Epicardial Ablation for Ventricular Tachycardia in Arrhythmogenic Cardiomyopathy

Arrhythmogenic cardiomyopathy (ACM) is an inherited or acquired myocardial disorder in which ventricular scar and electrical instability can produce recurrent ventricular tachycardia (VT), syncope, heart failure and sudden cardiac death. The disease may involve the right ventricle, left ventricle or both, and its phenotype can evolve over time. This variation makes treatment planning more complex than simply targeting a single, well-defined endocardial circuit.

For selected patients with drug-refractory VT, recurrent implantable cardioverter-defibrillator (ICD) therapies or a predominantly epicardial substrate, ablation from the outer surface of the heart can be an important part of care. Epicardial VT ablation requires careful integration of imaging, electroanatomical mapping, coronary anatomy, surgical backup and long-term disease management. Clinicians seeking current electrophysiology research and educational material can consult the Journal of Arrhythmia for peer-reviewed work relevant to these decisions.

Why arrhythmogenic cardiomyopathy produces ventricular tachycardia

The arrhythmic substrate in ACM commonly consists of fibrofatty replacement, patchy fibrosis and areas of surviving myocardium separated by conduction barriers. These channels can support re-entry, particularly when ventricular activation is slowed by scar. In arrhythmogenic right ventricular cardiomyopathy, the outflow tract, inferior wall and peritricuspid regions are frequently involved. Left-dominant or biventricular disease may create a more extensive substrate across the inferolateral left ventricle and interventricular septum.

The surface electrocardiogram, signal-averaged findings, ambulatory monitoring and cardiac magnetic resonance imaging each provide different information. T-wave inversion, ventricular ectopy with a left bundle branch block pattern, late gadolinium enhancement and progressive ventricular dysfunction can indicate a higher-risk phenotype, although no single finding defines the need for epicardial treatment. Genetic results may support diagnosis and family screening, but the ablation target is determined by the patient’s clinical VT and the distribution of electrical scar.

VT can arise from both endocardial and epicardial layers. In ACM, the epicardial component may be substantial even when the endocardial voltage map appears relatively limited. This is one reason recurrence can occur after an apparently successful endocardial procedure. A prior ablation, ongoing inflammation, genetic progression or incomplete lesion formation may expose additional channels over time.

Selecting patients for an epicardial strategy

Epicardial access is generally considered when VT persists despite appropriate antiarrhythmic therapy, when ICD shocks or antitachycardia pacing are recurrent, or when imaging and prior mapping suggest a predominantly epicardial circuit. It may be planned as a combined endocardial–epicardial procedure or used after recurrence following endocardial ablation. The decision should reflect symptom burden, ventricular function, procedural risk, comorbidities and the patient’s goals.

A detailed pre-procedure assessment is essential. Cardiac magnetic resonance can identify scar distribution and ventricular involvement, while computed tomography may clarify the relationship between the target substrate, coronary arteries and the phrenic nerve. Echocardiography assesses right and left ventricular function, valve disease and haemodynamic reserve. Device interrogation can reveal the clinical VT rate, morphology and response to programming, helping the team reproduce or target the relevant rhythm.

Patients with haemodynamic instability, severe ventricular failure, active myocarditis or extensive pericardial disease may require a different sequence of treatment. Mechanical circulatory support is considered in selected high-risk cases, particularly when sustained VT is expected to be poorly tolerated. The procedural plan should also account for anticoagulation, renal function, anaesthetic risk and the possibility that VT induction will be unsafe.

In Australia, referral pathways often concentrate complex VT care in tertiary electrophysiology centres in Sydney, Melbourne, Brisbane, Perth and other capital cities. Patients from regional or remote areas may need substantial travel and coordinated accommodation, follow-up and device monitoring. Medicare-supported consultations and hospital services can reduce some access barriers, but availability of advanced epicardial programmes remains uneven, making early referral valuable.

Mapping and accessing the epicardial substrate

Epicardial access is usually obtained by subxiphoid or inferior percutaneous puncture under fluoroscopic, echocardiographic and pressure guidance. The operator must distinguish the pericardial space from the right ventricle, liver and abdominal structures. Previous cardiac surgery, pericarditis or an existing pericardial effusion can make access more difficult and may favour a surgical or hybrid approach.

Once access is established, a high-density electroanatomical map can identify low-voltage regions, late potentials, fractionated electrograms and conduction channels. Pace mapping and entrainment may help connect the clinical VT to the mapped substrate, although VT induction is not always necessary. In sinus rhythm, abnormal electrograms can define a broader treatment field than a single induced circuit, especially in patients with multiple VT morphologies.

The operator must account for the course of the right coronary artery, circumflex artery, left anterior descending artery and their branches. Coronary angiography or integrated CT data may be used before energy delivery when the target lies near a major vessel. The phrenic nerve can also overlie an intended lesion set; pacing from the ablation catheter can help identify it, while techniques such as pericardial fluid, balloon displacement or altered catheter positioning may reduce injury risk.

Radiofrequency energy is the most established method for epicardial substrate modification. Irrigated catheters can create deeper lesions, but excessive power or prolonged applications increase the risk of steam pops, coronary damage and collateral injury. Contact force, impedance change, electrogram reduction and lesion continuity must be interpreted together rather than relying on one numerical endpoint. In selected centres, bipolar ablation or other advanced technologies may be considered for deep intramural substrate, although evidence remains more limited.

Managing complications and recurrent disease

Epicardial ablation carries risks that require a different safety framework from endocardial procedures. Haemopericardium, coronary injury, phrenic nerve dysfunction, pericarditis and delayed effusion are recognised complications. Bleeding can be particularly serious if the access tract traverses the myocardium or a coronary vessel. Continuous haemodynamic observation and immediate access to pericardiocentesis, blood products, cardiac surgery and coronary intervention are important components of a safe programme.

Post-procedure inflammation is common, and anti-inflammatory treatment may be used according to local protocols and the patient’s renal, gastrointestinal and bleeding risks. Follow-up should include clinical review, ECG assessment, device interrogation and echocardiography when indicated. New chest pain, dyspnoea, hypotension or persistent hiccups after discharge may signal pericardial, phrenic nerve or other complications and requires urgent assessment.

A useful reminder of procedural risk comes from broader structural electrophysiology experience: the Journal of Arrhythmia’s report on transseptal puncture complications illustrates why access-related outcomes deserve systematic surveillance. Epicardial procedures similarly benefit from consistent definitions, imaging follow-up and transparent reporting rather than focusing only on acute VT suppression.

Recurrence does not automatically indicate technical failure. ACM is a progressive myocardial disease, and new scar can develop after a technically complete lesion set. Recurrent VT should prompt review of ICD programming, medication adherence, ventricular function, new imaging findings and the possibility of a changing substrate. Repeat ablation, intensified medical therapy, heart failure treatment or transplantation assessment may each be appropriate in different clinical circumstances.

Building a long-term care pathway

Ablation should sit within a broader strategy that includes ICD management, antiarrhythmic medication, exercise counselling, family evaluation and psychological support. In many patients, reducing VT burden and ICD shocks is the immediate objective rather than eliminating every ventricular ectopic beat. ICD programming that uses appropriate detection intervals and antitachycardia pacing can reduce unnecessary shocks while preserving protection from malignant rhythms.

Exercise advice requires individual assessment. Vigorous endurance activity and competitive sport may increase arrhythmic risk in some ACM phenotypes, while complete inactivity can worsen general cardiovascular health and wellbeing. Recommendations should consider genotype, ventricular function, arrhythmia history and current guidelines. Practical plans are especially important for Australians whose daily routines may involve long drives, outdoor work, heat exposure or limited access to nearby cardiac services.

Genetic counselling helps identify relatives who may benefit from clinical review, ECG, imaging and cascade testing. Testing should be accompanied by appropriate counselling because variants may have uncertain significance and family decisions can be emotionally difficult. Privacy and health-information handling must also be considered within Australian legal and institutional requirements, especially when results are shared across family members or health services.

The Australian therapeutic market includes established catheter, mapping-system and ICD technologies, but access can vary according to hospital funding, procurement arrangements and specialist availability. Devices and procedural technologies are regulated through the Therapeutic Goods Administration, while local hospital policies govern credentialing, consent, infection control and emergency escalation. These realities make multidisciplinary governance important when adopting high-cost or emerging ablation tools.

Evidence continues to develop through registries, multicentre studies and genotype-informed research. The latest journal collections can help clinicians and trainees follow developments in ventricular arrhythmia, mapping, ablation and device therapy. Comparative studies are still needed to clarify the best timing of epicardial intervention, the value of prophylactic substrate modification and the role of newer energy sources.

Epicardial ablation offers a valuable option for carefully selected people with ACM and recurrent VT, particularly when the arrhythmic substrate extends beyond the endocardium. Its success depends on accurate phenotyping, meticulous access, coronary and nerve protection, realistic counselling and sustained follow-up. Centres that combine advanced imaging, experienced electrophysiology, cardiac surgery and inherited-heart-disease expertise are best placed to deliver this treatment safely.

Clinicians, researchers and trainees can use the Journal of Arrhythmia’s open-access resources to review current evidence, compare procedural approaches and share outcomes from Australian and international practice. Submitting well-designed registry analyses, mechanistic studies and carefully reported clinical experience will help refine epicardial VT ablation for the next generation of patients with arrhythmogenic cardiomyopathy.