316}$ Contact force is a strong determinant of lesion size and effectiveness;$^{317}$ a significant increase in freedom from atrial arrhythmia is obtained when achieving a target contact force and catheter stability.$^{318}$ Lesion formation indices are quantitative metrics used to assess ablation quality, incorporating parameters like power, contact force (over time), and impedance.$^{319-322}$ The use of such indices has been shown to lead to higher first pass PVI rates$^{323,324}$ and superior freedom from atrial arrhythmia.$^{325}$ During linear ablation, point-by-point RF delivery (≤35 W, interlesion distance ≤6 mm, ablation index ≥550) has demonstrated high first-pass block rates at the roof but not at the mitral isthmus, which often requires additional endocardial and epicardial RF applications due to its complex anatomical architecture.$^{326}$

High-power short-duration is an RF ablation strategy that creates lesions by prioritizing myocardial resistive heating while limiting conductive heat transfer. In in vivo and computational ablation models, high-power short-duration compared to standard RF settings resulted in lesions with greater surface area, similar depth, improved lesion uniformity and an increase in lesion contiguity.$^{327}$

Most of the high-power short-duration approaches, which were mainly developed for the treatment of AF, are performed using 45-60 W for 5-15 s.328 One system utilizes a catheter and temperature-

controlled generator that can deliver up to 90 W over 4 s, known as very high-power short-duration ablation. Thermocouples in the catheter provide real-time tissue-temperature feedback, allowing the system to titrate catheter irrigation and power, which might reduce the incidence of steam pops329 and improve AF procedural times without compromise to effectiveness or safety.330 Energy titration during these short RF deliveries does not play a major role in this workflow. The major concern about this approach is the lack of transmurality, especially in regions with relatively thick atrial tissue. In such scenarios, bipolar ablation 331,332 can be a helpful technique for effectively terminating tachycardias originating from deep intramural locations.333

An alternative temperature-controlled RF ablation system features six external thermocouples at its catheter tip imbedded in a network of industrial diamonds offering high thermal diffusivity.$^{334}$ Its efficiency has been demonstrated in preclinical models,$^{335}$ peritricuspid MRAT,$^{336}$ perimitral MRAT,$^{337}$ and AF ablation.$^{338}$ More evidence is needed to support the general application of high-power short-duration ablation in the treatment of AT.

4.6.2 Pulsed-field ablation

Among recent advances in cardiac electrophysiology, pulsed-field ablation (PFA) represents the most transformative development, offering a primarily non-thermal abative approach.$^{339-342}$ PFA utilizes intermittent, high-intensity electric fields for short durations (micro- vs. nano-seconds) to achieve irreversible cellular and tissue destruction.$^{343}$ Its potential advantage over thermal ablation lies in the preferential targeting of myocardial tissue with a reduction in collateral damage to the oe-sophagus or the phrenic nerve.$^{344-346}$

A variety of different PFA catheter designs and systems are being introduced, some of which are capable of combined PFA and RF ablation.$^{347,348}$ Clinical data are increasingly becoming available.$^{349,350}$ Early studies indicated safety and acute efficacy of posterior wall isolation.$^{345}$ as well as its use for targeted ablation of MRAT.$^{340,352}$ However, all studies noted that focal catheters would be better suited for creating focal and linear lesions. Focal catheters are now becoming increasingly available. Limited clinical data so far support their potential use in NRAT,$^{353}$ LRAT$^{354}$, and MRAT$^{354-356}$ ablation, indicating safety and acute efficacy in the RA and LA.$^{354}$

Unresolved issues surrounding PFA include long-term efficacy as well as safety concerns largely related to electrolysis, giving rise to micro-bubbles within the blood pool with the potential for micro-emboli, haemolysis-induced renal dysfunction in the case of extensive ablation, and coronary spasm/dimage with ablation directly over coronary arteries.$^{357,358}$

When energy is delivered adjacent to a coronary artery, PFA has been found to routinely provoke coronary vasospasm.$^{359}$ This has been observed mostly during the treatment of two common forms of AT: perimitral and peritricuspid MRAT.$^{360-362}$ It can be attenuated in most but not all patients by pre-treating with high doses of intravenous nitroglycerin (2-3 mg).$^{359,363}$ However, whether reducing spasm amelorates chronic injury to the coronary artery is unclear.$^{364}$ A recent study found a 10% narrowing of the coronary artery 3 months after PFA of the CTI.$^{365}$ The relative benefits and limitations of different PFA technologies in this context still require systematic evaluation. Noteworthy, the current availability of PFA systems varies widely across the world and rapid evolution is expected. It seems reasonable to consider PFA in challenging situations requiring ablation on the posterior wall or near the phrenic nerve.$^{344-346}$

4.6.3 Ethanol injection/ablation

Vein of Marshall (VoM) ethanol ablation may be performed either empirically for persistent AF or as a targeted therapy in patients with .364.$^{366}$ $^{39}$ It uses in the treatment of NRAT,$^{370}$ LRAT,$^{371}$ and MRAT$^{211}$ has been described. Reentrant AT involving the Marshall bundle network has been found in up to 30% of left-sided AT after AF

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 ablation, mostly perimitral MRAT.$^{211}$ Achieving mitral isthmus block, therefore, often necessitates further ablation to be performed epicardially within the CS. This may be challenging due to anatomical constraints and the presence of fibrofatty tissue insulating the VoM. VoM-related AT should be strongly suspected when arrhythmia recurs after extensive ablation, including endocardial mitral isthmus ablation.$^{131}$

Ethanol ablation in the VoM is an adjunct method to achieve perimiral block, with multiple studies demonstrating high success rates of 98–100% for the achievement of block in this fashion, with shorter procedure duration.$^{372-375}$ We suggest the use of ethanol ablation for perimiral MRAT or LRAT$^{211}$ using the VoM, either as an adjunct to RF or as a primary strategy (Figure 14). A learning curve in successfully cannulating and ablating the VoM should be considered.$^{376}$

4.6.4 Cryoablation

Alongside advances in RF technology, cryoablation has also evolved. While cryoballoons are mainly used for PVI, focal cryocatheters offer the advantage of creating reversible test' lesions. This might improve safety in para-Hisian AT not accessible from adjacent structures, such as the aortic root or LA, or when catheter stability is problematic.$^{377,378}$ The ability of the catheter to stick to the tissue when frozen can also increase stability in areas such as around the anterior lip of the tricuspid valve.$^{379}$ More recently, catheters capable of ultra-low temperature

cryoablation have emerged to provide more durable focal and linear le-sions. This can increase the cryogenic power available using a high-pressure 'near-critical' nitrogen refrigerant (near its boiling tempera-ture of -196°C). In animal models, this has been shown to produce durable transmural lesions,$^{380}$ with safety and acute success in AF abla-tion,$^{381}$ although not yet in AT ablation.

4.6.5 Combined ablation forms and other

Despite recent advances in RF-, cryo-, PFA, and ethanol-ablation approaches, some patients still suffer from therapy-refractory AT. Consequently, several innovative approaches are under development.$^{382,383}$ but so far, lack appropriate evidence for systematic recommendations. The most solid evidence so far is available for combining RF with ethanol-ablation for perimitral MRAT.$^{372-375}$ The feasibility of utilizing a focal ablation catheter toggling between RF and PFA has been demonstrated in patients with AF, including mitral isthmus, LA roof, and CTI lines in some patients.$^{384}$ Also, bipolar ablation has been found to be useful for therapy-refractory arrhythmias,$^{332,385,386}$ especially for intramural septal AT.$^{331}$

4.6.6 Robotic ablation

Remote navigation systems were developed to overcome the manual skill dependency inherent in conventional CA. Robotic ablation may enable precise lesion placement, thereby producing more contiguous

Management of patients with atrial tachycardia

lesions. Historically, two predominant navigation systems have been introduced: One magnetically driven system$^{387}$ and one using a hollow robotically steered sheath,$^{388}$ with the former being internationally available.

Remote navigation may not only improve catheter stability,$^{389}$ but also have the potential advantage of reduced fluoroscopy exposure for the operator.$^{390}$ Cardiac tamponade rates appear to be relatively low with the magnetically driven system,$^{391,392}$ as the distal tip of the catheter is soft. Furthermore, for experienced operators it allows easier access to the LA via a retrograde approach, which may be useful in some patients with congenital heart disease (CHD).

However, whilst radiation can be reduced, procedure times can be prolonged due to the time needed to set up the system. Clinical outcomes have not been shown to improve in limited randomized controlled trials despite the theoretical advantages over conventional manual ablation.$^{393}$⁻$^{395}$ Further disadvantages have been the significant learning curve in the use of this technology and both the initial purchase price of the system and the costs per procedure. For these reasons, robotic AT ablation should be performed in experienced centres and reserved for patients with anatomy in which conventional manual navigation would be challenging.

4.7 Ablation strategies

|Choice of ablation strategy|Strength of evidence| |---|---| |Advised TO DO|| |Side-to-side comparison of activation and voltage maps is advised to identify the critical area and design the most effective lesion set.|| |The endpoint of AT ablation is advised to include tachycardia termination during ablation (without an ectopic beat interrupting a circuit), confirmation of completion of the targeted lesion set, and non-inducibility.|| |The endpoint of linear lesions is confirmation of bidirectional block across the ablation line.|| |If pacing manoeuvres are borderline or inconclusive, repeat mapping and ablation is advised.|| |If isoprenaline is utilised during tachycardia induction, it is advised to be also used in testing for non-inducibility after ablation.|| |May be appropriate TO DO|| |Advanced local signal analysis in combination with entrainment mapping at critical sites may be appropriate to identify the ablation target area.|| |For bidirectional block of a mitral isthmus line, ethanol infusion may be reasonable to eliminate residual epicardial conduction.||

4.7.1 Targeted critical area ablation

Identifying the optimal ablation target area is essential in achieving desirable procedural and clinical outcomes. A comprehensive review of

mapping data, including active and passive loops as well as structural and functional substrates, can guide targeted ablation of critical areas (Figure 15). The critical isthmus of reentrant circuits was initially characterized in several animal models and during surgical mapping.$^{396-398}$ It is defined as the area of atrial myocardium that is essential for the maintenance of a reentrant AT, resulting from scars and/or anatomical obstacles, often accompanied by slow conduction. Ablation resulting in conduction block at the critical isthmus leads to tachycardia termination and prevention of its recurrence.$^{3,399}$ The local bipolar atrial electrogram, especially in scar-related AT, commonly shows low amplitude, and long fractionated signals denoting a low voltage area and slow conduction, respectively.$^{72,400}$ High-resolution activation mapping with small multielectrode catheters helps identify the critical area, typically corresponding to the narrowest or slowest part of the activation wavefront.$^{248,401-405}$ The local electrogram at the critical isthmus may differ markedly from that at the anatomical isthmus, e.g. in peritricuspid or perimital MRAT. Peak frequency analysis can assist in identifying critical regions.$^{406}$ Entrainment at the critical site can confirm circuit involvement and improve acute ablation success with fewer lesions.$^{399,407}$ Side-to-side comparison of activation and bipolar voltage maps can additionally help to determine the most effective lesion set.$^{131}$

NRAT originates from discrete sites and several mapping techniques are helpful to identify the earliest activation, where the unipolar electrogram typically displays an initial negative deflection.$^{408,409}$

4.7.2 Anatomically guided linear ablation

Linear ablation joining anatomical structures to interrupt atrial arrhythmias was first inspired by the surgical Cox maze procedure.$^{410}$ RF ablation was subsequently used to create anatomical lines to interrupt AT, including patients after corrective surgery for CHD.$^{411}$ Anatomical barriers and atrial scarring from surgical incisions, patches, prior ablation, or tissue degeneration can create critical isthmuses that facilitate reentrant AT.$^{412}$ Furthermore, linear ablation strategies used in the treatment of persistent AF were also used to treat AT. Examples of these include mitral isthmus ablation and a LA roof line in roof-dependent MRAT.$^{413}$,$^{414}$ Depending on the underlying substrate, ablation of the anatomical or practical isthmus may be reasonable.

The anatomical isthmus is defined as the portion of the reentrant circuit bounded by anatomical obstacles (alone or in combination with scar), irrespective of local electrogram characteristics (see also Chapter 2, Table 5). The practical isthmus is defined as the narrowest pathway between scars and/or anatomical obstacles, which is anticipated to be the most appropriate site for ablation; it can be determined based on anatomical length, local activation/electrogram characteristics indicating slow construction, entrainment mapping, tissue thickness, and finally catheter stability (Figure 16). Both the anatomical and the practical isthmus usually encompass the critical isthmus but may differ depending on the applied criteria, leading to distinct ablation strategies. One drawback of long linear lesions is that residual gaps, even with advanced ablation techniques, may predispose to further AT.$^{304,354,415}$

4.7.3 Substrate modulation and other strategies

Substrate modulation primarily targets low voltage areas that may serve as critical isthmuses, aiming to homogenize scar tissue and prevent recurrence.$^{416,417}$ Related strategies were initially described for the treatment of persistent AF and later adopted for AT.$^{162,418,419}$ It can be applied, for example, to the ablation of AT with alternating or variable CLs and activation patterns, particularly in patients with adult congenital heart disease (ACHD) and multiple potential isthmuses.$^{420-422}$ Additionally, several functional atrial substrate mapping strategies during SR have been proposed, partly adapted from ventricular substrate-based ablation techniques.$^{423-427}$ Although current evidence is limited, these approaches may be useful when a clinical AT is absent, non-inducible, or difficult to map (see also Chapter 4.2.2, Figure 17 and Supplementary material online, Table S2). In such cases, residual

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![graph TD\n A1[Anatomical MRAT Perimital Posterolateral line(MA-LIPV) Anterolateral line(MA-LSPV) Anteromedial line(MA-RSPV) LA roof-dependent LA roof line Pericardipud CTI ablation] --> A2[Non-anatomical MRAT Ablate given isthmus (identified by voltage/activation/EGM analysis(+ entrainment))]\n A3[MRAT] --> A2\n A4[LRAT] --> A5[Ablate critical site (and add linear lesions towards anatomical/surgical barriers)]\n A5 --> A2\n A6[NRAT] --> A7[Ablate site of earliest activation]\n A7 --> A2\n](1/parseimages/figure6eaab291867d4a489b6556c53c9d3319_0_2.png) myocardial strands within scar areas may enable slow conduction and sustain reentry. Progression of the atrial substrate may result from ageing, hypertension, diabetes, obesity, structural heart disease, or long-standing arrhythmia, leading to histological remodelling and scar formation.$^{429}$ A retrospective multicentre study indicated that substrate-based linear lesions combined with prophylactic CTI ablation were associated with favourable outcomes in patients with scar-related upper-loop reentry.$^{416}$ Additional strategies include ethanol ablation of the VoM, which can eliminate AT involving the LA ridge or mitral isthmus.$^{430,431}$ In post-AF ablation AT, re-solation of the PVs and closure of conduction gaps in previous linear lesions, alongside ablation of the clinical AT, represent reasonable pre-emptive measures to reduce recurrence.

4.7.4 Procedural endpoints and validation of ablation strategy

Various procedural endpoints for AT ablation—used alone or in combination—have been applied in multiple cohort studies.$^{108,299,432}$ Common endpoints include tachycardia termination during ablation (without a causative ectopic beat interrupting the circuit), non-inducibility tested by programmed stimulation or atrial burst pacing to atrial refractoriness or a minimum CL of 200 ms (with or without isoprenaline), and complete bidirectional block across ablation lines confirmed by differential pacing or high-resolution mapping.$^{433}$

A small randomized study in patients with AT after prior ablation for persistent AF found no association between post-procedural inducibility and outcome, and no benefit of additional ablation targeting inducible AT to achieve non-inducibility.$^{432}$ Moreover, even after successful termination of the clinical AT and achievement of non-inducibility, considerable recurrence rates have been reported during follow-up, mainly due to non-index AT, most commonly perimtral, followed by roof-dependent forms.$^{109,131}$ In these scenarios, durable mitral isthmus and roof block have therefore been found to be key determinants of a successful outcome in AT ablation.$^{131,432,434}$ Current evidence also indicates that AT inducibility after elimination of the clinical AT (see also Chapter 9.1) may rather represent a prognostic marker of a more advanced arrhythmogenic substrate than a procedural target.

Considering these data, validation of bidirectional block across ablation lines as the procedural endpoint for linear lesions has received

increasing scientific attention in recent years.$^{301,302}$ Historically, mostly performed by differential pacing,$^{413,414,435,436}$ high-resolution mapping has been found to be useful for the evaluation of residual conduction. In a prospective study, high-resolution mapping identified residual conduction in 38%, 47%, and 29% of CTI, roof, and mitral isthmus lines, respectively, often missed by differential pacing.$^{301}$ Patients with a complete block of all lines confirmed by high-resolution mapping showed an encouragingly lower AT recurrence rate compared to those with at least one unblocked line (4.6% vs. 68.1% at one year). In patients with previous AF ablation, durable PVI and bidirectional linear block in addition to ablation of the clinical AT seems sufficient irrespective of the presence of gap-related AT.$^{432}$

If isoprenaline is utilized during tachycardia induction, it should also be used in testing for non-inducibility. Additionally, if induction is successful during local anaesthesia and conversion to monitored anaesthesia is conducted mid-procedure, post-ablation re-induction should be evaluated when the patient regains consciousness, if feasible.

5. Focal AT

Focal AT

Advised TO DO

Ablation of NRAT is advised to be performed at the site of earliest activation after exclusion of a pseudo-focal AT.

5.1 Definition

FAT is defined as atrial activation emanating from a discrete focus separate from the sinus node spreading centrifugally (Figure 18).$^{3}$,$^{4}$,$^{3}$,$^{4}$,$^{3}$,$^{3}$

Management of patients with atrial tachycardia

 Traditionally, FAT includes activation mapping covering up to 75% of the TCL rather than up to 100% seen in reentrant AT.$^{438}$ Exceptions occur particularly in patients with previous cardiac interventions where continuous activity encompassing nearly the entire CL may be observed within a confined region.$^{439}$

NRAT, representing 'true' FAT, may occur in bursts lasting seconds to minutes as opposed to reentrant AT which is usually sustained due to a stable circuit. However, (pseudo-)focal micro-reentrant AT (MiRAT) may be stable and sustained as well.

5.2 Mechanism

FAT accounts for up to 10% of all AT.$^{437}$ It is important to note that ‘focal’ refers to a pattern of activation on an electroanatomic map and not an electrophysiological mechanism.

Two non-reentry mechanisms underlie FAT:

(1) Enhanced automaticity—acceleration or burst of activity from an automatic focus due to an increase in the slope of phase 4 depolarization, shortening of the refractory period or decrease in the threshold for excitation; (2) Triggered activity—the result of afterdepolarizations which are focal electrical events that result in repeat depolarization at phase 2, 3, or 4 of the action potential and accordingly may be referred to as early or late.

Advances in high-resolution mapping have established MiRAT and SRAT as subtypes of LRAT, sometimes showing a centrifugal activation pattern. Differentiating MiRAT from true focal AT can, however, be challenging or even impossible, as subendocardial micro-reentry may appear focal on 3D maps while the underlying mechanism cannot

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Workflow for difficult AT mapping situations

 Figure 17 Workflow for difficult AT mapping situations. Flow chart suggesting a structured workflow for difficult AT mapping situations. Note that before careful review, slow continuous activation at the bottom of the inferior LIPV was not observed, and instead, centrifugal activation from the lateral LA (yellow star) was observed. Magnification of the area of interest (white dotted square) and automatically acquired electrograms in this region demonstrated that discrete activation was displayed, suggesting focal activity. Note that after careful review, slow continuous activation at the bottom of the inferior LIPV was clearly displayed (red arrow). Magnification of the area of interest (white dotted square) and automatically acquired electrograms in this region demonstrated that continuous activation was displayed, suggesting reentrant activity. Abbreviations: AT, atrial tachycardia; LAA, left atrial appendage; LIPV, left inferior pulmonary vein; LSPV, left superior pulmonary vein; RIPV, right inferior pulmonary vein; RSPV, right superior pulmonary vein; and SR, sinus rhythm. Adapted from Takigawa et al.$^{428}$

 Figure 18 Non-reentrant AT. (A) Schematic drawing of an NRAT displaying centrifugal activation. (B) Right atrial electroanatomy displaying a FAT mapping pattern. The map indicates a NRAT as the underlying mechanism. The local atrial electrogram at the earliest atrial activation site displays an initial negative deflection. Abbreviations: IVC, inferior vena cava; and SVC, superior vena cava.

Management of patients with atrial tachycardia

always be reliably determined during an electrophysiological study (see also Chapters 4, 6, and 7; pseudo-focal AT).

Histological studies mostly reported normal myocardium at the AT focus; however, abnormal myocardium may provide the substrate for abnormal automaticity.$^{26}$ NRAT can be multifocal, especially in older patients, while children more frequently demonstrate a single automatic focus.$^{439}$ During an electrophysiological study, triggered activity may be initiated or terminated by programmed stimulation. In contrast, NRAT, due to abnormal automaticity, occurs spontaneously or in response to isoprenaline and is not induced by programmed extrastimuli.$^{26}$

Isoprenaline may be useful to distinguish the mechanisms of FAT in the EP lab. MIRAT will remain at a stable CL in response to adenosine. Triggered activity may abruptly terminate with adenosine, while automaticity will have transient termination and then reinitiation.$^{440}$

5.3 Localization

FAT does not occur randomly throughout the atria, but clusters at specific anatomic locations.$^{437}$ Sites of FAT origin are often characterized by alterations in myocardial fibre orientation. In a series of 126 patients with FAT, AT arose in the RA in 63% and LA in 37%.$^{64}$ Common sites for AT include the tricuspid annulus, crista terminals, PVs, and the paraseptal region.$^{441}$ Paraseptal sites involve: perinodal, septal tricuspid annulus, CS ostium, left septum, superior mitral annulus, and the non-coronary cusp. The latter should be considered in case of early para-hisian atrial activity.

The localization of FAT can generally be determined from an unen-cumbered P wave on the 12-lead ECG. An algorithm integrating P wave morphology with intra-atrial multipolar activation patterns and timing has also been reported to be useful for the localization of non-PV sites.$^{442}$ Lead V1 has been found to be the most useful lead to differ-tate between LA and RA foci (see also Chapter 2).

$\bullet$ Negative or biphasic positive/negative: likely RA origin

$\cdot$ Biphasic negative/positive: likely paraseptal origin

* Positive: likely LA origin (except crista terminalis)

A P wave algorithm can guide targeted mapping, particularly when inducibility is limited (see Figure 6).

5.4 Mapping and ablation strategy

5.4.1 General

Given the limited efficacy and side effects of AADs, ablation is the preferred therapy for most patients with NRAT. CA relies on accurate mapping of the site of origin, typically using catheters with small electrodes.$^{437}$ A discrete P wave can help guide the starting point for detailed mapping, while pacing manoeuvres (e.g. ventricular overdrive with post-pause observation) can clarify morphology when obscured. The onset of the P wave can also serve as a useful reference, since sites activating at or after this point are unlikely to represent the tachycardia origin. CS activation can help determine whether mapping should begin in the right or left atrium (see also section 4.1.2). Determining the FAT mechanism can aid in accurate mapping: triggered AT usually exhibits a discrete electrogram 20–30 ms before the P wave, while LRAT often shows long, fractionated signals occupying >50% of the CL. However, the exit region from an automatic focus may also show fractionated electrograms.$^{443-445}$ The unipolar 'QS' morphology indicates centrifugal propagation from the focal site.$^{446,447}$

Atrial overdrive pacing may help confirm the origin, as the PPI approximates the CL in MiRAT and triggered AT.$^{263}$ but commonly exceeds it in automatic AT.$^{448}$ However, overdrive suppression can

challenge this manoeuvre. Because many FAT are triggered or micro-reentrant, identifying the site where the PPI best matches the CL can guide ablation, though pacing must be minimized to avoid termination. A pacing CL of ≤20 ms faster than the CL has been demonstrated to rarely terminate stable AT.$^{274}$ Typically, a detailed high-resolution map is acquired first, followed by potential overdrive pacing at candidate ablation sites. A major limitation to procedural success can be insufficient ectopy or tachycardia to identify the site of origin and define an accurate procedural endpoint.$^{437}$

To minimize insufficient ectopy, the use of light sedation is recommended. In cases of non-inducibility, which may occur with a greater likelihood depending on the sedatives used,$^{218}$ escalating the dose of isoprenaline and, occasionally, intravenous calcium may facilitate induction.$^{449}$

5.4.2 Challenging anatomical areas

Up to two-thirds of right-sided FAT arise from the crista terminalis.$^{450}$ Since ablation in this area carries a small risk of right phrenic nerve injury, high-output atrial pacing should be performed before RF energy delivery to confirm the absence of diaphragmatic capture.$^{26}$ Electroanatomic characterization of sinus node activity may further enhance procedural safety, particularly in elderly patients, where sinus node injury is more likely.$^{451-455}$ Cautiousness is advised when ablation is performed near the sinus node during isoprenal infusion or pacing, as this may mask signs of sinus node injury. A progressive CL prolongation without acute termination or acceleration beyond expected automaticity can be potential warning signs.$^{162}$

FAT may also originate from within the superior vena cava$^{456}$ (as well as a persistent left superior vena cava$^{251}$) with automaticity,$^{457}$ triggered activity$^{458}$ and MiRAT$^{459}$,$^{460}$ as reported underlying mechanisms. Proximal isolation of the superior vena cava using a limited number of energy deliveries$^{461}$⁻$^{466}$ may be more effective than focal RF ablation within the superior vena cava, which carries a risk of superior vena cava stenosis.$^{467}$

Para-hisian FAT requires careful mapping from adjacent structures (especially non-coronary cusp and/or LA, septal tricuspid/mitral annulus, CS ostium, aorto-mitral continuity). If the earliest activation is at the His bundle, ablation should be attempted first from alternative sites such as the aortic root. For mid-septal origins, cautious energy titration or focal cryoablation is advised.

FAT from the PVs may occur after incomplete PVI or spontaneously in younger patients. These may be evanescent and difficult to induce in the EP lab. Most operators favour antral isolation of the PVs to reduce AT recurrence and minimize the risk of PV stenosis or phrenic nerve injury, particularly for FAT originating from sites distal to the ostium.$^{468}$

FAT originating from the LAA is less common. However, they are often incessant and challenging to map because the pliability and movement of the appendage may lead to confusing delineation of tachycardia origin. Use of a circular mapping catheter in the LAA to maintain a fixed reference may be helpful. Catheter manipulation needs to be performed with caution because of the thin and heterogeneous tissue structure, as the risk of perforation is higher than in other atrial regions. In rare cases, surgical appendage removal may be required.$^{469,470}$ Also, whenever possible, LAA isolation should be avoided, considering the otherwise higher cardiovascular risk.$^{471}$ Finally, while most of the AT related to atrial incisions are MRAT, FAT can arise from surgical scars. Due to the presence of lines of block from surgical incisions, atrial activation may mimic a MRAT. Entrainment/PPI mapping can help to confirm the diagnosis and origin of FAT in these challenging situations.

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6. Localized reentrant AT

6.1 Definition

Localized reentrant AT

Advised TO DO

To discriminate LRAT from NRAT, it is advised to use intracardiac electrogram characteristics (indicating a local dominant rotational activation with prolonged, highly fractionated signals).

To treat LRAT, it is advised to target the critical istmus whenever possible, while additional creation of linear lesions can be reasonable.

  Following its first description >25 years ago,$^{82}$ various definitions have been used to describe AT with a relatively small circuit. These arrhythmias commonly circle around a dense scar or a line of block (Figure 19). Mainly, the terms localized reentrant tachycardia (LRAT),$^{6,472}$ small circuit reentry (SRAT),$^{473}$ and micro-reentrant AT (MiRAT)$^{162}$ have been used in the literature with partly overlapping definitions (see Supplementary material online, Table S3). Considering its well-established terminology (localized reentry AT in >460 PubMed hits), the writing group recommends summarizing these tachycardias as LRAT as a subgroup of reentrant AT (Figure 1). MIRAT and SRAT can be understood as subforms of the umbrella definition LRAT, although overlapping arrhythm characteristics exist.

Based on consensus, a LRAT is defined by a circuit that is typically not around a fixed anatomical obstacle but associated with atrial disease or fibrosis and confined to a circuit diameter of approximately <2 cm. This threshold ensures a clear mechanistic separation from MRAT, which is classically characterized by a PPI equal to the TCL at sites >2 cm apart.$^{3}$ A circuit size of 3 cm may also frequently extend across more than one anatomical atrial segment (e.g. anterior and septal), although exceptions exist, especially depending on atrial size. The path length is typically determined by local electrophysiology with a small or no excitable gap. LRAT can be readily initiated and terminated by programmed stimulusation and burst pacing.$^{6,141,472}$

SRAT is defined as an LRAT with circumferential local activation that may spread away centrifugally to the periphery. Electrograms at the origin are typically characterized by fractionated (diastolic) potentials which encompass >50% of the CL over a small diameter. MiRAT is defined as a centrifugal atrial spread radiating from a (very) small circuit that can be readily initiated with programmed electrical stimulation as the marker of reentry. The electrogram at the site of origin is typically of long-duration, fractionated, and localized to a very small diameter.

6.2 Mechanism

In patients with atrial cardiomyopathy$^{429}$ and/or previous cardiac interventions, among all AT, LRAT accounts for 11–40%.$^{5,474}$ Localized reentrant circuits, which often occur in scarred areas, typically have multiple corridors of slow conduction that contribute to AT maintenance and have an isthmus width of <10 mm.$^{253,475}$ The activation pattern often appears as small rotatory actions or 'carousels' around a scarred area and as rectangular when running around a linear incision.$^{253,475}$ Compared to NRAT, intracardiac electrogram characteristics of LRAT show a dominant rotational activation commonly, but not

exclusively, with prolonged, highly fractionated signals.$^{141,472}$ Importantly, pseudo-reentries must be carefully excluded, which may occur in regions of wavefront turning or collision, or may result from annotation artifacts due to noise or interpolation in areas of incomplete mapping.$^{476}$ Electrograms in the candidate circuit and activation in the wider surrounding region should be reviewed to distinguish pseudo-reentry from LRAT.

SRAT, as a subform of LRAT, has a circumferential local activation that may spread away centrifugally to the periphery in some cases depending on zones of advanced remodelling (with lines of block in some directions and preferential conduction in others). It can also be present as part of a figure-of-eight and other dual-loop or rarely triple-loop AT, which might challenge the identification of the critical AT site for successful ablation.$^{266}$ In such scenarios, combining arrhythmia topology with electrogram features may enable activation and entrainment mapping to support prompt termination to SR with ablation.$^{477}$ MiRAT is commonly characterized by centrifugal atrial spread beyond the re-entrant circuit itself.$^{26,478}$

The CL of MiRAT has been found to be considerably shorter than that of NRAT.$^{255}$

6.3 Localization

LRAT has been observed in multiple areas of both atria, including the thoracic veins.$^{266,479}$ In patients with suggested atrial cardiomyopathy without a history of previous cardiac interventions, the most common site of localization is the anterior LA wall.$^{109,253,292}$ In patients with previous ablation, the critical part of the circuit is often located close to previously ablated regions, such as the PVs or other linear lesions. Typical localizations include the anterior LA (13-53%), the LAA (13-60%), the LA ridge (37-40%), the interatrial septum (13-32%), and the PVs (16-20%).$^{131,253,292,299,475}$

6.4 Mapping and ablation strategy

6.4.1 General

High-resolution activation mapping in recent years has significantly advanced our understanding of LRAT. Concurrently, the integration of targeted electrogram analysis remains essential for both mechanistic insights and therapeutic success.$^{253,417}$ The electrogram at the critical region of a LRAT is typically 'long and fractionated', often comprising >50% of the CL (≥35% up to ≥90%, see Supplementary material online, Table S3) on a single electrode or multiple closely spaced electrodes.$^{255,260,474}$ In SRAT, critical electrograms are typically characterized by fractionated signals on >1 electrode, while in MiRAT, the electrograms have been found to be fractionated at some anatomical sites but not necessarily at others.$^{6,19,260,480}$ Atrial overdrive pacing may help to identify and characterize LRAT.$^{481}$ Entrainment with a PPI equivalent to the TCL is observed in a relevant proportion of cases, but may be limited, especially in extensively scarred atria.$^{277}$

Ablation of LRAT commonly involves ablation at the critical site, with creation of linear lesions bidging the nearest anatomical-surgical barriers, or extension of the existing lines of conduction block to reach large anatomical barriers, e.g. one of the PVs or the mitral annulus, or scar regions due to previous ablation or atrial cardiomyopathy. Depending on the critical area of slow conduction and reentrant size, a single ablation often results in early AT termination, while additional consolidation is recommended.$^{249,476}$ The necessity of adjunct PVI should be considered in patients who show evidence for atrial myopathy presenting with non-focal left-sided AT without previous interventions.$^{141,249}$

6.4.2 Challenging anatomical areas

The LAA was early described as a potential site of origin for LRAT (see also 5.4.2).$^{479}$ High-resolution mapping strategies have enabled more

Management of patients with atrial tachycardia

 precise localization and characterization of multiple origins, including the LAA ostium.$^{131,482,483}$ De novo and post-AF ablation MiRAT has been repeatedly observed to arise from either the anterior base or the LA ridge (between the left PVs and the posterior base of the LAA). In these regions, limited ablation without linear or circumferential lesions, avoiding electrical isolation of the LAA, has been shown to result in successful termination without any recurrences of the index AT during mid-term follow-up.$^{482}$ In some patients, LRAT depends on the Marshall bundle network and may be targeted at the Marshall bundle-LA junction at the LA ridge, correlating with the arborization of the VoM and suggesting a potential epicardial-endocardial breakthrough.$^{211}$

7. Macro-reentrant AT

MRAT are one of the most common forms of reentrant tachycardias, which are now well described with their multiple underlying mechanisms. It is commonly defined as a circuit around an anatomical obstacle where the CL is determined by the obstacle and the presence of regions of markedly slowed conduction. Careful mapping, including advanced signal analysis in combination with the standardization of procedural workflow and novel ablation strategies nowadays, allows SMART-AT care, translating into overall high acute procedural success in about 90% of patients (see Supplementary material online, Figure S1). It may be initiated or terminated either by atrial burst pacing or

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programmed electrical stimulation. The latter is mostly limited to MRAT when there is a zone of markedly slowed conduction easily susceptible to unidirectional block. However, in the case of peritricuspid MRAT, e.g. initiation with programmed stimulation is rare and would require burst pacing to achieve unidirectional local block.$^{484-486}$

Macro-reentrant AT

Strength of evidence

Advised TO DO

In patients with previous cardiac interventions, it is advised to know the ablation/surgical strategy used during the index procedure as it may affect the arrhythmia mechanism by creating complex and atypical circuits.

In dual- and multiple-loop circuits, the use of high-resolution 3D mapping in combination with entrainment is required to understand each circuit, identify an eventual common isthmus, and guide the ablation strategy.

When an ablation line is performed to treat a MRAT, a complete bidirectional block of conduction across the line should be demonstrated by means of pacing manoeuvres and/or activation mapping.

May be appropriate TO DO

VoM ethanol infusion is reasonable to facilitate achieving block in the lateral mitral isthmus in patients with perimitral MRAT.

  

7.1 Periticuspid macro-reentrant AT

The overall incidence of peritricuspid MRAT is 88/100 000 person-years and is 2.5 times more frequent in men. Predisposing factors include age, chronic obstructive pulmonary disease, and heart failure.$^{176}$ Although recognized as one of the most common forms of MRAT, the exact epidemiology of peritricuspid MRAT is not known with certainty, as various forms of (peritricuspid) MRAT and AF often coexist. Peritricuspid MRAT is characterized by a right-sided MRAT circuit with a broad activation wavefront rotating around the tricuspid annulus. The circuit has anatomical boundaries represented by the crista terminals-eustachian ridge/inferior vena cava posteriorly and the tricuspid annulus anteriorly and commonly uses the CTI as the narrowest segment of the circuit.$^{487-489}$ Beyond that classic description, several variations have been described mainly concerning the upper part of the circuit (anterior or posterior to the superior vena cava).$^{488,490}$

The counter-clockwise presentation, the most common MRAT, is characterized by a downward RA free wall activation, followed by the CTI and the right septum. This activation results in regular atrial activation at a rate of 250–330 bpm, with classical saw-tooth waves in the inferior leads (see also chapter 2.5).$^{491}$ In the rarer clockwise presentation, the circuit of arrhythmia is the same but activated in the opposite direction, resulting in a different and often more variable ECG pattern with broad, mostly positive waves in the inferior leads.$^{3}$,$^{71}$

Occasionally, peritricuspid MRAT may appear with an atypical ECG pattern, especially in the case of previous cardiac surgery involving atrial

incision, after extensive RF ablation, or in the presence of native atrial scar.$^{73,102,492}$ Nevertheless, preventive linear ablation at the CTI or other common sites for MRAT in patients undergoing AF ablation is not recommended.$^{493}$

Treatment

CA is the most effective treatment for peritricuspid MRAT.$^{103,104}$ The principle of ablation is to create a line of block between the tricuspid annulus and the eustachian ridge at the anterior aspect of the inferior vena cava, generating complete bidirectional conduction block across the isthmus, as demonstrated by differential pacing or activation mapping in challenging situations.$^{435,494}$

7.2 Perimitral macro-reentrant AT

Perimitral MRAT was initially reported as a frequent form of left-sided MRAT occurring in patients with large spontaneous atrial scar.$^{82,142}$ The perimitral circuit is characterized by an activation wavefront circulating around the mitral annulus and using atrial scar and PVs as boundaries (Figure 20). As such, perimitral MRAT is frequently observed after AF ablation, especially when substrate modification is combined with PVI, or after cardiac surgery with atrial intervention.$^{131,299,306,418,495-499}$ The ablation strategy used during the index procedure is critical to know, as it may affect the arrhythmia by creating complex and atypical circuits.$^{299,300}$ Owing to the complex nature of the atrial substrate and arrhythmia circuit, the 12-lead ECG is usually non-specific in perimitral MRAT.$^{500}$ Since one myocardial layer can bypass another and lead to a downstream centrifugal propagation at their interface, they can also present as pseudo-focal AT in an activation map.$^{269}$ When 3D mapping systems display a centrifugal activation from the ostium of the LAA and the top of the LA ridge,$^{501}$ mid-low regions of the LA ridge,$^{502}$ or the neighbouring areas around the left inferior PV, reentrant (pseudo-focal) AT using the VoM$^{252,269}$ should be differentiated from true FAT. Whereas a short PPI at the site opposite to the breakthrough site demonstrates a MRAT despite centrifugal propagation in the activation map,$^{269}$ multiple breakthroughs rule out the possibility of a true FAT and the 12-lead ECG (P wave duration), a typical QS pattern with a sharp dV/dt in the unipolar electrogram at the origin, as well as a high-resolution activation map with a global activation histogram further enable accurate differentiation.$^{252}$ A combination of activation mapping and entrainment along the circuit is commonly required to confirm the diagnosis.

Treatment

The ablation strategy is similar to peritricuspid MRAT, namely the achievement of a stable line of block at the narrowest isthmus of the arrhythmia. Originally, the preferred isthmus was the atrial region between the left inferior PV and the mitral annulus (named ‘mitral isthmus’).$^{413,503}$ This approach has several advantages: (1) short length (17–51 mm);$^{503,504}$ (2) preservation of natural LA activation:$^{505}$ and (3) relationship with the CS for epicardial ablation.$^{413,498,506}$ In spite of this, long-term block of the mitral isthmus remains challenging, mainly due to epicardial fibres along the CS and VoM that bypass the line.$^{131,211,498,506-511}$ Recent studies have demonstrated the superiority of adding ethanol in fusion in the VoM to improve acute and long-term mitral isthmus block.$^{369,372,373,5212-516}$ Other ablation approaches have been reported, including the anterior mitral line and the superolateral line, both with high acute success rates.$^{517-519}$ However, they are also associated with important anatomic challenges, such as Bachmann’s bundle, and may impair atrial function.$^{520-522}$

3.3 LA roof-dependent macro-reentrant AT

Roof-dependent MRAT represents the second most common form of MRAT occurring after AF ablation.$^{299,418,496,497}$ As with perimitral

Management of patients with atrial tachycardia

  MRAT, roof-dependent MRAT is frequently diagnosed in patients with severe native atrial scar or after heart surgery.$^{142,299,499}$ The typical circuit is characterized by an activation wavefront that rotates around a set of PVs, left or right, resulting in a commonly perivenous MRAT. The

narrowest path of the circuit is usually located between both sets of PVs. 3D activation mapping and entrainment are required to confirm the diagnosis, as atypical variants are frequently described, especially if the patient has a history of substrate-based AF ablation (Figure 21).$^{299,300}$

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Treatment

The ablation strategy consists of achieving a line of bidirectional block between the two sets of PVs, often but not necessarily performed as a ‘roof line’.$^{414}$ Generally considered less technically challenging to complete than the mitral line, the roof line is associated with a high acute success rate (90–98%) although the septo-pulmonary bundle, an epicardial structure insulated from the atrial body by fat, can bypass the line.$^{414,523}$ As such, it may affect lesion transmurality and reduce acute and long-term results.$^{524,525}$

In some situations, a low posterior line (floor line) may be an easier one to perform and block than the roof line. As with any line between the left and right PVs, this line will also eliminate roof-dependent MRAT. Due to a higher risk of oesophageal injury, the floor line should be limited to cases with failed roof line attempts.$^{526,527}$ The use of PFA might allow delivery of a posterior line more safely with higher efficacy than thermal ablation.

7.4 Figure-of-eight and complex dual-loop circuits

Dual-loop circuits are characterized by the coexistence of two simultaneously documented loops, each fulfilling the definition of a reentrant circuit. A figure-of-eight circuit is defined as a specific type of dual-loop reentry involving two coexisting loops rotating in opposite directions and sharing a common segment of unidirectional activation.$^{492}$ Similar to single-loop circuits, these arrhythmias are favoured by severe atrial scar (post-ablation, post-surgery, or spontaneous) and may represent 20–50% of AT in these complex substrates.$^{131,142,266,299,496,528,529}$B. Multiple studies from several centres around the globe in the last two decades demonstrated that these arrhythmias are more common than previously thought.$^{266,477,492,530}$ The most frequent circuit is a combination of perimitral and roof-dependent MRAT, although many variations have been described (Figure 22).$^{299,529,531}$ The use of high-resolution 3D mapping associated with entrainment is required to understand each circuit, differentiate active from passive macroreentrant loops, identify an eventual common isthmus, and guide the ablation strategy.$^{267,299,528,529,532}$ The identification of two critical boundaries—defined as sequential activation around a given barrier, spanning ≥90% of the CL—can be additionally helpful to identify a critical isthmus and terminate an AT to stable SR by a single-line ablation strategy.$^{533,534}$ This can be of importance since an identified narrow, slowly conducting isthmus may be a critical isthmus or a non-critical isthmus.

7.5 Multiple-loop AT

Multiple-loop AT are defined as those composed of >1 independent active loop sharing one common isthmus, including dual-loop AT and triple-loop AT, with the entire CL included in each of the circuits.$^{266,535}$ Multiple sequential AT are another frequent clinical presentation of multiple AT.$^{299,536}$ In these cases, only the main loop is ‘active’ and constantly resets the secondary loops in which a part of the CL is missing. Termination of the main loop reveals the secondary loop(s) until SR is restored. The underlying substrate is similar to a dual-loop circuit and is characterized by the presence of atrial scar. Multiple-loop AT are frequent and may represent 20% of post-AF ablation AT. The circuits usually include LA macro-reentry and the PVs (Figures 22 and 23).

Treatment

Dual- or multiple-loop AT require customized approaches for complete and effective ablation. The operator has the option of targeting each arrhythmia circuit individually, at a central common isthmus, or targeting two separate limbs. However, as classic MRAT (perimitral and roof-dependent AT) are involved in the majority of cases, the optimal ablation strategy often requires ablation of the anatomical isthmuses.$^{532}$

7.6 Biatrial AT

Biatrial tachycardia is a rare form of MRAT in which both atria constitute essential components of the circuit. It typically occurs when a large electrical obstacle on the septum is present, e.g. as a result of either extensive substrate ablation or previous anterior mitral line attempt.$^{515,537-539}$ In such cases, a comprehensive 3D map of both atria, complemented by en-trainment, is required to confirm the diagnosis. The circuit typically involves preserved interatrial connections, with Bachmann's bundle forming one limb and the CS or anterior septum the other.$^{537,540,541}$ Three different loops have been reported with different ablation strategies.$^{540}$ It is important to keep in mind that interatrial connections are anatomically robust, and may be resistant to RF ablation.$^{515}$

7.7 Epicardial components

Beyond the knowledge of typical atrial anatomy, often considered as a 2D structure, it is important to understand the concept of epicardial connections between adjacent structures, as it can strongly influence our ability to create transmural lesions. Specific structures separated from the atrial body by a layer of fat may be incompletely eliminated with RF ablation and create an atypical substrate for recurrent tachycardia.$^{542-544}$ Marshall's bundle is certainly the most frequent and is responsible

Management of patients with atrial tachycardia

 for a wide spectrum of arrhythmias, whilst Bachmann's bundle, the PVs, and septo-pulmonary bundle are also implicated in these recurrent arrhythmias.$^{211}$,$^{269}$,$^{508}$,$^{510}$,$^{513}$,$^{521}$,$^{545}$ High-resolution 3D mapping is required to understand these complex arrhythmias and adjust the ablation strategy. Ethanol-infusion in the VoM is an effective technique to eliminate Marshall's bundle-related arrhythmias.$^{514}$,$^{515}$,$^{546}$

8. AT following previous cardiac interventions

8.1 AT after catheter ablation of AF

AT after CA of AF remains a recognized challenge of growing importance, despite clinical and technological advances, particularly given the rising number of procedures.$^{547-553}$

The reported incidence of AT after AF ablation varies from 2.5–43.3%, highly dependent on index ablation strategies (see Supplementary material online, Figure S2).$^{306,418,554,555}$ Factors contributing to these differences include the specific ablation strategy, completeness of the ablation lines, and the presence of conduction gaps, which can facilitate reentrant circuits. MRAT is the most common form of AT post-AF ablation, but LRAT and NRAT also occur in up to 30% and 10% of all post-PVI AT.$^{109,299,556}$ Although rare, MRAT can also occur in patients

without obvious structural heart disease and unrelated to previous cardiac surgery or catheter intervention. It may for example be related with septal reentrant circuits as an expression of atrial myopathy.$^{139,140}$ Identification of the exact AT mechanism is crucial, requiring detailed 3D mapping to pinpoint and terminate the reentrant circuit.

8.1.1 AT after pulmonary vein isolation

Early studies using segmental or circumferential PVI found that the most common mechanism of AT was focal activity from reconnected PVs.$^{495}$ More recent studies demonstrated that the prevailing mechanisms include various forms of reentry with or without involvement of the reconnected PV antrum (Figure 23). Of interest, in one study in patients with AT following prior cryoballoon ablation, all patients with left-AT presented with low voltage areas in the LA, suggesting a more progressive underlying fibrotic disease in these patients. To which extent patient-specific substrates rather than ablation gaps play a key role in the current era deserves further investigation.$^{557}$

With the advent of PFA, the incidence of AT appears comparable to that observed with RF and cryoablation.$^{557,558}$

8.1.2 AT after electrogram-guided ablation

Several historical techniques of AF ablation included the extensive ablation of complex atrial fragmented electrograms. The creation of regions of altered conduction has been linked with recurrences of

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mostly MRAT and LRAT, with an incidence of 7.6-24%.$^{559,560}$ Mapping and ablation of AT during and after AF ablation also remains of clinical relevance, with novel ablation strategies being currently under development.$^{561-565}$ Considering its emerging importance, novel approaches may include the use of artificial intelligence for AT prediction and for improved procedural planning and guidance.$^{562-565}$ Management of AT post-ablation of complex atrial fragmented electrograms typically involves repeat CA targeting the specific AT circuit. However, while the acute success rate is high, the long-term success rate may be lower, and the risk of multiple recurrences necessitates a careful balance between procedural intervention and medical therapy.

8.1.3 AT after additional linear ablation

Beyond PVI, anatomic isthmus transection has been proposed as an adjunct strategy for persistent AF to improve the success rate.$^{56}$,$^{56}$,$^{57}$ These lines aim to compartmentalize the atrium, thereby reducing AF recurrence. When these lines are not entirely transmural or continuous, they can paradoxically become sources of reentrant AT$^{56}$,$^{58}$ with an incidence variable from 15-30% (see Supplementary material online, Figure S2)$^{51}$,$^{56}$ Identifying gaps at these lines is crucial for effective management: 3D mapping is essential during repeat ablation procedures to locate and close these gaps (see also chapter 4.7.4).

8.2. AT after cardiac surgery

8.2.1 Anatomical and surgical considerations

The development of AT following cardiac surgery is determined by different anatomical and surgical factors.$^{569-571}$ Understanding these factors is crucial for predicting, preventing, and managing postoperative atrial arrhythmias.

inconvective barriers, while incomplete ablation lines or gaps in surgical lesions can be conduits for reentrant circuits. Specific cardiac surgeries, such as those involving the mitral or tricuspid valves, the atrial septum, or atrial appendages, particularly increase the risk due to their extensive atrial involvement. Main surgical procedures predisposing to AT in CHD include atrial baffles (Mustard and Senning surgeries) and Single ventricle palliation (Fontan surgeries).$^{572,573}$ The RA may be prone to developing a perincional localized reentrant circuit since its complex anatomy includes the crista terminals, the CTI, and the connections to the superior and inferior vera cava. The ex-tent and position of the atriotomy at the RA free wall significantly influence the rate of occurrence. The LA, which is targeted in procedures like mitral valve repair, PVI, and LAal occlusion, also exhibits significant pro-arrhythmic changes post-cardiac surgery. Anterior LA atriotomy may offer the perfect substrate for the development of MRAT or LRAT with single- or dual-loops.

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1. Understanding the specific surgical modifications and the resultant electrophysiological implications is crucial for effectively managing and preventing AT in this patient population. Atriotomy-related arrhythmias and others have been described after heart transplantation.$^{574-577}$ Combining CTI and lateral RA ablation has been found to result in a favourable long-term arrhythmia-free survival after orthotonic biatrial heart transplantation.$^{578}$

8.2.2 Hybrid ablation

PVI remains the cornerstone of AF ablation and surgical ablation can be performed via a thoracoscopic approach in the management of patients with (long-standing) persistent AF. Noteworthy, there is a recognized risk of developing AT, especially MRAT or FAT,$^{579}$ as a consequence of the lesion set.$^{580}$ Additionally, not all lesions can be exclusively addressed epicardially, such as the mitral or CTI line.$^{581}$ Endocardial mapping and ablation can be performed after epicardial surgical ablation to assess the lesion set and avoid atrial tachyarrhythmias if linear gaps or incomplete PVI are detected ('the hybrid approach').$^{582}$ A recent meta-analysis indicated that hybrid AF ablation is associated with a greater long-term freedom from atrial tachyarrhythmias when compared with isolated thoracoscopic ablation.$^{581}$

8.2.3 Mechanisms and other specifics

The MAZE procedure has seen numerous changes, with lesion size and technique variations. The traditional 'cut and sew' approach has mostly been replaced by intraoperative ablation techniques, utilizing energy sources like RF and cryoablation. The overall incidence of post-surgery AT in large single-centre studies is estimated to range from 5-15%.$^{583,584}$ The mechanisms underlying AT after cardiac surgery are multifactorial. Peritricuspid MRAT is the most common AT late after open heart surgery, other MRAT become progressively more common with more extensive atrotomy. In patients with postoperative right-sided MRAT after extended right atriotomy, ablation of both the CTI and the periincisional isthmus has been shown to reduce arrhythmia re-currences.$^{585}$ While RA incisional tachycardia is the dominant non-peritricuspid MRAT after RA atriotomy, perimitral or roof-dependent MRAT circuits can be expected after LA operations.$^{499,570}$ Understanding these mechanisms is essential for targeted therapeutic strategies, including critical area ablation to eliminate the underlying ar-rhythmogenic substrate.$^{432}$ Related approaches ensure a tailored and effective treatment, reducing the recurrence of AT and improving the overall outcomes for patients post-cardiac surgery.$^{411,586}$

8.3. AT in ACHD

8.3.1 Anatomical and surgical considerations

8.3.1 Anatomical and surgical considerations

AT in ACHD

Strength of evidence

Advised TO DO

It is advised to refer patients with moderate and severe CHD complexity and documented AT to a centre with expertise in ACHD patients and treatment of ACHD-related AT.

It is advised to consider CA for symptomatic sustained AT in patients with ACHD provided that the procedure is performed in experienced centres.

It is advised to target all induced AT by ablation provided that they are mappable (haemodynamically tolerated and sustained AT), and the additional procedural risk is considered to be low.

It is advised to access the CT(M)I from the systemic and pulmonary venous atrium if bidirectional conduction block cannot be achieved from the systemic venous atrium in case of surgical exclusion of parts of the isthmus.

It is advised to use intracardiac or transoesophageal echocardiography to identify baffle leaks or fenestations and to guide transbaffle or transcaval cardiac puncture.

May be appropriate TO DO

It may be appropriate to routinely perform imaging (cardiac magnetic resonance imaging or computed tomography) in ACHD patients with complex anatomy and expected transbaffle access to the systemic venous atrium.

CT(M) = cavotricuspid or cavotiral isthmus in L-looped ventricles.

CT(M) = cavotricuspid or cavotiral isthmus in L-looped ventricles.

systemic venous atrium. transbaffle access to the systemic venous atrium.

Management of patients with atrial tachycardia

 Late AT in ACHD are common with a prevalence between 15% and 75%, being highest after Fontan palliation and atrial switch operation.$^{587}$ Mapping and ablation can be technically challenging and require specific operator and departmental expertise.$^{588}$

Surgical incisions, patch material, valve annuli, and PVs form regions of conduction block that create anatomical isthmuses.$^{101}$ Interstitial fibrosis due to longstanding cyanosis, pressure and/or volume overload, ageing, and pathological hypertrophy can provide the substrate for slow conduction within anatomically defined isthmuses, explaining the high incidence of MRAT, whereas FAT frequently arises along suture lines or areas of scar tissue.$^{589}$

Surgical approaches and the timing of intervention have changed significantly, affecting the incidence and substrates for AT. The complexity of the AT substrate is mainly determined by the type of atrial

surgery.$^{572,590}$ Knowledge of the underlying CHD, prior surgical reports, and how to access the atria is mandatory.$^{588}$

Evolution of surgical approaches in CHD and potential impact on AT substrates

Surgical approaches in CHD and their potential impact on the development of AT have changed over the last decades. For atrial septal defect closure, repair of tetralogy of Fallot, or as part of other corrective surgeries, a large vertical approach previously used has been developed into a limited oblique RA incision (Figure 24).$^{573,591}$

For tricuspid atresia, single ventricle circulation (e.g. hypoplastic right and left heart syndromes) or other univentricular hearts, the classic Fontan procedure (direct atrio-pulmonary connection) has been

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advanced to the lateral tunnel technique (intra-atrial patch to connect the inferior vena cava to the superior vena cava, which is connected to the pulmonary artery)$^{592}$ and to the extracardiac conduit (extracardiac connection between the inferior vena cava and the right pulmonary artery (Gore-TexR conduit).$^{573,593}$ After the lateral tunnel, a significant decrease in late AT (15-year AT-free survival of 87% compared with 61% after the classic Fontan) has been shown.$^{594}$ However, considering the time dependency of an evolving arrhythmogenic substrate, a longer follow-up is required.

For dextro-transposition of the great arteries, the classical Senning or Mustard procedure (atrial switch operations using the atrial septum or a baffle from pericardium or synthetic material to redirect the blood flow from the caval veins to the left ventricle) has been exchanged by an anatomical correction with the arterial switch.$^{573,595,596}$ The arterial switch for simple dextro-transposition of the great arteries does not require any atriotomy; however, many centres perm atriotomies to close residual atrial septal defects following balloon atrial septectomy (Rashkind procedure)$^{596}$ Moreover, dextro-transposition of the great arteries may also have a ventricular septal defect, which is usually closed through an atrial approach.

8.3.2 Common substrates and mechanisms

Detailed 3D EAM studies of clinically documented and induced AT have identified common AT mechanisms and substrates with slightly different frequencies for batrial anatomy, atrial switch, and Fontan pallation.$^{572}$ More than one AT mechanism per patient is common.$^{572,597,598}$

Common AT mechanisms

The most common AT mechanisms in CHD are peritricuspid (or cavomitral in L-looped ventricles) MRAT (40–60% of all AT), incisional IART using a suture line or prosthetic material as central obstacle in the systemic venous atrium (20–40% of all AT) and non-automatic FAT in the systemic or pulmonary venous atrium (5–10% of all AT).$^{572,597,599}$

MRAT or LRAT using other structures is rare (≤3%).$^{572,599}$ Non-inducible patients (31% in a recent large multicentre cohort) may benefit from an empirical substrate ablation approach. Targeting the CTI and/or connecting the systemic venous atrium incision to an unexcitable boundary resulted in a similar outcome compared to inducible patients, supporting empirical ablation, provided that predefined endpoints have been reached.$^{572}$

Special aspects

Fontan

After the classic Fontan procedure, multiple IART circuits at various locations are frequently encountered, whereas FAT is rare.$^{572,606}$ Haemodynamic instability during induced AT may occur in 18% of patients.$^{600}$ During repeat procedures, IART commonly occurs at different sites. After the lateral tunnel modification, peritricuspid (or cavomitral in L-looped ventricles) MRAT usually requires access to the pulmonary venous atrium.$^{601}$ Pericaval reentry is common with an area of slow conduction associated with the lower margin of the crista terminalis or low systemic venous atrium surgical scars (e.g. the cannulation site).

Dextro-transposition of the great arteries with atrial switch

The tricuspid valve and variable portions of the CTI are located in the pulmonary venous atrium, dependent on the surgical variant. Peritricuspid MRAT is the dominant subtype, accounting for 73–76% of all AT.$^{572,602}$ In 81%, access to the CTI cannot be achieved via a systemic (venous) route but requires a transbaffle puncture or a transaortic access through the AV valve. AT recurrence after Senning may

involve the posterior anastomosis (anterior edge of atriotomy sewn posteriorly to lateral edge of the incision close to the right PVs).$^{602}$

8.3.3 Mapping and ablation strategy

3D EAM voltage and activation mapping can be performed during stable SR to identify boundaries of potential reentrant circuit isthmuses. Sites with no atrial potential distinguishable from noise (generally ≤0.03 mV) may be considered dense scar/unexcitable tissue, which can be further supported by no-capture following high-output pacing (10 mA/2 ms). Unexcitable sites can be displayed together with the caval veins, valve annuli, and lines of double potentials. Double potentials may be located between the caval veins and the posterolateral systemic venous atrium, consistent with the crista terminals, but may also indicate atriotomy and suture lines. The feasibility of high-resolution, multielectrode mapping has been demonstrated, allowing for detailed activation mapping of complex circuits and FAT.$^{777,603,604}$ Whether the use of multielectrode mapping will improve outcomes requires further studies.

After delineation of boundaries that create intervening isthmuses, these isthmuses can be targeted by a linear RF lesion. Fractionated elec- trograms are consistent with slow conduction and may indicate the po- tential origin of a FAT. Contact force measurement or catheter visualization by intracardiac echocardiography can be helpful to exclude poor contact. Long, steearable sheaths can be helpful to improve con- tact. The use of an irrigated tip catheter has increased acute procedural success in ACHD.$^{605}$,$^{606}$ Image integration (multi-slice computed tom-ography, cardiac magnetic resonance imaging) can facilitate ablation by visualizing the complex anatomy and its relation to the catheter position.

Access to the pulmonary venous atrium

In the absence of fenestrations or leaks, a transbaffle puncture can be guided by TOE or intracardiac echocardiography with acute success rates of up to 96%, if performed in experienced centres.$^{607}$ In selected cases, RF-assisted transseptal puncture may be considered.

In patients with surgically excluded CTI (or cavomitral in L-looped ventricles), bidirectional conduction block often requires a systemic venous and either a retrograde transaortic approach or transbaffle access.$^{608}$

In the extracardiac conduit, Fontan access to the pulmonary venous atrium can be obtained via direct conduit puncture, pre-existing fenetration, or transcaval cardiac puncture. The feasibility of transcaval cardiac puncture can be predicted by preprocedural computed tomography or cardiac magnetic resonance imaging.$^{609}$

Remote-controlled magnetic navigation systems in combination with a 3D mapping system and integration of pre-acquired images (computed tomography or cardiac magnetic resonance imaging) may allow for an exclusively retrograde approach to the pulmonary venous atrium and can potentially overcome navigation difficulties.$^{610}$

Endpoints of ablation

Bidirectional isthmus block is an established endpoint for pertricuspid (or cavomitral in L-looped ventricles) MRAT and has improved long-term outcome in patients after atrial switch operations.$^{608}$ Complete procedural success defined as termination of all clinical and induced FAT by RF and verification of bidirectional block along all ablation lines for clinical and induced IART and non-inducibility of any AT at the end of the procedure (including isoprenaline administration) was an independent predictor for AT-free survival in two recent cohorts.$^{572,611}$

Despite uniform endpoints, AT recurs after the index procedure in 27–54% of patients after a median follow-up of 30–34 months.$^{572,611}$ The mechanism of AT recurrences may differ from the initial AT mechanism. Recovery of an initially targeted substrate was reported in 63–64% of patients in two series.$^{572,612}$ Of note, in an important number of patients, who underwent a second procedure, peritricuspid MRAT

Management of patients with atrial tachycardia

or IART in the systemic venous atrium have been targeted as a new substrate.$^{611-613}$ This finding may support additional empirical ablation of these potential substrates during the index procedure.

8.4 Specifics in the paediatric population

8.4.1 Ablation indication in the paediatric population

|Ablation indication in the paediatric population|Strength of evidence| |---|---| |Advised TO DO|| |Medical treatment should be used in infants with AT to achieve conversion to SR or rate control.|| |Synchronized cardioversion should be used for conversion to SR in infants with non-self-limiting MRAT or in unstable older patients with MRAT or AF.|| |CA is advised in symptomatic and drug-refractory patients >15 kg or in those with left ventricular dysfunction.||

FAT is quite rare in childhood. Spontaneous resolution is more frequent in infants (90%) than in older children (45%).$^{614}$ Infants are often asymptomatic until the development of AiCMP.$^{615}$ Medical therapy is necessary in symptomatic infants and often applied long-term before ablation. Beta-receptor blockers are the first-line treatment and class IC or class III AADs may be used as adjunctive therapy or in cases where beta-receptor blockers are insufficient.$^{615}$ Ivabradine has also shown promising effects with a potentially haemodynamically more favorable profile compared to other AADs in paediatric patients, especially in those with severe left ventricular dysfunction.$^{616,617}$ Whereas infants aged <3 years typically respond to AAD therapy, beyond infancy, FAT are often persistent and the response to AADs is worse.$^{614}$ Consequently, CA should be considered especially in symptomatic and drug-refractory patients or in those with left ventricular dysfunction.$^{618}$ In rare cases, atrial appendectomy may be used if CA fals.$^{619}$

Multifocal AT mainly affects infants and is often associated with Raso-pathies, CHD or a giant right atrial appendage in older children.$^{572,620,621}$ As conversion to SR is often challenging to achieve, rate control is an important therapeutic option. CA of multifocal AT may be of limited efficacy. A surgical approach—e.g. in the case of a giant right atrial appendage as the AT source—might be helpful in selected patients.$^{622,623}$ Long-term cardiovascular and developmental outcome depends principally on the underlying condition; for otherwise healthy children, multifocal AT has a favourable prognosis.$^{623,624}$

Periticuspid MRAT occurs rarely in children with structurally normal hearts$^{625}$ and is usually associated with cardiomyopathies,$^{626}$ channelopathies or inherited arrhythmogenic conditions, progressive cardiac conduction disease or CHD.$^{59}$ Periticuspid MRAT can occur in infants and often foal manifestations.$^{627}$ It is well tolerated and generally lasts 2 or 3 days.$^{625,627}$ However, synchronized electrical cardioversion restores SR,$^{628}$ while transoesophageal overdrive stimulation is less effective. Recurrences are unlikely and prophylactic therapy is generally not necessary.$^{627}$

In older paediatric patients with MRAT, synchronized cardioversion should be used in unstable patients, keeping in mind that about 9% of cases present with intracardiac thrombi.$^{629}$ The recommended drugs are digoxin with the addition of flecanide or amiodarone.$^{630}$ CA should be considered in symptomatic and drug-refractory patients.

In alignment with previous guidelines,$^{1,631}$ it is advised to consider patient weight as a more important factor than age in determining the risk-benefit ratio for ablation. A threshold of approximately 15 kg is commonly used, while recognizing that a strict cut-off for weight or age is not universally applicable.$^{631}$ Ablation in infants (≤1 year) and small children (≤15 kg) remains controversial, as studies have not consistently defined these groups. The only clear exception is neonates and very small infants, in whom age may also be a determining factor in certain cases.

8.4.2 Interdisciplinary management

The vast majority of paediatric patients with AT do not have any underlying noncardiac diseases.$^{615,627}$ However, AT can also be associated with viral infections (e.g. respiratory syncytial), various syndromes (e.g. Raso-pathies including Costello, Rett, Williams, cardio-facio-cutaneous syndrome, etc.), neurological, metabolic or endocrine disorders.$^{620,632-620,634-620}$

$^{634}$ Therefore, a multidisciplinary interaction is essential in the diagnostic process and therapeutic decision-making. For the performance of ablation procedures including monitoring of anaesthesia, relevant experience in paediatrics is required. Compared with the adult population, paediatric patients often need deeper sedation to guarantee motionlessness and preserve comfort.$^{635}$ Whereas general anaesthesia has historically been the preferred strategy for ablation procedures in paediatrics, data suggest no difference between general and monitored anaesthesia care in tachycardia inducibility, acute ablation success and major complications.$^{636}$

9. Efficacy, safety, and institutional requirements

9.1 Acute procedural success

According to the consensus of the writing group members, acute complete success should be differentiated from partial success.$^{572,605}$ Acute complete procedural success is defined as non-inducibility, while partial success is characterized by non-inducibility of the clinical AT, but inducibility or spontaneous occurrence of other sustained AT. Acute complete procedural success of AT ablation ranges between 76.7–100%, depending on the present AT mechanisms, localizations and the underlying substrate.$^{637}$ Ablation of NRAT remains more often acutely successful compared to MRAT, with a higher success for pertricuspid vs. non-pertricuspid� MRAT.$^{246,637,638}$ Considering different AT localizations, one-sided AT, especially right-sided, non-septal ones, go along with a higher acute success rate than biatrial AT.$^{245}$

Whether and to what extent partial success differs from complete success with respect to quality of life, need for antiarrhythmic medication, rehospitalization rate, and other cardiovascular endpoints during long-term follow-up is incompletely understood and deserves further investigation. $^{63}$,$^{13}$,$^{43}$,$^{43}$ Therefore, a staged approach can be reasonable in some scenarios considering the individual risk/benefit ratio.

Tachycardia characteristics predicting acute failure are multifocal sites or changing activity, as well as ectopy recurrence for NRAT, and a broader width, faster conduction velocity and higher bipolar voltage of the mid-diastolic isthmus or a faster CL for MRAT.$^{639,640}$ Additional procedural reasons include incomplete mapping or lesion generation, e.g., due to extended hypertrophy/fibrosis$^{641}$ or high risk for unintended damage to the specific conduction system.$^{572}$ Considering the underlying substrate, the acute success rate is higher in patients operated for acquired heart disease compared to those operated for CHD, without significant differences between those with simple or complex CHD.$^{572,638}$

Patient- and procedure-related factors should be evaluated for shared decision-making regarding arrhythmia recurrence following AT ablation (Figures 8 and 9). Considering the heterogeneity of success in the literature, standardized reporting of patient characteristics,

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procedural data, and follow-up (patient-reported symptoms/outcome and intermittent/continuous ECG monitoring) is needed.

9.2 Recognition and management of complications

Recognition and prompt management of complications remain essential, as AT ablation remains one of the most technically demanding procedures in electrophysiology, despite recent improvements in quality indicators such as acute success rates, procedural times, and fluoroscopy times.$^{642}$ The most relevant complications include pericardial e-fusion or tamponade (0.2–0.6%), (thrombo)embolic events (0.1–0.5%), coronary injury (<0.01%), phrenic nerve palsy (<0.01%), sinus or AV node injury (<0.01%), oesophageal thermal injury (<0.01%), and vascular access complications (1–5%).$^{109,239,642–644}$ The recognition, presentation, diagnostic evaluation, treatment, and methods to prevent such complications have been described in detail elsewhere.$^{162}$ Overall risk is determined by both clinical and procedural complexity, particularly in relation to individual anatomical and arrhythmia characteristics. Current evidence suggests that complication rates are higher in left-compared with right-sided AT and in MRAT compared with FAT,$^{643,644}$ although these observations are limited by methodological constraints and heterogeneous study designs. The complication rates in patients undergoing ablation of consecutive AT appear similar to those observed during AF ablation, although no direct comparative studies are available.

9.3 AF and AT during follow-up

Long-term arrhythmia freedom after successful AT ablation depends on the underlying arrhythmogenic substrate, AT mechanisms, and the patient's history, including previous cardiac interventions.$^{6,97,249,266}$ Arrhythmia recurrences after AT ablation have been reported in 5-66%$^{6,80,97,249,266}$ comprising mainly non-index AT but also AF. Ablation of NRAT has a favourable outcome compared to reentrant AT. However, with the growing number of observational studies on patients with NRAT and the increasing use of mobile ECGs for self-monitoring, arrhythmia recurrences after NRAT ablation are now reported more frequently, occurring in up to 32% of patients (including index and non-index AT).$^{66,239,478}$

Whereas a blanking period following AT ablation, especially in patients with a history of AF is widely accepted, early recurrences have been demonstrated to predict late recurrences, independent of the timing of early recurrence.$^{240}$

Repeat ablation has been reported to be performed in 8–29% of patients$^{4,82,109,249}$ and is mainly conducted for novel AT different from the one(s) targeted during the index procedure. In the case of recurrent AT originating from the initially targeted localization, AT are more often MRAT or LRAT than NRAT$^{4}$ and rather localized in the LA than in the RA,$^{139}$ with a higher recurrence rate for perintal MRAT$^{109,266,299,498}$ or septal AT.$^{245,246}$ in patients with scar-related AT without a history of previous cardiac interventions and AF, peritricuspid MRAT as well as AF are common, when AT ablation only is performed during the index procedure.$^{141,478,645}$

9.4 Training and institutional requirements

The management of AT remains one of the most challenging arrhythmias considering potential clinical complexity (heterogeneous patient populations, comorbidities, often long arrhythmia history and related extensive substrates) and procedural complexity (including an increasing number of previous cardiac interventions like AF ablation, patent foramen ovale/atrial septal defect occlusion/septal patch, valvular interventions, LAA occlusion, etc.). Therefore, CA of AT requires advanced

skills and continuous training in clinical cardiac electrophysiology on top of established standards (beyond Level III training)$^{646}$ including (repeat) AF ablation.$^{162}$ In addition to the general training and institutional requirements for complex ablation procedures.$^{647}$ clinicians and institutions should document appropriate training, standard operating procedures, and facilities to ensure safety and efficacy in AT management, including patient follow-up after ablation.

The following aspects are relevant for the management of patients with AT for strategic and (peri-)procedural planning (see also Figures on clinical (Figure 8) and procedural (Figure 9) complexity):

* Stepwise approach to AT management (including timing/monitoring of medication/cardioversion/ablation and device-related decision mapping (including indication/device selection/programming, etc.) * Possibilities and limitations: When, whom and how to ablate (including risk classification), * How to rapidly characterize AT origin (left vs. right atrium), mechanism (reentry vs. non-reentry), type (MRAT vs. LRAT and related subforms), and circuit locations (perimitral, roof-dependent etc.) * Advanced sedation and monitoring techniques * Successful and safe procedural execution and intraprocedural management of comorbidities * Challenging transseptal puncture (especially after previous cardiac interventions, including septum closure, etc.) * Haemodynamic, respiratory, and metabolic management during prolonged procedures, including frail patients * Specifically careful mapping/stimulation manoeuvres (to avoid AT termination/degeneration to AF which might challenge acute therapeutic success in some patients) * Biophysics of ablation (especially in patients with previous cardiac interventions/ablation)

* Standardized care during follow-up, including patient-reported outcomes and advanced ECG monitoring (like individualized usage of wearables, etc.)

* Skills, strategies, and infrastructure to manage early, late, and/or inces- sant AT recurrences, including patients with haemodynamic deterioration.$^{94}$

Whenever available, institutional requirements should include certified physicians as well as other certified health professionals.$^{648}$

They should further include access to advanced therapies for complex cases, as well as multidisciplinary teams, including anaesthesia support and dedicated care teams (nurses, technicians) for peri-ablation management (in and out of the EP lab); they must also have access to providers to assist in acute complication needs. Finally, ablation after-care resources (staffing and clinic), along with qualified intermediary review to provide for education and improvement opportunities, are needed.

10. Gaps of knowledge and future directions

As outlined in the present document, in recent years, multiple efforts around the globe have evolved diagnostic, prognostic, and therapeutic concepts that improved the management of patients with AT in the present era of CA. The resulting interpretation of the given evidence by the writing group is the present SMART-AT framework.

Despite several evolutionary steps promoting present best clinical practice, relevant open questions remain to be answered to guide future SMART-AT improvement from a clinical and scientific perspective. Selected key areas are addressed in Table 7.

First, precise ECG- and mapping-based diagnosis of AT mechanisms and their underlying aetiologies warrants further improvements, especially to predict and optimize long-term outcomes. Next, the morphological and functional atrial substrate in patients with and without various forms of structural heart disease still remains incompletely understood. Cut-off values for voltage mapping and other (imaging)

AT prevention

AT prevention

• Optimal risk factor management • Optimized PVI to prevent AT • Optimized substrate modulation/linear lesion settings for AF ablation strategies to avoid the creation of areas of slow conduction and consecutive AT • Optimal lesion set during repeat ablation in AF patients and isolated PVs to treat AF while preventing AT • Optimized AT ablation lesion sets to prevent future (other) AT (including the role of the functional atrial arrhythmogenic substrate) without compromising safety Diagnostics • Advanced automatic ECG analysis including state-of-the-art (wearable) technologies • Standardized definition of low voltage criteria to identify scar/fibrosis/arrhythmogenic substrates • Automatic AT map interpretation including artificial intelligence-based applications • Predictive value of blood-based biomarkers • Dedicated algorithms for AT detection in (wearable) devices Insights to special populations and arrhythmia substrates

• Characterization of atrial arrhythmia substrate in SR vs. AT • Value of (novel) imaging modalities • Systematic evaluation of surgical strategies to avoid consecutive AT Aetiology + comorbidities

• Identification of imaging modalities/cardiac magnetic resonance imaging parameters to predict AiCMP in patients with AT and subsequently newly diagnosed heart failure

• Identification of patients at risk and characterization of the course of AiCMP • Usefulness of blood-based biomarkers Stroke prevention

• General risk stratification of various patient populations with/without AT ablation • Characterization of stroke risk in patients with AT • Differentiation of stroke risk in patients with AT vs. AF • Risk prediction in patients after successful AT treatment • Additional evaluation of the performance of TOE and other imaging modalities prior to cardioversion/AT ablation Mechanisms/mapping

• Rapid precise critical AT site detection and prediction of future AT Ablation • Optimal ablation strategy in MRAT and LRAT • Optimal energy source and their potential combinations (RF/PFA, RF/ethanol, etc.)

• Optimal linear lesion sets with respect to reverse atrial remodelling following AT ablation (while avoiding accidental intra-atrial conduction delay and/or stiff atrial syndromes)

• Targeted ablation strategy for prevention of future AT (beyond initial clinical AT)

Procedural endpoint

• Ablation of clinical only vs. all (inducible) AT • Preventive LA (linear) ablation (especially considering low voltage areas)

• Evaluation of functional and/or structural 'substrate modification'

Optimizing long-term outcomes

• Standardized reporting of patient characteristics, procedural data, and follow-up for individualized success prediction considering AT aetiology and patient history (patient-reported symptoms/outcome and intermittent/continuous ECG monitoring)

• Evaluation of the predictive value of early AT recurrence • Evaluation of the need for a blanking period for specific patient populations • Evaluation of optimal management of early recurrence • Value of hybrid therapy (ablation + medication)

• Timing + value of AT ablation in elderly cohorts • Timing + value of AV nodal ablation in patients with therapy-refractory AT • Relevance of asymptomatic AT Data integration

• Using big data and machine learning to predict patient outcomes and personalize therapy • Multicentre clinical trials are needed to determine optimal therapy and ablation strategy Management of patients with atrial tachycardia

References

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modalities in SR and during ongoing AT need to be determined in detail for different patient populations to develop potential preventive ablation strategies. Also, the clinical implications of various mapping catheters and related algorithms need to be determined in detail. Electrogram characteristics indicating atrial scarring are well known to depend on atrial rate, electrode size, spacing, design, orientation, and direction of wavefront, and standardization of these variables might facilitate AT management. Mechanistically, additional important questions remain to be answered. Reentry AT associated with atrial myopathy in the absence of previous iatrogenic interventions is of particular interest, as haemodynamic, proteomic, metabolomic, and genomic characterization might offer valuable insights.

Recently, personalized atrial digital twins generated from late gadolinium enhancement-magnetic resonance images have been shown to enable preprocedural prediction of scar-related AT occurrence after ablation. This approach has further been suggested to identify target locations where ablation with lower power may decrease the risk of AT, thereby avoiding extensive linear ablation and laying the foundation for further development of AT ablation strategies.$^{649}$ In this context, knowledge gaps include optimal energy parameters, catheter design, and lesion durability, as well as safety and efficacy data, including novel PFA platforms for NRAT, LRAT, and MRAT in the presence of atrial scar.

Considering recent translational and clinical studies addressing the 'topology' of AT might additionally improve strategic intraprocedural ablation planning.$^{477,330}$ The construct, rooted in mathematical principles and validated in computational and clinical AT, implies that reentry involves paired rotation around two critical boundaries. In atra with three boundaries or more, this appears to translate often into the invariable presence of two, mostly asymmetric loops with passive activation around one or more non-critical boundaries. These findings suggest that adequate ablative therapy requires differentiation of critical and non-critical boundaries and connection of both critical ones. Further translation of these and other novel insights with respect to improved patient outcome (including arrhythmia-free survival, hospitalization, stroke prevention, cardiac mortality etc.) needs to be supported by future data integration and urgently warranted randomized controlled trials to shape future SMART-AT care.

Supplementary material

Supplementary material is available at Europace online.

Acknowledgements

The authors thank Kalyamam Shivkumar and Shumpei Mori for providing an anatomical image from the Amara Yad Project, Mattias Duytschaever and Nele Vandersickel for valuable contribution on AT topology, Lauren Tapp (EHRA/ESC) and Henrike Goebels (EVK Düsseldorf) for excellent logistic support. Part of the Figures 5, 8–11 was created with BioRender.com.

Conflict of interest: The authors have provided declaration of interest information for all relationships that might be perceived as real or potential sources of conflicts of interest. The full disclosures can be viewed in the Supplementary material online for this article, available online at [URL].

Data availability

The data underlying this article are available in the article including its citations and in its online supplementary material.

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