Catheter ablation of ventricular tachycardia.

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 substratespecific strategies used in the electrophysiology laboratory.