Substrate Ablation of VT in Unstable Post-Infarct Patients

Survivors of myocardial infarction remain exposed to a long tail of electrical instability, and ventricular tachycardia arising from the resulting scar is a dominant driver of sudden cardiac death in the months and years after the index event. Modern reperfusion has changed who reaches the clinic: large infarcts that would once have been fatal are now survived, only to present later with re-entrant arrhythmias arising from heterogeneous border zones. The lesions that substrate ablation targets are slow-conducting channels of surviving myocytes woven through dense fibrosis, where unidirectional block and slowed conduction sustain macroreentry.

When ventricular tachycardia becomes haemodynamically intolerable, the usual tools of activation and entrainment mapping fall away. The operator cannot sustain VT long enough to localise a circuit, and pharmacological termination returns the patient to sinus rhythm without showing where the circuit lies. Substrate ablation closes this gap by treating the scar itself as the target, working in sinus rhythm to identify abnormal electrograms and deliver lesions that interrupt potential re-entry paths regardless of whether VT is running at the moment of ablation.

This review walks through the rationale, patient selection, mapping strategy, lesion delivery, and outcomes for substrate ablation in post-infarct patients with haemodynamic instability, and frames those considerations against the realities of Australian practice, where referral pathways, retrieval services, and access to mechanical circulatory support shape pacing.

Pathophysiology of post-infarct VT substrate

The arrhythmic substrate after myocardial infarction is not uniform scar. It is a layered landscape of dense fibrosis, surviving myocyte bundles, and intermediate zones of preserved but partially depolarised tissue, and the borders between these layers are where re-entry circulates. Conduction through surviving bundles is slowed by gap junctional remodelling, and the resulting zig-zag propagation produces the fractionated, late-potential-bearing electrograms that define the target for substrate-based intervention.

Critical isthmuses responsible for clinical VT tend to be narrow, often only a few millimetres wide, and they can be missed by catheters that record at standard density. Modern multipolar mapping tools have substantially improved the resolution with which these channels can be visualised in sinus rhythm, and the resulting high-density maps make it possible to identify corridors of slowed conduction that were effectively invisible a decade ago. Identifying these corridors is the bridge between mechanical entrapment of the circuit and successful elimination.

Choosing candidates for substrate ablation in Australian practice

Patient selection is driven by three recurring clinical pictures in Australian tertiary centres: recurrent VT despite antiarrhythmic therapy, electrical storm, or haemodynamic intolerance of VT that precludes conventional activation mapping. Most of these procedures are concentrated in a small group of high-volume units, including those at Royal Melbourne Hospital, Westmead Hospital, The Alfred, and MonashHeart, which together cover catchment populations that span thousands of kilometres. Patients from regional and remote areas frequently arrive by retrieval through state-based aeromedical networks or the Royal Flying Doctor Service, which adds pressure to complete the intervention in a single admission rather than staged across multiple visits.

Screening tools that flag patients at risk before the first VT episode are increasingly relevant, and AI-based ECG interpretation now offers a way to surface silent atrial fibrillation and other subtle conduction abnormalities in post-infarct cohorts followed in the community. Identifying these abnormalities matters because coexisting atrial arrhythmia and ventricular disease often travel together, and a flagged ECG may be the trigger for a referral that prevents the first arrhythmic event rather than the tenth.

Local guidelines from the Cardiac Society of Australia and New Zealand broadly align with international recommendations, but the threshold for offering invasive therapy is often influenced by the logistics of retrieval and follow-up. A patient in western Queensland or the Northern Territory may face a four-hour flight to reach a lab, which shifts the calculus toward earlier intervention when the substrate is clearly defined.

Mapping approaches when haemodynamic tolerance is poor

Substrate-based approaches begin in sinus rhythm and rely on the assumption that abnormal electrograms recorded during stable rhythm mark the regions capable of supporting VT. Late potentials, fractionated signals, and low-voltage areas are used to construct a three-dimensional reconstruction of the scar and its borders, and corridors of abnormal signal are then targeted for ablation. Distinct from catheter ablation in patients who tolerate VT, this approach sacrifices some circuit-specific information in exchange for safety and reproducibility.

When VT is poorly tolerated but termination is achievable with medication, brief inductions can be used to validate that the targeted channels actually correspond to a clinical circuit. More recent approaches use catheter ablation during VT supported by mechanical circulatory support, and percutaneous Impella or VA-ECMO support is offered at major Australian centres for carefully selected patients in whom mapping during VT would otherwise be unsafe. This approach allows activation mapping to be completed despite hypotension, but it brings its own procedural complexity and requires close coordination between electrophysiology, cardiac anaesthesia, and perfusion teams.

High-density mapping catheters, sometimes combined with image integration from pre-procedural cardiac MRI or CT, have become routine. When late gadolinium enhancement imaging clearly highlights the core and border zone of the scar, the reconstructed three-dimensional model can be merged with the electroanatomic map to guide ablation in regions that would otherwise be ambiguous.

Ablation energy, lesion design, and endpoints

Radiofrequency ablation delivered through an irrigated-tip catheter remains the workhorse, and lesion depth is influenced by contact force, power, duration, and irrigation. Contemporary workflows aim for an impedance drop and a reduction in local electrogram amplitude as markers of effective lesion formation, and operators typically target an ablation index that balances lesion depth against the risk of steam pop. Where standard unipolar ablation fails to reach epicardial or mid-myocardial circuits, operators can use an epicardial approach via subxiphoid access, simultaneous unipolar ablation from two catheters, or a coronary venous approach.

Endpoints vary between operators and institutions. Non-inducibility at the end of the procedure is a common goal, but it is not a perfect surrogate for freedom from recurrent VT, and many patients with negative induction studies still have arrhythmia recurrence. A more substrate-focused endpoint aims to eliminate all late potentials and abnormal electrograms within the scar, accepting a longer procedure and more extensive ablation in exchange for what appears to be a more durable result. Complications from the procedure include phrenic nerve injury, cardiac tamponade, and vascular complications, and these occur in a small but real proportion of patients.

Lessons from other scar-based VT substrates

The post-infarct substrate is one of several scar-mediated VT substrates encountered in clinical practice, and operators have learned from the management of related conditions. Decisions about timing, energy choice, and endpoint definition in arrhythmogenic right ventricular cardiomyopathy share many features with the post-infarct setting, and timing and strategy in ARVC ablation often informs how operators plan their approach to fibrofatty replacement in the right ventricle.

There are important differences. Post-infarct substrate tends to be left ventricular, subendocardial or transmural, and driven by ischaemic border zone re-entry, whereas ARVC substrate is right ventricular, often epicardial, and prone to progressive fibrofatty replacement. The shared principles of substrate identification, elimination of late potentials, and use of high-density mapping translate across conditions, but the procedural access, complications profile, and need for serial procedures differ. Operators familiar with one approach tend to combine strategies rather than reinventing workflows for every condition.

Outcomes, complications, and follow-up in the Australian context

Acute procedural success, defined as non-inducibility of the targeted VT at the end of the case, is achieved in the majority of patients at experienced Australian centres, and freedom from recurrent VT at one year varies widely depending on case mix, definition, and follow-up rigor. Long-term freedom is harder to achieve: VT recurs in a substantial minority over five years, often from new circuits within the same scar. Repeat ablation is feasible and frequently performed, and the morbidity of repeat procedures is generally low.

Complications mirror those reported elsewhere and include vascular access complications, cardiac tamponade, conduction system injury requiring permanent pacing, and, less commonly, embolic stroke. The use of mechanical support adds its own complications, including limb ischaemia and access-site bleeding, and these must be weighed against the benefit of mapping during VT in patients who cannot tolerate sustained arrhythmia. Follow-up after ablation in Australia is typically shared between the procedural centre and the local cardiology service, with device interrogation used to gauge arrhythmia recurrence where an ICD is in place. For patients living far from the procedural centre, telehealth review and remote device monitoring have taken the sting out of long-haul travel to the big smoke for what would otherwise be a brief check, and have made long-term follow-up more practical than it once was. These arrangements matter because ongoing management of heart failure, antiarrhythmic therapy, and device programming continues long after the last ablation lesion is delivered, and they are particularly important for Aboriginal and Torres Strait Islander patients, in whom ischaemic heart disease and arrhythmic complications carry a disproportionate burden.

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