Substrate-Based Ablation for Ventricular Tachycardia in Ischaemic Scar

Ventricular tachycardia (VT) arising from an ischaemic myocardial scar remains a major cause of recurrent implantable cardioverter-defibrillator (ICD) therapy, hospital admission and impaired quality of life. The arrhythmia often depends on surviving myocardial fibres that course through or around dense fibrosis, creating slow-conduction channels capable of sustaining re-entry. Treating the substrate, rather than pursuing each clinical VT as an isolated event, has become central to modern electrophysiology.

For Australian clinicians, this strategy must be adapted to a geographically dispersed health system. Complex ablation is concentrated in metropolitan centres such as Sydney, Melbourne, Brisbane, Perth and Adelaide, while patients from regional areas may travel long distances for mapping, repeat procedures and device follow-up. Careful risk assessment, pre-procedure imaging and coordination between local cardiologists and tertiary electrophysiology teams are therefore as important as the lesion set delivered in the laboratory.

How Ischaemic Scar Sustains Ventricular Tachycardia

Following myocardial infarction, replacement fibrosis and interspersed surviving myocyte bundles produce regions of conduction slowing and unidirectional block. These channels may connect areas of viable tissue within the infarct border zone to the surrounding myocardium. When the circuit reaches a critical length and conduction velocity is sufficiently reduced, a stable monomorphic VT can develop. The surface ECG may provide clues about the infarct territory and likely exit, but it rarely defines the complete re-entry circuit.

Scar-related VT can be clinically tolerated, allowing activation mapping during the arrhythmia. More commonly, however, the rhythm causes hypotension, chest pain, pulmonary oedema or loss of consciousness and must be terminated quickly. Multiple morphologies may reflect different exits from the same substrate rather than separate mechanisms. A comprehensive procedure therefore seeks to identify the shared arrhythmogenic region, including conducting channels, abnormal electrograms and the border zone surrounding dense scar.

Late gadolinium enhancement cardiac MRI can help estimate scar location, transmurality and tissue heterogeneity before the procedure. MRI may be limited by device compatibility, renal function, image quality or local access, so contrast-enhanced CT and detailed review of prior angiography can also contribute. The pre-procedure assessment should include ventricular function, coronary anatomy, valve disease, anticoagulation, renal status and the likelihood that anaesthesia or haemodynamic support will be required.

Mapping the Arrhythmogenic Substrate

Three-dimensional electroanatomical mapping during sinus rhythm or paced rhythm is often the foundation of substrate modification. Bipolar voltage mapping identifies areas of dense scar and low-voltage border zone, while unipolar voltage can suggest deeper or intramural disease that is less apparent from the endocardial surface. Mapping density matters: widely spaced points may miss narrow channels, particularly around papillary muscles, the mitral isthmus or the ventricular septum.

Operators look for local abnormal ventricular activities, fractionated potentials, isolated late potentials and sharp signals separated from the far-field ventricular electrogram. These findings can identify surviving bundles within scar that participate in re-entry. Pace mapping from candidate sites may reproduce the clinical QRS morphology, whereas entrainment during tolerated VT can establish whether a site lies in the circuit, near the exit or within a bystander region. When VT is unstable, pace mapping and substrate-based techniques become particularly valuable.

Ablation may involve targeting late potentials, abolishing local abnormal ventricular activities, closing conducting channels or creating a more extensive scar homogenisation strategy. The most appropriate endpoint depends on scar architecture and the procedural goal. Elimination of inducible sustained monomorphic VT is useful, although noninducibility does not guarantee that every potential circuit has been removed. Conversely, aggressive ablation should be balanced against the risk of injury to the conduction system, coronary arteries, valves and viable myocardium.

Endocardial, Epicardial and Advanced Approaches

An endocardial approach is appropriate for many patients with prior anterior or inferior infarction, especially when the scar is predominantly subendocardial. Transseptal or retrograde aortic access may be selected according to ventricular anatomy, target location and operator experience. Intracardiac echocardiography can improve catheter contact assessment, identify thrombus and support transseptal puncture, while real-time imaging helps reduce complications in a ventricle that may already have limited reserve.

Epicardial mapping should be considered when the suspected substrate is subepicardial, when endocardial ablation fails, or when the ECG and imaging suggest an epicardial exit. It carries additional risks, including bleeding, coronary injury, phrenic nerve damage and pericarditis. Previous cardiac surgery, anticoagulation and adhesions can make access more difficult. A staged procedure may be safer than attempting extensive endocardial and epicardial work in a single session, particularly in a frail patient with advanced heart failure.

Intramural septal scar, papillary muscle VT and deep channels may remain difficult to treat with conventional unipolar radiofrequency energy. Bipolar ablation, needle or needle-like technologies, half-normal saline irrigation and other specialised techniques are used in selected centres, but each has procedural limitations and a developing evidence base. Energy delivery should be guided by anatomy and tissue thickness rather than by a desire to create the largest possible lesion.

Procedural safety also includes anticipating the effects of anaesthesia. General anaesthesia can suppress sympathetic tone and alter VT inducibility, while prolonged hypotension may worsen myocardial injury. In Australia, temporary mechanical circulatory support is available mainly through selected tertiary services, so referral decisions should account for local expertise, retrieval logistics and the patient’s distance from a capable centre.

Timing, Outcomes and Long-Term Care

Ablation is indicated for recurrent monomorphic VT, repeated ICD shocks or electrical storm despite suitable medical therapy, and it may be considered earlier in selected patients with ischaemic cardiomyopathy. The VANISH study helped establish the role of catheter ablation over escalation of antiarrhythmic medication in appropriate patients with recurrent VT and ICDs. The benefit is often a reduction in VT episodes and shocks rather than elimination of mortality risk, so ablation should sit within a broader heart-failure and secondary-prevention plan.

Timing is clinically important. An unstable patient with electrical storm may require sedation, correction of potassium and magnesium abnormalities, treatment of ischaemia, sympathetic blockade and intravenous antiarrhythmic therapy before mapping. Once stabilised, early referral can prevent repeated shocks and progressive decompensation. In a public hospital setting, bed availability and transfer pathways may influence timing, while private care may involve different access and funding arrangements. Clear communication prevents patients from interpreting a delayed procedure as a lack of urgency.

After ablation, ICD programming should be reviewed, including detection intervals, antitachycardia pacing and shock thresholds. Antiarrhythmic drugs may be continued temporarily or long term, depending on ventricular function, recurrence risk and adverse effects. Guideline-directed therapy for heart failure, revascularisation when appropriate, management of diabetes and renal disease, and smoking cessation remain essential. Cardiac rehabilitation can support exercise confidence and medication adherence, with local services varying substantially between metropolitan and regional communities.

Follow-up should combine device interrogation, symptom review, ECG assessment and consideration of repeat imaging. Recurrent VT does not always mean procedural failure: it may represent a new channel, incomplete lesion formation, disease progression or a different mechanism. Patients travelling from the Northern Territory, regional Queensland or rural Western Australia may need remote ICD monitoring and coordinated local review to reduce unnecessary long-distance journeys.

Building Evidence and Expertise

Substrate-based ablation continues to evolve through improved mapping resolution, high-density multipolar catheters, better imaging integration and automated identification of abnormal electrograms. Research is also examining the role of cardiac sympathetic denervation, stereotactic body radiotherapy and novel energy sources for patients with refractory VT. These options should be viewed within specialist programmes and clinical trials rather than as substitutes for careful substrate assessment.

Education is particularly valuable because procedural success depends on interpreting signals in anatomical context. Australian trainees may encounter different case volumes across metropolitan electrophysiology units, and exposure to complex VT can be supplemented through multidisciplinary conferences, simulation and international literature. The Journal of Arrhythmia’s arrhythmia collections provide a useful route to themed research and educational material spanning ablation, devices and electrophysiology.

Publishing high-quality local data can also clarify how substrate modification performs across varied healthcare settings. Reports on referral delay, Indigenous health access, rural retrieval, device follow-up and outcomes after VT storm may add practical value to the international literature. Authors preparing such work should follow transparent reporting, define procedural endpoints carefully and describe antiarrhythmic, ICD and heart-failure management alongside ablation details. The journal’s author guidelines outline the requirements for submitting original research, reviews and clinical material.

Technology developed in other electrophysiology fields may also inform ventricular ablation, although it must not be transferred uncritically. For example, discussion of high-power ablation safety illustrates how power, contact, lesion depth and collateral injury must be considered together. In ventricular scar, tissue thickness, impedance, cooling and proximity to coronary arteries make lesion assessment especially complex.

A practical pathway begins with early recognition of recurrent VT, stabilisation, imaging and referral to a centre capable of advanced mapping and rescue support. The procedural plan should be individualised to scar distribution, VT tolerance, comorbidities and patient goals. Continued collaboration between Australian regional services, tertiary electrophysiologists, device clinics and heart-failure teams can make this highly specialised care more accessible. Clinicians and researchers can contribute to that progress by applying rigorous substrate assessment, sharing outcomes and engaging with the growing evidence base in cardiac electrophysiology.