Endocardial or Epicardial Ablation in ARVC: Predictors of Success

Arrhythmogenic right ventricular cardiomyopathy (ARVC), historically termed arrhythmogenic right ventricular dysplasia, is an inherited cardiomyopathy characterised by myocyte loss, fibro-fatty replacement and ventricular electrical instability. Disease usually involves the right ventricular free wall, outflow tract and peritricuspid region, producing ventricular tachycardia (VT), syncope or sudden cardiac death. Genetic findings support diagnosis and family assessment, while ventricular arrhythmia burden helps refine risk. Cardiac magnetic resonance imaging and the task-force and Padua frameworks provide further diagnostic support.

Endocardial versus epicardial ablation is not a simple choice of two techniques. Endocardial catheter ablation is established, whereas epicardial access can expose substrate that is concealed or electrically separated from the endocardial surface. A combined approach may be required for extensive arrhythmogenic right ventricular disease. Treatment also remains multimodal: an implantable cardioverter-defibrillator (ICD) may prevent fatal rhythms, while drugs or ablation reduce recurrent VT.

Success should be separated into acute procedural success and durable VT freedom. The first means terminating the targeted arrhythmia and eliminating inducibility; the second means no recurrent VT or ICD therapy over years. Predictors differ, and neither technical endpoint guarantees freedom from a progressive inherited cardiomyopathy.

Selecting the ablation strategy

Selection begins with symptoms, ECG and imaging. Clinicians review VT morphology, syncope, prior shocks, device data, medication response, right ventricular function, scar distribution and left ventricular involvement. Ambulatory monitoring and a 12-lead ECG are often arranged through a general practitioner, while inherited cardiomyopathy assessment should involve an electrophysiologist familiar with ARVC.

Endocardial ablation is commonly the first procedure for monomorphic VT with a reproducible and accessible circuit. It can target late potentials, fractionated electrograms, conduction channels and scar borders in the right ventricular outflow tract or tricuspid annulus. Structural overlap with congenital disease can complicate imaging and device planning; the journal’s practical guide to adult congenital heart disease provides a useful model for multidisciplinary review.

Epicardial ablation is favoured when endocardial mapping shows an inadequate target, when the circuit lies on the outer ventricular wall, or when epicardial substrate is expected to dominate. Combined endocardial–epicardial ablation can improve target coverage in selected patients, especially with extensive free-wall disease. The decision should reflect arrhythmia complexity, ventricular function, pericardial access, operator expertise and the consequences of leaving a clinically important circuit untreated.

Defining the arrhythmogenic substrate

High-density mapping should identify the mechanism of each clinical VT before committing to a lesion set. An activation map can establish a late activation or re-entry circuit, while abnormal electrograms reveal slow conduction at tissue borders. Electrogram morphology, activation timing, pacing manoeuvres and exclusion of inadvertent mechanical artefacts help distinguish arrhythmogenic substrate from normal myocardium.

Endocardial and epicardial voltage maps often show different disease boundaries. Epicardial mapping can demonstrate late, isolated or fractionated potentials with no convincing endocardial counterpart, particularly near the right ventricular free wall and peritricuspid region. Conversely, septal and intracavitary structures may be easier to define from inside the ventricle. Comparing maps can prevent a procedure from becoming an indiscriminate exercise in voltage abolition.

Cardiac MRI with late gadolinium enhancement and CT assessment of wall thickness, fat and coronary anatomy complement invasive mapping. Scar burden and biventricular involvement provide prognostic context, although a visible scar does not prove that every low-voltage area is arrhythmogenic. The practical endpoint is usually elimination of the clinical VT and relevant substrate, assessed with repeat induction when haemodynamics permit. Non-inducibility is encouraging, yet new substrate can develop as the cardiomyopathy advances.

Predicting procedural and long-term success

The most reproducible favourable markers are preserved ventricular function, limited scar, absence of significant left ventricular involvement and a small number of monomorphic VT circuits. A stable, clinically concordant VT that can be mapped is more amenable to targeted ablation than rapid polymorphic VT or multiple unstable morphologies. Lower pre-procedure arrhythmia burden and fewer prior ICD therapies also indicate a less electrically unstable cardiac substrate.

Conversely, recurrent VT is more likely with advanced right ventricular dysfunction, extensive scar, low right ventricular ejection fraction, left ventricular involvement and polymorphic ventricular arrhythmias. Previous failed ablation, multiple VT morphologies and difficult haemodynamics complicate both substrate access and the likelihood of complete circuit elimination. These factors should not be used to deny ablation; they should trigger earlier referral, more careful planning and realistic counselling about repeat procedures.

Complete elimination of mapped abnormal electrograms and the clinical VT is a stronger procedural objective than stopping at one anatomical site. Failure to achieve electrical non-inducibility predicts recurrence, although some patients remain VT-free despite residual inducible signals. Conversely, a non-inducible procedure cannot prevent future arrhythmia arising from new scar. Genetic subtype, age and sex have shown associations in selected cohorts, but no validated score currently combines them into a reliable individual prediction tool. Most outcome cohorts are observational and centre-based, and comparative evidence does not establish universal superiority for any ablation strategy.

Long-term success also depends on modifiable disease activity. Continued high-intensity endurance exercise can accelerate arrhythmic disease in genetically susceptible people, while appropriate beta-blockade, review of stimulant excess and management of thyroid or electrolyte abnormalities can reduce triggers. Exercise restriction and adaptation should be individualised with cardiology and sports medicine advice, with the aim of reducing arrhythmic risk while preserving safe activity.

Weighing complications and recurrence

Endocardial ablation carries risks of vascular injury, perforation, tamponade, embolisation and inadvertent damage to the conduction system, particularly near the tricuspid annulus and His bundle. Epicardial access introduces pericardial bleeding, myocardial injury, coronary artery injury, phrenic nerve injury and post-ablation pericarditis. Combined procedures may improve substrate coverage while increasing procedural complexity, so expected benefit should be weighed against additive risk.

Anticoagulation reduces thromboembolic risk, while careful access planning reduces bleeding and mechanical complications, but neither prevents all injury. Pericardial drainage capability, immediate cardiac imaging support and access to advanced cardiac surgery are essential for higher-risk procedures. Anaesthesia, haemodynamic monitoring and ICD backup should match the expected arrhythmia burden rather than the simplicity of the planned ablation.

Recurrence after a first procedure can result from incomplete lesion placement, an unmapped circuit, evolving scar or a new ventricular arrhythmia mechanism. Repeat endocardial ablation may address gaps, while repeat epicardial or combined ablation can be considered for persistent epicardial or free-wall substrate. Remote device interrogation, ambulatory ECG, exercise review and interval imaging help distinguish electrical recurrence from non-arrhythmic events such as heart failure or medication effects.

Translating evidence into Australian practice

ARVC ablation expertise is concentrated in tertiary electrophysiology programs, including services in Melbourne, Sydney and Brisbane, with further capability in Adelaide and Perth. This concentration matters for people living in rural New South Wales, northern Queensland, Tasmania or Western Australia, where referral may involve travel and prolonged public waiting times. Some centres provide remote device checks and transmitted ECG monitoring, although hands-on mapping still requires an experienced team.

Australian care commonly spans a public hospital and private outpatient system. General practitioner referrals support Medicare-subsidised specialist consultations, and eligible investigations and ablation attract Medical Benefits Schedule rebates; complex ablation can still produce a gap payment, while private insurance may cover part of the pathway. Prescription benefits support drugs such as sotalol or amiodarone when prescribed appropriately. Patients should be counselled about medicine effects, pregnancy considerations where relevant and the practical burden of repeated follow-up.

Daily habits shape risk outside the electrophysiology laboratory. Running, cycling, rowing, swimming and gym-based endurance training are common in Australia, so an ARVC diagnosis requires an individual exercise plan, ideally developed with sports cardiology. Syncope and ICD therapies also affect driving. Clearance periods differ across state transport authorities, and patients need written advice on when resumption is safe rather than relying on general reassurance.

Regulation and governance are equally practical. Implantable devices and ablation tools used in Australia are overseen by the Therapeutic Goods Administration through the Australian Register of Medical Devices. Consent and record handling should explain device transmission, imaging uploads and data sharing under the Privacy Act 1988 and applicable state health-records legislation. For teams building a service protocol or prospective registry, the journal’s author guidance provides current information for turning clinical data into publishable research.

Early referral to an ARVC-experienced electrophysiology centre is the most useful immediate action for patients with recurrent VT, syncope, ICD therapies or suspected disease. The referral should include the ECG, device interrogation, imaging reports, medication history and VT recordings, allowing the receiving team to consider endocardial, epicardial and combined strategies before another sustained episode occurs.

Patients can support that plan by bringing records to every appointment, reporting palpitations or syncope promptly, adhering to medicines and agreed exercise advice, and asking for a written driving plan after any loss of consciousness or ICD therapy. These steps make the next ablation decision more precise while preserving shared decision-making across the patient, family, cardiology and genetics team.