[Early after-depolarization in polymorphic ventricular tachycardia without QT prolongation].

Endocardial monophasic action potentials (MAP) were recorded at different sites of the right ventricle in a patient with a history of syncope and recurrent polymorphic ventricular tachycardia (pVT) without QT prolongation. The MAP recording from the infero-septal wall demonstrated persisting early afterdepolarizations (EAD) during sinus rhythm with no cycle length dependence. Programmed ventricular stimulation at this site provoked a pVT rapidly degenerating into ventricular fibrillation. Iodine-123-meta-iodobenzylguanidine (MIBG) scintigraphy indicated a defective sympathetic innervation in inferior and apical sectors of the left ventricle. Intravenous verapamil resulted in marked sinus bradycardia and nevertheless completely suppressed the pVT. These observations support the hypothesis that the mechanism of pVT is EAD-induced triggered activity that is due to an intrinsic defect of the myocardial cell with alteration of the calcium channels. This regulation defect of ionic channels might possibly be induced by an abnormality in the sympathetic innervation. Both conditions may lead to dispersion of repolarization causing triggered activity. In our case the regionally restricted findings explain the absence of QT prolongation. The effect of verapamil provides evidence that bradycardia is not an essential condition in the genesis of pVT.