Ventricular tachycardia (VT) most commonly develops in patients with structural heart disease. Myocardial infarction results in collagen replacement interspersed with surviving myocardium, which alters impulse propagation, facilitating re-entry.1 Aside from the postinfarction substrate, scar-mediated VT occurs in patients with nonischemic cardiomyopathy, Chagas disease, sarcoidosis, arrhythmogenic right ventricular cardiomyopathy, and postsurgical congenital heart disease. In structurally normal hearts, VT results from intracellular calcium overload or an abnormal response to adrenergic stimulation, promoting triggered activity or automaticity, respectively. There are 3 treatment options for VT, although many patients require a combination: an implantable cardioverter-defibrillator (ICD), antiarrhythmic medications, and catheter ablation. An ICD provides abortive “rescue” therapy but cannot prevent the heart from going into VT. Antiarrhythmic therapy has limited efficacy and has the potential for multiple side effects, including proarrhythmia.2 In this Clinician Update, we discuss 3 different VT clinical scenarios that are amenable to catheter ablation to highlight the range of substrate-specific strategies used in the electrophysiology laboratory. An 18-year-old man presented with palpitations and fatigue. Over a period of 5 months, he had been unable to play sports owing to dyspnea on exertion. A resting ECG demonstrated sinus rhythm with frequent monomorphic premature ventricular contractions. An echocardiogram revealed an ejection fraction of 35% with global hypokinesis. Previous treatment with β-blockers and flecainide was unsuccessful, and he was referred for evaluation for catheter ablation. The patient underwent electrophysiological study, and activation mapping was performed in the right and left ventricular outflow tracts to locate the earliest site of origin. A single application of radiofrequency energy at the earliest site below the left coronary cusp resulted in complete abolition of the premature ventricular contractions (Figure 1). Figure 1. A 12-lead ECG of ventricular bigeminy with left bundle-branch morphology and inferior axis with early precordial transition ( top ). Earliest site of activation ( bottom …