Eight children, age between 4.5 and 19 years were treated with moricizine for supraventricular tachycardia during the last 3 years. The tachycardia was documented by surface electrocardiogram (EGG), and/or by ambulatory ECG in all the children and the mechanism of tachycardia was determined by previously published surface ECG and electrophysiologic criteria in all but one child. Of the eight children, three had atrial ectopic tachycardia, three had automatic junctional ectopic tachycardia, one had atrioventricular (AV) nodal reentry tachycardia and one had atrial reentry. All the children except one had failed trial of two or more antiarrhythmic drugs prior to moricizine therapy. The duration of moricizine therapy ranged from 4 days to 25 months. In three of the eight children (patients 3, 5 and 7), who presented with AV nodal reentrant tachycardia, automatic junctional ectopic tachycardia and atrial ectopic tachycardia, respectively, moricizine therapy was effective in restoring sinus rhythm and controlling the clinical tachycardia. Only one child (patient 1) developed proarrhythmia, an episode of fast, narrow-QRS supraventricular tachycardia lasting for 30 s, on the third day of therapy. This was subsequently confirmed by electrophysiologic study to be AV nodal reentrant tachycardia. The other side effects noted were non-cardiac, not dose-dependant and did not require discontinuation of therapy. Based on our small series and those of others, moricizine, a newer class I anti-arrhythmic agent, has a limited but useful role in the management of recalcitrant type of supraventricular tachycardia, such as ectopic atrial and junctional tachycardia in children.