Defining the Substrate in Scar-Related Ventricular Tachycardia

Scar-related monomorphic ventricular tachycardia is sustained by a limited re-entry circuit within a much larger field of diseased myocardium. Late gadolinium enhancement cardiac magnetic resonance and cardiac computed tomography define scar distribution, channel architecture, wall thickness, and tissue composition, but cannot demonstrate conduction or circuit participation. Voltage mapping and abnormal electrograms identify electrically abnormal myocardium, although their appearance depends on activation sequence, catheter geometry, contact, and annotation. Functional mapping reveals rate-dependent slowing, decrement, and block that may be concealed during baseline rhythm. Mapping during ventricular tachycardia (VT) provides the most direct evidence of circuit participation, but is often limited by hemodynamic instability, noninducibility, or incomplete surface representation of a 3-dimensional circuit. This review examines how to weight these findings when defining the arrhythmogenic substrate. Structural imaging establishes where a circuit could reside and how it may be accessed. Baseline electroanatomic mapping characterizes the electrical expression of surviving myocardium, while functional mapping tests whether conduction deteriorates with changes in wave front or coupling interval. Activation and entrainment provide the strongest evidence that a region participates in a specific VT. These findings should be integrated hierarchically rather than by simple spatial overlap, adjusting interpretation for disease phenotype, substrate depth, mapped surface, and recording conditions. The arrhythmogenic substrate is best understood as surviving myocardium within scar whose 3-dimensional architecture and electrophysiological behavior permit re-entry. A reproducible definition will require standardized acquisition and annotation, explicit reporting of the evidence linking a region to VT, and prospective validation using mapped circuits.