A majority of patients with structural heart disease and scar-related ventricular tachycardia (VT) have fast, hemodynamically unstable VT.1 In fact, up to one-fifth of the patients have only unstable VT, which precludes detailed activation and entrainment mapping.2 In addition, even in those with well-tolerated VT, procedural success can be complicated by acute heart failure as a consequence of prolonged episodes of induced VT and intravascular volume expansion; and one consequence of this acute decompensated heart failure is a significant increase in the short-term morbidity and mortality of the procedure.
