Ablation for ventricular tachycardia: is more always better? How much more is too much?

Ventricular tachycardia (VT) remains one of the major causes of morbidity and mortality after myocardial infarction (MI) (1,2). Surviving myofibers within scar tissue have been shown to represent the arrhythmogenic substrate of post-infarction VT (3). Identification of these myocytes and myofiber bundles is possible by recording electrograms from the scarred endocardium with a mapping catheter (4). This can be best achieved while the patient is in VT. Unfortunately, most VTs are not hemodynamically tolerated, and therefore mapping during VT is not possible (5). Identification of specific electrograms, mainly isolated potentials during sinus rhythm, has been linked to critical sites of VT,