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 (ECG), 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 dis-continuation 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.