FormalPara TABLE OF CONTENTS
  1. Section 1

    Introduction .......................................in this issue

    1. 1.1.

      Document Scope and Rationale ...........in this issue

    2. 1.2.

      Methods .................................................in this issue

  2. Section 2

    Background ........................................in this issue

  3. Section 3

    Clinical Evaluation .............................in this issue

    1. 3.1.

      Clinical Presentation .............................in this issue

    2. 3.2.

      Diagnostic Evaluation ...........................in this issue

      1. 3.2.1.

        Resting 12-Lead Electrocardiogram ...in this issue

      2. 3.2.2.

        Assessment of Structural Heart Disease and Myocardial Ischemia ......................in this issue

      3. 3.2.3.

        Risk Stratification in the Setting of Frequent Premature Ventricular Complexes ...in this issue

      4. 3.2.4.

        Longitudinal Follow-up in the Setting of Frequent Premature Ventricular Complexes ...in this issue

  4. Section 4

    Indications for Catheter Ablation .......in this issue

    1. 4.1.

      Idiopathic Outflow Tract Ventricular Arrhythmia ...

    2. 4.2.

      Idiopathic Nonoutflow Tract Ventricular Arrhythmia ..........................................in this issue

    3. 4.3.

      Premature Ventricular Complexes With or Without Left Ventricular Dysfunction ................in this issue

    4. 4.4.

      Ventricular Arrhythmia in Ischemic Heart Disease ...in this issue

    5. 4.5.

      Nonischemic Cardiomyopathy .............in this issue

    6. 4.6.

      Ventricular Arrhythmia Involving the His-Purkinje System, Bundle Branch Reentrant Ventricular Tachycardia, and Fascicular Ventricular Tachycardia ...........................................in this issue

    7. 4.7.

      Congenital Heart Disease .....................in this issue

    8. 4.8.

      Inherited Arrhythmia Syndromes ..........in this issue

    9. 4.9.

      Ventricular Arrhythmia in Hypertrophic Cardiomyopathy ..................................in this issue

  5. Section 5

    Procedural Planning ...in this issue

  6. Section 6

    Intraprocedural Patient Care ..............in this issue

    1. 6.1.

      Anesthesia .............................................in this issue

    2. 6.2.

      Vascular Access .....................................in this issue

    3. 6.3.

      Epicardial Access ..................................in this issue

    4. 6.4.

      Intraprocedural Hemodynamic Support ...in this issue

    5. 6.5.

      Intraprocedural Anticoagulation ...........in this issue

  7. Section 7

    Electrophysiological Testing ..............in this issue

  8. Section 8

    Mapping and Imaging Techniques ....in this issue

    1. 8.1.

      Overview ...............................................in this issue

    2. 8.2.

      Substrate Mapping in Sinus Rhythm ...in this issue

    3. 8.3.

      Intraprocedural Imaging During Catheter Ablation of Ventricular Arrhythmias ....................in this issue

    4. 8.4.

      Electroanatomical Mapping Systems and Robotic Navigation ...in this issue

  9. Section 9

    Mapping and Ablation .......................in this issue

    1. 9.1.

      Ablation Power Sources and Techniques ..in this issue.

    2. 9.2.

      Idiopathic Outflow Tract Ventricular Arrhythmia ...in this issue

    3. 9.3.

      Idiopathic Nonoutflow Tract Ventricular Arrhythmia ...in this issue

    4. 9.4.

      Bundle Branch Reentrant Ventricular Tachycardia and Fascicular Ventricular Tachycardia ...in this issue

    5. 9.5.

      Postinfarction Ventricular Tachycardia ...in this issue

    6. 9.6.

      Dilated Cardiomyopathy ......................in this issue

    7. 9.7.

      Ventricular Tachycardia Ablation in Hypertrophic Cardiomyopathy ...................................in this issue

    8. 9.8.

      Brugada Syndrome ...............................in this issue

    9. 9.9.

      Polymorphic Ventricular Tachycardia/Ventricular Fibrillation Triggers ..............................in this issue

    10. 9.10.

      Arrhythmogenic Right Ventricular Cardiomyopathy ..............................in this issue

    11. 9.11.

      Mapping and Ablation in Congenital Heart Disease ...............................................in this issue

    12. 9.12.

      Sarcoidosis ..........................................in this issue

    13. 9.13.

      Chagas Disease ...................................in this issue

    14. 9.14.

      Miscellaneous Diseases and Clinical ScenariosWith Ventricular Tachycardia ...in this issue

    15. 9.15.

      Surgical Therapy ...in this issue

    16. 9.16.

      Sympathetic Modulation ....................in this issue

    17. 9.17.

      Endpoints of Catheter Ablation of Ventricular Tachycardia ........................................in this issue

  10. Section 10

    Postprocedural Care .........................in this issue

    1. 10.1.

      Postprocedural Care: Access, Anticoagulation, Disposition .........................................in this issue

      1. 10.1.1.

        Postprocedural Care: Access ...in this issue

      2. 10.1.2.

        Postprocedural Care:Anticoagulation ...in this issue

    2. 10.2.

      Incidence and Management of Complications ...in this issue

    3. 10.3.

      Hemodynamic Deterioration and Proarrhythmia ...in this issue

    4. 10.4.

      Follow-up of Patients Post Catheter Ablation of Ventricular Tachycardia ......................in this issue

  11. Section 11

    Training and Institutional Requirements and Competencies ..................................in this issue

    1. 11.1.

      Training Requirements and Competencies for Catheter Ablation of Ventricular Arrhythmias ...in this issue

    2. 11.2.

      Institutional Requirements for Catheter Ablation of Ventricular Tachycardia ..................in this issue

  12. Section 12

    Future Directions .............................in this issue

  13. Appendix 1

    Author Disclosure Table ................in this issue

  14. Appendix 2

    Reviewer Disclosure Table ............in this issue

1 Introduction

1.1 Document Scope and Rationale

The field of electrophysiology has undergone rapid progress in the last decade, with advances both in our understanding of the genesis of ventricular arrhythmias (VAs) and in the technology used to treat them. In 2009, a joint task force of the European Heart Rhythm Association (EHRA) and the Heart Rhythm Society (HRS), in collaboration with the American College of Cardiology (ACC) and the American Heart Association (AHA), produced an expert consensus document that outlined the state of the field and defined the indications, techniques, and outcome measures of VA ablation [1]. In light of advances in the treatment of VAs in the interim, and the growth in the number of VA ablations performed in many countries and regions [2, 3], an updated document is needed. This effort represents a worldwide partnership between transnational cardiac electrophysiology societies, namely, HRS, EHRA, the Asia Pacific Heart Rhythm Society (APHRS), and the Latin American Heart Rhythm Society (LAHRS), and collaboration with ACC, AHA, the Japanese Heart Rhythm Society (JHRS), the Brazilian Society of Cardiac Arrhythmias (Sociedade Brasileira de Arritmias Cardíacas [SOBRAC]), and the Pediatric and Congenital Electrophysiology Society (PACES). The consensus statement was also endorsed by the Canadian Heart Rhythm Society (CHRS).

This clinical document is intended to supplement, not replace, the 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death [4] and the 2015 ESC Guidelines for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death [5]. The scope of the current document relates to ablation therapy for VAs, from premature ventricular complexes (PVCs) to monomorphic and polymorphic ventricular tachycardia (VT) and triggers of ventricular fibrillation (VF). Due to its narrower scope, the consensus statement delves into greater detail with regard to indications and technical aspects of VA ablation than the above-mentioned guidelines.

Where possible, the recommendations in this document are evidence based. It is intended to set reasonable standards that can be applicable worldwide, while recognizing the different resources, technological availability, disease prevalence, and health care delivery logistics in various parts of the world. In addition, parts of this document, particularly Section 9, present a practical guide on how to accomplish the procedures described in a manner that reflects the current standard of care, while recognizing that some procedures are better performed, and some disease states better managed, in settings in which there is specific expertise.

1.2 Methods

The writing group was selected according to each society’s procedures, including content and methodology experts representing the following organizations: HRS, EHRA, APHRS, LAHRS, ACC, AHA, JHRS, PACES, and SOBRAC. Each partner society nominated a chair and co-chair, who did not have relevant relationships with industry and other entities (RWIs). In accordance with HRS policies, disclosure of any RWIs was required from the writing committee members (Appendix 1) and from all peer reviewers (Appendix 2). Of the 38 committee members, 17 (45%) had no relevant RWIs. Recommendations were drafted by the members who did not have relevant RWIs. Members of the writing group conducted comprehensive literature searches of electronic databases, including Medline (via PubMed), Embase, and the Cochrane Library. Evidence tables were constructed to summarize the retrieved studies, with nonrandomized observational designs representing the predominant form of evidence (Supplementary Appendix 3). Case reports were not used to support recommendations. Supportive text was drafted in the “knowledge byte” format for each recommendation. The writing committee discussed all recommendations and the evidence that informed them before voting. Initial failure to reach consensus was resolved by subsequent discussions, revisions as needed, and re-voting. Although the consensus threshold was set at 67%, all recommendations were approved by at least 80% of the writing committee members. The mean consensus over all recommendations was 95%. A quorum of two-thirds of the writing committee was met for all votes [6].

Each recommendation in this document was assigned a Class of Recommendation (COR) and a Level of Evidence (LOE) according to the system developed by ACC and AHA (Table 1) [7]. The COR denotes the strength of the recommendation based on a careful assessment of the estimated benefits and risks; COR I indicates that the benefit of an intervention far exceeds its risk; COR IIa indicates that the benefit of the intervention moderately exceeds the risk; COR IIb indicates that the benefit may not exceed the risk; and COR III indicates that the benefit is equivalent to or is exceeded by the risk. The LOE reflects the quality of the evidence that supports the recommendation. LOE A is derived from high-quality randomized controlled trials; LOE B-R is derived from moderate-quality randomized controlled trials; LOE B-NR is derived from well-designed nonrandomized studies; LOE C-LD is derived from randomized or nonrandomized studies with limitations of design or execution; and LOE C-EO indicates that a recommendation was based on expert opinion [7].

Table 1 ACC/AHA Recommendation System: Applying Class of Recommendation and Level of Evidence to Clinical Strategies, Interventions, Treatments, and Diagnostic Testing in Patient Care*
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Unique to this consensus statement is the systematic review commissioned specifically for this document as part of HRS’s efforts to adopt the rigorous methodology required for guideline development. The systematic review was performed by an experienced evidence-based practice committee based at the University of Connecticut, which examined the question of VT ablation vs control in patients with VT and ischemic heart disease (IHD) [8]. The question, in PICOT format, was as follows: In adults with history of sustained VT and IHD, what is the effectiveness and what are the detriments of catheter ablation compared with other interventions? Components of the PICOT were as follows: P = adults with history of sustained VT and IHD; I = catheter ablation; C = control (no therapy or antiarrhythmic drug [AAD]); O = outcomes of interest, which included 1) appropriate implantable cardioverter defibrillator (ICD) therapies (ICD shock or antitachycardia pacing [ATP]), 2) appropriate ICD shocks, 3) VT storm (defined as three shocks within 24 hours), 4) recurrent VT/VF, 5) cardiac hospitalizations, and 6) all-cause mortality; and T = no time restrictions.

An industry forum was conducted to achieve a structured dialogue to address technical questions and to gain a better understanding of future directions and challenges. Because of the potential for actual or perceived bias, HRS imposes strict parameters on information sharing to ensure that industry participates only in an advisory capacity and has no role in either the writing of the document or its review.

The draft document underwent review by the HRS Scientific and Clinical Documents Committee and was approved by the writing committee. Recommendations were subject to a period of public comment, and the entire document underwent rigorous peer review by each of the participating societies and revision by the Chairs, before endorsement.

2 Background

This section reviews the history of VT ablation, details the mechanisms of VT, and provides definitions of frequently used terms (Table 2), including anatomic definitions (Table 3), as well as illustrating some types of sustained VA (Fig. 1).

Table 2 Definitions
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Table 3 Anatomical terminology
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Fig. 1
figure 1

Monomorphic (a), pleomorphic (b), and polymorphic (c) VT. Reproduced with permission of the Heart Rhythm Society from Aliot et al. EHRA/HRS expert consensus on catheter ablation of ventricular arrhythmias. Heart Rhythm 2009;6:886–933. VT = ventricular tachycardia

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3 Clinical Evaluation

This section discusses clinical presentations of patients with VAs and their workup as it pertains to documentation of arrhythmias and appropriate testing to assess for the presence of SHD.

3.1 Clinical Presentation

3.2 Diagnostic Evaluation

3.2.1 Resting 12-Lead Electrocardiogram

3.2.2 Assessment of Structural Heart Disease and Myocardial Ischemia

3.2.3 Risk Stratification in the Setting of Frequent Premature Ventricular Complexes

3.2.4 Longitudinal Follow-up in the Setting of Frequent Premature Ventricular Complexes

4 Indications for Catheter Ablation

Following are the consensus recommendations for catheter ablation of VAs organized by underlying diagnosis and substrate. These recommendations are each assigned a COR and an LOE according to the current recommendation classification system [47]. In drafting each of these recommendations, the writing committee took into account the published literature in the specific area, including the methodological quality and size of each study, as well as the collective clinical experience of the writing group when published data were not available. Implicit in each recommendation are several points: 1) the procedure is being performed by an electrophysiologist with appropriate training and experience in the procedure and in a facility with appropriate resources; 2) patient and procedural complexity vary widely, and some patients or situations merit a more experienced operator or a center with more capabilities than others, even within the same recommendation (eg, when an epicardial procedure is indicated and the operator or institution has limited experience with this procedure, it might be preferable to refer the patient to an operator or institution with adequate experience in performing epicardial procedures); 3) the patient is an appropriate candidate for the procedure, as outlined in Section 5, recognizing that the level of patient suitability for a procedure will vary widely with the clinical scenario; and 4) the patient’s (or designee’s) informed consent, values, and overall clinical trajectory are fundamental to a decision to proceed (or not) with any procedure. Therefore, in some clinical scenarios, initiation or continuation of medical therapy instead of an ablation procedure may be the most appropriate option, even when a class 1 recommendation for ablation is present. There may also be scenarios not explicitly covered in this document, and on which little or no published literature is available, in which the physician and patient must rely solely on their own judgment.

Figure 2 provides an overview of care for the patient with congenital heart disease (CHD) and VA.

Fig. 2
figure 2

Congenital heart disease and sustained VT. For further discussion of ICD candidacy, please see PACES/HRS Expert Consensus Statement on the Recognition and Management of Arrhythmias in Adult Congenital Heart Disease [48] and 2012 ACCF/AHA/HRS Focused Update of the 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities [49]. ACA = aborted cardiac arrest; CHD = congenital heart disease; DORV = double outlet right ventricle; ICD = implantable cardioverter defibrillator; TOF = tetralogy of Fallot; VT = ventricular tachycardia

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4.1 Idiopathic Outflow Tract Ventricular Arrhythmia

4.2 Idiopathic Nonoutflow Tract Ventricular Arrhythmia

4.3 Premature Ventricular Complexes With or Without Left Ventricular Dysfunction

4.4 Ventricular Arrhythmia in Ischemic Heart Disease

4.5 Nonischemic Cardiomyopathy

4.6 Ventricular Arrhythmia Involving the His-Purkinje System, Bundle Branch Reentrant Ventricular Tachycardia, and Fascicular Ventricular Tachycardia

4.7 Congenital Heart Disease

4.8 Inherited Arrhythmia Syndromes

4.9 Ventricular Arrhythmia in Hypertrophic Cardiomyopathy

5 Procedural Planning

This section includes preprocedural risk assessment (Table 4), preprocedural patient preparation, and preprocedural arrhythmia documentation with a focus on the regionalizing information of the ECG regarding the origin of VAs (Figs. 3 and 4). Furthermore, the capabilities of multimodality imaging in localizing the arrhythmogenic substrate are discussed in detail. Topics including the required equipment, personnel, and facility are detailed in this section.

Table 4 The PAAINESD Score, developed to predict the risk of periprocedural hemodynamic decompensation
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Fig. 3
figure 3

Examples of 12-lead ECGs of premature ventricular complexes from different LV sites, as corroborated by successful focal ablation. a shows 12-lead ECG patterns of common ventricular arrhythmia origins in patients without SHD [1–9] from the left ventricle. All leads are displayed at the same amplification and sweep speed. These locations are illustrated in b based on 3D reconstruction of a cardiac computed tomography using the MUSIC software that was developed at the University of Bordeaux. The reconstruction shows an anterolateral view of the left ventricle, aorta, and left atrium. Also shown are the coronary arteries (red), the coronary venous system (blue), and the phrenic nerve (green). AIV = anterior interventricular vein; AL PAP = anterolateral papillary muscle; AMC = aortomitral continuity; ECG = electrocardiogram; GCV = great cardiac vein; ant. MA = anterior mitral valve annulus; PM PAP = posteromedial papillary muscle; R/L = right-left; SHD = structural heart disease; SoV = sinus of Valsalva

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Fig. 4
figure 4

Examples of 12-lead ECGs of premature ventricular complexes from different right ventricular sites, as corroborated by successful focal ablation. All leads are displayed at the same amplification and sweep speed. a shows the 12-lead ECG pattern of common origins of right ventricular arrhythmias in patients without SHD [1–6]. The locations are detailed in a 3D reconstruction of the computed tomography using the MUSIC software that was developed at the University of Bordeaux. The reconstruction shown in b illustrates the septal view of the right ventricle. Indicated are the pulmonary artery, the tricuspid valve annulus, and the right ventricular apex. ECG = electrocardiogram; PA = pulmonary artery; RVOT= right ventricular outflow tract; SHD = structural heart disease; TVA = tricuspid valve annulus

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6 Intraprocedural Patient Care

Important aspects regarding intraprocedural sedation and its potential problems are highlighted in this section. Furthermore, vascular access, epicardial access with its many potential complications are discussed in detail, as well as anticoagulation and the indications for the use of hemodynamic support (HS) during VT ablation procedures.

6.1 Anesthesia

6.2 Vascular Access

6.3 Epicardial Access

6.4 Intraprocedural Hemodynamic Support

6.5 Intraprocedural Anticoagulation

7 Electrophysiological Testing

The benefits and limitations of PES are detailed in this section.

8 Mapping and Imaging Techniques

8.1 Overview

Activation mapping with multipolar catheters, entrainment mapping (Figs. 5 and 6), and pace mapping are the main techniques used to map VAs. This section reviews these techniques including the technique of substrate mapping aiming to identify the arrhythmogenic substrate in sinus rhythm. Furthermore, intraprocedural imaging as it pertains to procedural safety and to identification of the arrhythmogenic substrate is reviewed in this section.

Fig. 5
figure 5

Entrainment responses from components of reentrant VT circuit. CL = cycle length; PPI = postpacing interval; VT = ventricular tachycardia. Adapted with permission from Elsevier (Stevenson et al. J Am Coll Cardiol 1997;29:1180–1189)

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Fig. 6
figure 6

Pacing from the protected isthmus of a VT circuit. Entrainment mapping during VT. The VT CL is 620 ms, and pacing is performed at a CL of 580 ms. A low-voltage electrogram is located in diastole on the recordings of the ablation catheter (Map). The stimulus-QRS interval is 230 ms and matches with the electrogram-QRS interval. The postpacing interval is equal to the VT CL. The stimulus-QRS/VT CL ratio is 0.37, indicating that the catheter is located in the common pathway. CL = cycle length; PPI = postpacing interval; VT = ventricular tachycardia

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8.2 Substrate Mapping in Sinus Rhythm

8.3 Intraprocedural Imaging During Catheter Ablation of Ventricular Arrhythmias

8.4 Electroanatomical Mapping Systems and Robotic Navigation

9 Mapping and Ablation

This section is designed as a “how-to” section that details the procedural steps of VT ablation in different patient populations ranging from ablation of PVCs in patients without heart disease to ablation of VT/VF in patients with different types of SHD (Figs. 7, 8, 9, 10, 11 and 12 and Tables 5, 6, 7 and 8). Bullet points summarize the key points in this section.

Fig. 7
figure 7

Anatomical boundaries of the LV summit, with the inaccessible [1] and accessible [2] parts. Shown are the left anterior descending artery (LAD), the circumflex artery (Cx), the great cardiac vein (GCV), the anterior interventricular vein (AIV), and the first and second diagonal branch of the LAD (D1, D2)

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Fig. 8
figure 8

Intraprocedural imaging during ablation of papillary muscle arrhythmias. a Anatomical map of the left ventricle (CARTO, Biosense Webster) showing contact of the ablation catheter (Abl) with the posteromedial papillary muscle (PMPAP). b Intracardiac echocardiogram showing real-time visualization of the ablation catheter during ablation on the anterolateral papillary muscle (ALPAP)

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Fig. 9
figure 9

Overview of the workflow for catheter ablation of VT in patients with IHD. Not all of these steps might be required, and steps can be performed in a different sequence. For instance, repeat VT induction can be deferred in patients with hemodynamic instability. In addition, the operator might have to adapt to events that arise during the case, for instance, to take advantage of spontaneous initiation of stable VT during substrate mapping and switch to activation mapping. IHD = ischemic heart disease; PES = programmed electrical stimulation; SR = sinus rhythm; VT = ventricular tachycardia

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Fig. 10
figure 10

Epicardial substrate ablation in a patient with Brugada syndrome and appropriate ICD shocks for VF. Image integration of a preacquired CT with the electroanatomical epicardial substrate map is shown in (A). Purple represents bipolar voltage >1.5 mV. Fractionated potentials (arrows) are tagged with black dots, and a representative example is displayed. Widespread fractionated potentials were recorded from the epicardial aspect of the RVOT extending down into the basal RV body. Ablation lesions are tagged with red dots. Some fractionated potentials could not be ablated due to the proximity of the acute marginal branches of the right coronary artery. Panel (B) shows the significant transient accentuation of the Brugada ECG pattern during the application of radiofrequency energy at one of these sites. CT = computed tomography; ECG = electrocardiogram; ICD = implantable cardioverter defibrillator; PA = pulmonary artery; RA = right atrium; RCA = right coronary artery; RFA = radiofrequency ablation; RV = right ventricle; RVOT = right ventricular outflow tract; VF = ventricular fibrillation

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Fig. 11
figure 11

Right ventricular voltage maps from cases of moderate (upper row) and advanced (lower row) arrhythmogenic right ventricular cardiomyopathy (ARVC) are shown. Purple represents a voltage >1.5 mV in the bipolar maps (left and right) and >5.5 mV in the unipolar maps (center); red represents a voltage <0.5 mV in the bipolar maps and <3.5 mV in the unipolar maps. Moderate ARVC is defined as having a bipolar/unipolar low-voltage area ratio of <0.23 and is associated with epicardial arrhythmogenic substrate area (ASA) (defined by the presence of electrograms with delayed components of >10 cm2. Advanced ARVC displays a bipolar/unipolar endocardial low-voltage area of ≥0.23, which is associated with an epicardial arrhythmogenic substrate area of ≤10 cm2. Adapted with permission from Oxford University Press (Berruezo et al. Europace 2017;19:607–616)

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Fig. 12
figure 12

Anatomical isthmuses (AI) in repaired tetralogy of Fallot according to the surgical approach and variation of the malformation. RV = right ventricular; TA = tricuspid annulus; VSD = ventricular septal defect

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Table 5 Types of bundle branch reentrant tachycardia
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Table 6 Fascicular ventricular tachycardias
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Table 7 Select recent radiofrequency catheter ablation studies in patients post myocardial infarction with a focus on substrate-based ablation strategies
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Table 8 Catheter ablation of ventricular arrhythmias in cardiac sarcoidosis
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9.1 Ablation Power Sources and Techniques

Key Points

  • An impedance drop ≥10 ohms or a contact force ≥10 g is commonly used as a target for radiofrequency energy delivery.

  • The use of half normal saline generates larger ablation lesions but can result in steam pops.

  • Simultaneous bipolar or unipolar ablation can result in larger ablation lesions.

  • Cryoablation can be beneficial for achieving more stable contact on the papillary muscles.

  • Ethanol ablation can generate lesions in areas where the arrhythmogenic substrate cannot be otherwise reached, provided that suitable target vessels are present.

  • Stereotactic radiotherapy is an emerging alternative to ablation, requiring identification of a region of interest that can be targeted prior to the radiation treatment.

9.2 Idiopathic Outflow Tract Ventricular Arrhythmia

Key Points

  • The RVOT, pulmonary arteries, SVs, LV epicardium and endocardium contain most of the outflow tract arrhythmias.

  • Activation mapping and pace mapping can be used to guide ablation in the RVOT.

  • Imaging of coronary artery ostia is essential before ablation in the aortic SVs.

  • The LV summit is a challenging site of origin, often requiring mapping and/or ablation from the RVOT, LVOT, SVs, coronary venous system, and sometimes the epicardial space.

  • Deep intraseptal VA origins can be challenging to reach.

9.3 Idiopathic Nonoutflow Tract Ventricular Arrhythmia

Key Points

  • VAs originating from the papillary muscles can be challenging due to multiple morphologies of the VA and the difficulty in achieving and maintaining sufficient contact during ablation.

  • VAs originate in LV papillary muscles more often than in RV papillary muscles; they more often originate from the posteromedial than the anterolateral papillary muscle and occur more often at the tip than at the base.

  • Pace mapping is less accurate than in other focal VAs.

  • ICE is particularly useful for assessing contact and stability.

  • Cryoablation can also aid in catheter stability during lesion delivery.

9.4 Bundle Branch Reentrant Ventricular Tachycardia and Fascicular Ventricular Tachycardia

Key Points

  • Bundle branch reentry can occur in a variety of patients in whom the conduction system can be affected, including patients with dilated cardiomyopathy (DCM), valvular heart disease, myocardial infarction, myotonic dystrophy, Brugada syndrome, and ARVC, among others.

  • Ablation of either the right or left bundle branch eliminates bundle branch reentrant ventricular tachycardia (BBRVT) but does not eliminate other arrhythmic substrates.

  • A correct diagnosis of BBRVT is crucial and should employ established criteria prior to ablation of either of the bundle branches.

  • Ablation of the AV node does not cure BBRVT.

  • Ablation of either bundle branch does not cure interfascicular VT.

  • For posterior fascicular VTs, the P1 potential is targeted during VT; if P1 cannot be identified or VT is not tolerated, an anatomical approach can be used.

  • Purkinje fibers can extend to the papillary muscles, and these can be part of the VT circuit.

  • For anterior fascicular VTs, the P1 potential is targeted with ablation.

  • Focal nonreentrant fascicular VT is infrequent and can occur in patients with IHD; however, it cannot be induced with programmed stimulation, and the target is the earliest Purkinje potential during VT.

9.5 Postinfarction Ventricular Tachycardia

Key Points

  • In cases of multiple inducible VTs, the clinical VT should be preferentially targeted.

  • Elimination of all inducible VTs reduces VT recurrence and is associated with prolonged arrhythmia-free survival.

  • For tolerated VTs, entrainment mapping allows for focal ablation of the critical isthmus.

  • For nontolerated VTs, various ablation strategies have been described, including targeting abnormal potentials, matching pace mapping sites, areas of slow conduction, linear lesions, and scar homogenization.

  • Imaging can be beneficial in identifying the arrhythmogenic substrate.

  • Epicardial ablation is infrequently required, but epicardial substrate is an important reason for VT recurrence after VT ablation in patients with prior infarcts.

9.6 Dilated Cardiomyopathy

Key Points

  • Identifying the location and extent of scarring on CMR is beneficial in procedural planning and has improved the outcomes of ablation in patients with DCM.

  • The ablation strategy is similar to postinfarction VT.

  • An intramural substrate is more frequently encountered in DCM than in postinfarction patients and requires a different ablation strategy than for patients with either epicardial or endocardial scarring.

  • Epicardial ablation is beneficial if the scar is located in the epicardium of the LV free wall.

  • For intramural circuits involving the septum, epicardial ablation is not beneficial.

  • In the absence of CMR, unipolar voltage mapping has been described as a method to indicate a deeper-seated scar.

9.7 Ventricular Tachycardia Ablation in Hypertrophic Cardiomyopathy

Key Points

  • Polymorphic VT and VF are the most common VAs in HCM; monomorphic VT is less common.

  • The arrhythmogenic substrate in HCM often involves the septum but can extend to the epicardium, often necessitating combined endocardial and epicardial ablation procedures to eliminate the VT.

  • VT associated with apical aneurysms is often ablated endocardially.

9.8 Brugada Syndrome

Key Points

  • PVC-triggered VF or polymorphic VT are the most prevalent VAs that motivate device therapy in patients with Brugada syndrome.

  • Monomorphic VT is less frequent but can be caused by BBRVT in patients with Brugada syndrome.

  • The arrhythmogenic substrate is located in the RV epicardium and can be demonstrated by sodium channel blockers.

  • Ablation targets include fractionated prolonged electrograms on the epicardial aspect of the RV.

9.9 Polymorphic Ventricular Tachycardia/Ventricular Fibrillation Triggers

Key Points

  • Recurrent PVC-induced VF is most often triggered by PVCs originating from Purkinje fibers, located in the RVOT, the moderator band, or the LV.

  • Patients with a single triggering PVC are better ablation candidates; however, there are often multiple triggers.

  • Patients with healed myocardial infarction often require extensive ablation of the Purkinje fiber system within or at the scar border.

  • Ischemia should be ruled out as a trigger for VF prior to ablation.

9.10 Arrhythmogenic Right Ventricular Cardiomyopathy

Key Points

  • The arrhythmogenic substrate in ARVC is located in the epicardium and can involve the endocardium in advanced stages.

  • The most commonly affected areas are the subtricuspid and RV outflow regions.

  • LV involvement is not uncommon.

  • Endocardial-epicardial ablation is often required and results in higher acute success and lower recurrence rates compared with endocardial ablation alone.

  • Conventional mapping and ablation techniques, including entrainment mapping of tolerated VT, pace mapping, and substrate ablation, are used.

9.11 Mapping and Ablation in Congenital Heart Disease

Key Points

  • Patients with a VT substrate after congenital heart defect surgery include those with repaired tetralogy of Fallot, repaired ventricular septal defect, and repaired d-transposition of the great arteries (D-TGA), as well as Ebstein’s anomaly among other disease processes.

  • VT isthmuses are often located between anatomical barriers and surgical incisions or patch material.

  • An anatomical isthmus can be identified and targeted during sinus rhythm.

  • For tolerated VTs, entrainment mapping is the method of choice for identifying critical components of the reentry circuit.

9.12 Sarcoidosis

Key Points

  • The arrhythmogenic substrate in cardiac sarcoidosis is often intramurally located but can include the endocardium and epicardium.

  • A CMR is beneficial in planning an ablation procedure in cardiac sarcoidosis.

  • The arrhythmogenic substrate can be complex and can include areas of active inflammation and chronic scarring.

  • The VT recurrence rate after ablation is high.

9.13 Chagas Disease

Key Points

  • The pathogenesis of Chagas disease is poorly understood but often results in an inferolateral LV aneurysm.

  • The arrhythmogenic substrate is located intramurally and on the epicardial surface, often necessitating an epicardial ablation procedure.

9.14 Miscellaneous Diseases and Clinical Scenarios With Ventricular Tachycardia

Key Points

  • Lamin cardiomyopathy often has a poor prognosis, progressing to end-stage heart failure.

  • VT ablation is challenging due to intramural substrates

  • VT recurrence rate is high after ablations.

  • VT in patients with noncompaction tends to originate from regions of noncompacted myocardium where scar can be identified in the midapical LV.

  • VT ablation in patients with LV assist device can be challenging due to the limitation of preprocedural imaging, and the electromagnetic noise generated by the LV assist device.

9.15 Surgical Therapy

Key Points

  • Surgery-facilitated access to the epicardium via a limited subxiphoid incision can be helpful in the case of adhesions.

  • Cryoablation via thoracotomy is possible for posterolateral substrates and via sternotomy for anterior substrates.

9.16 Sympathetic Modulation

Key Points

  • Sympathetic modulation targeting the stellate ganglia by video-assisted thoracoscopy may be considered for failed VT ablation procedures or VF storms.

  • A temporary effect can be obtained with the percutaneous injection or infusion of local anesthetics.

9.17 Endpoints of Catheter Ablation of Ventricular Tachycardia

Key Points

  • Noninducibility of VT by PES after ablation is a reasonable endpoint and predictor for VT recurrence after VT ablation in patients with SHD.

  • Due to the limitations of programmed stimulation, endpoints other than noninducibility have been described, including elimination of excitability, elimination of late potentials or local abnormal ventricular activity, dechanneling, substrate homogenization, core isolation, image-guided ablation, and anatomically fixed substrate ablation.

10 Postprocedural Care

Access-related issues, anticoagulation (Table 9), and complications (Table 10), as well as the management thereof, are reviewed in this section. Furthermore, assessment of outcomes and determinants of outcomes are detailed (Fig. 13).

Table 9 Postprocedural care in prospective studies of ventricular tachycardia catheter ablation
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Fig. 13
figure 13

Factors influencing outcomes post VA ablation. ICD = implantable cardioverter defibrillator; LVAD = left ventricular assist device; VA = ventricular arrhythmia; VT = ventricular tachycardia

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10.1 Postprocedural Care: Access, Anticoagulation, Disposition

10.1.1 Postprocedural Care: Access

10.1.2 Postprocedural Care: Anticoagulation

10.2 Incidence and Management of Complications

Table 10 Major complications of ventricular arrhythmia ablation in patients with structural heart disease
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10.3 Hemodynamic Deterioration and Proarrhythmia

10.4 Follow-up of Patients Post Catheter Ablation of Ventricular Tachycardia

11 Training and Institutional Requirements and Competencies

This section contains the general training and institutional requirements with an emphasis on lifelong learning, professionalism, and acquisition and maintenance of knowledge and skills. In addition, institutional requirements for specific procedures are reviewed.

11.1 Training Requirements and Competencies for Catheter Ablation of Ventricular Arrhythmias

11.2 Institutional Requirements for Catheter Ablation of Ventricular Tachycardia

12 Future Directions

This section summarizes ongoing trials and the need for prospective evaluation of different clinical problems. It further reviews recent advances and limitations of various mapping techniques and addresses unanswered questions requiring future investigations.