Mapping ventricular tachycardia in nonischemic cardiomyopathy

In nonischemic cardiomyopathy, sustained ventricular tachycardia may arise from a relatively small region of fibrosis that is difficult to identify from the surface electrocardiogram alone. As ventricular function and disease activity change, re-entry pathways can reorganise, making an electroanatomic map a snapshot rather than a permanent blueprint. Mapping helps localise abnormal tissue, conduction barriers and arrhythmia circuits for catheter ablation.

Endocardial and epicardial mapping answer complementary questions. Endocardial catheters can define activation, voltage and late potentials within the ventricular chamber and venous structures. Epicardial access reveals disease on the myocardial surface, where scar may be prominent in several nonischemic conditions. A limited endocardial map does not exclude epicardial substrate, while epicardial mapping cannot fully assess deep septal or intramural disease.

The distinction has practical consequences for patients treated in Australia. Recurrent ventricular tachycardia can cause syncope, implantable cardioverter-defibrillator shocks and uncertainty about driving or work. Patients living outside metropolitan areas may also need to travel to a centre with advanced electrophysiology, cardiac imaging and pericardial expertise, making an efficient, well-planned procedure particularly valuable.

This review examines the technical foundations of ventricular tachycardia mapping, the strengths and limitations of each approach, and the factors that should shape procedural and follow-up decisions. The emphasis is on integrated interpretation: electrical findings, arrhythmia behaviour, imaging, comorbidities and the consequences of ablation for the individual patient.

Why nonischemic ventricular tachycardia needs a broader map

Nonischemic ventricular tachycardia usually reflects an arrhythmogenic substrate involving myocardial fibrosis, inflammation, genetic disease or a combination of these processes. Idiopathic dilated cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis, myocarditis and inherited channelopathies may all present with ventricular arrhythmias, although their substrate distribution differs substantially.

Arrhythmogenic right ventricular cardiomyopathy and cardiac sarcoidosis frequently involve the epicardial surface and can produce a mismatch between the apparent origin on the electrocardiogram and the tissue responsible for maintenance of the tachycardia. In other cardiomyopathies, critical sites may be intramural, around the papillary muscles, within the interventricular septum or near the left ventricular summit. A single imaging plane or voltage criterion cannot reliably represent all of these locations.

Clinical clues can guide investigation but cannot replace mapping. Younger age, a familial history, right ventricular dilatation, regional wall-motion abnormalities and conduction disease may suggest a particular substrate. Recurrent syncope, exercise-related symptoms or sustained tachycardia may increase concern, yet the electrocardiogram alone cannot define the circuit. Electroanatomic mapping translates those suspicions into a three-dimensional account of activation and abnormal tissue.

Building and interpreting the electroanatomic map

Modern mapping platforms combine catheter locations with electrogram timing and voltage information to reconstruct the arrhythmia substrate. Activation maps display the sequence of depolarisation, while voltage maps identify areas with reduced amplitude consistent with scar. Fragmented electrograms, prolonged activation and late potentials can indicate diseased tissue or slow conduction that participates in re-entry.

A mapping session usually begins with anatomical reconstruction using fluoroscopy, intracardiac echocardiography or computed tomography angiography. The ventricular geometry is then annotated with reference locations such as the His bundle, coronary ostia and valve annuli. Additional points are acquired during sinus rhythm, pacing or tachycardia to assess conduction, capture potential and regions of interest relevant to ablation.

Interpretation requires more than labelling visibly abnormal voltage. Signal noise, electrode contact, motion, oedema and mapping thresholds can all influence the apparent size of a scar. Arrhythmogenic tissue may also be electrically heterogeneous, with a narrow zone of slow conduction surrounded by apparently normal myocardium. Confirming a critical site may require entrainment, pacing manoeuvres or repeated mapping during different rhythm states.

Ventricular tachycardia presents further constraints. Mapping during haemodynamic instability demands close communication with anaesthesia and prompt termination of poorly tolerated episodes. Antiarrhythmic medication, blood loss, autonomic changes and evolving ventricular function can also modify the recorded signals. For this reason, the map should be interpreted as an evolving physiological model rather than a fixed representation of structural disease.

Endocardial mapping and ablation

Endocardial mapping is performed through femoral arterial or venous access and may include retrograde aortic, transseptal or transvenous approaches to the left and right ventricles. Familiar catheter routes provide access to the ventricular cavities, valve annuli, papillary muscles, septal surfaces and the left ventricular summit. These landmarks are also important when defining ablation targets and avoiding unintended injury.

The approach is established, reproducible and generally avoids the specific complications associated with entering the pericardial space. It is particularly suitable when the suspected circuit is endocardial, when the patient has a high bleeding risk from pericardial access, or when epicardial involvement appears limited. Endocardial ablation may be definitive in selected forms of idiopathic cardiomyopathy and can form part of a combined strategy in more extensive disease.

Radiation reduction is increasingly achievable through catheter navigation, intracardiac imaging and electroanatomical localisation. The journal’s practical account of zero-fluoroscopy protocols describes how operators can build on three-dimensional mapping while limiting fluoroscopic exposure. Such protocols require training in image registration, catheter visualisation and safe access because fluoroscopy still provides important information during difficult punctures or unexpected anatomical courses.

Epicardial mapping and access strategies

Epicardial mapping requires access to the pericardial space, most often through a subxiphoid approach with a steerable sheath or through a surgical window. The pericardium can then be mapped systematically around the right ventricle, inferior and lateral left ventricular walls, apex, anterior septum and posterior wall. Precise catheter positioning and recognition of coronary anatomy are essential throughout the procedure.

Surface mapping can expose extensive epicardial scar that is poorly represented on endocardial recordings. This is particularly relevant in arrhythmogenic right ventricular cardiomyopathy, cardiac sarcoidosis and selected cases of idiopathic dilated cardiomyopathy. Isolated late potentials, fragmented signals and activation barriers identified on the epicardium may provide additional ablation targets and explain why an apparently endocardial circuit terminates or changes behaviour after epicardial intervention.

Epicardial access also introduces distinct risks. These include coronary artery injury, vessel perforation, pericardial bleeding, tamponade, pericardial inflammation and injury to nearby structures such as the oesophagus or diaphragm. Posterior mapping requires careful assessment of coronary branches and collateral vessels, while ablation near the oesophagus may benefit from cooling, oesophageal temperature monitoring or alternative energy delivery. Access should therefore be undertaken where surgical backup and advanced imaging are immediately available.

Choosing and combining the mapping approaches

The decision between epicardial and endocardial access should be based on substrate distribution, arrhythmia characteristics and patient-specific risk. Epicardial mapping is favoured when the clinical picture or imaging suggests surface disease, particularly in arrhythmogenic right ventricular cardiomyopathy or sarcoidosis. Endocardial mapping may suffice when the circuit is well defined within the chamber and epicardial access carries excessive risk.

Combined procedures remain an important option. Endocardial activation and voltage data can define the ventricular anatomy and guide later epicardial access, while epicardial findings may reveal targets not visible from within the chamber. The sequence can vary according to operator preference, haemodynamic stability and the anticipated burden of epicardial disease. A staged strategy may be safer when a prolonged combined procedure would expose a high-risk patient to unnecessary anaesthesia or bleeding.

Evidence for a universally superior approach is limited by procedure selection, differences in disease aetiology and the strong influence of operator experience. Comparisons of recurrence and complication rates must therefore consider VT termination, renal and neurological injury, mortality, repeat procedures and subsequent defibrillator therapy. Device infection, abandoned transvenous leads and complex implanted hardware can add another layer of planning; the journal’s discussion of pre-extraction risk assessment illustrates the value of multidisciplinary preparation when future access or device management may be affected.

Bringing advanced mapping into Australian practice

Australia’s advanced ventricular arrhythmia services are concentrated in major metropolitan hospitals, including networks in Melbourne, Sydney and Brisbane. Medicare-supported public services and private health insurers fund much of the specialist care, while access to mapping systems, electrophysiology staffing and pericardial surgical backup varies between centres. Public waiting times and the cost of capital equipment can influence referral pathways, particularly for patients travelling from regional, rural or remote areas.

Everyday Australian life shapes the consequences of recurrent ventricular tachycardia. Long commutes, driving on rural roads, physically demanding occupations and limited access to immediate medical care make syncope and haemodynamic instability especially consequential. Medication schedules, exercise routines and the timing of implantable cardioverter-defibrillator shocks should therefore be incorporated into discharge planning. Fitness to drive is considered under state and territory rules for private drivers, with separate national requirements applying to commercial drivers.

Devices and research in this field are overseen within Australian frameworks. The Therapeutic Goods Administration regulates the inclusion and supply of mapping, ablation and implanted cardiac devices, while research participation generally requires approval through a human research ethics committee and alignment with National Health and Medical Research Council expectations. These processes support rigorous evidence generation, but they also highlight the need for consistent outcome reporting, transparent follow-up and equitable access beyond the largest cities.

For clinicians, trainees and researchers seeking deeper understanding of ventricular tachycardia, electrophysiology and device-based arrhythmia management, the journal’s scope provides access to original research, reviews, guidelines, special collections and submission information. Reading the current evidence and sharing it through peer-reviewed publication can help refine substrate-based ablation, strengthen multidisciplinary decision-making and improve care for patients with complex nonischemic ventricular arrhythmias.