The electrophysiologic effects and therapeutic efficacy of intravenous and oral
flecainide were studied in 15 patients with spontaneous and inducible sustained
paroxysmal supraventricular tachycardia (SVT). Twelve patients had atrioventricular (AV) reentrance using an accessory pathway for retrograde conduction and 3 had AV nodal reentrance. Fourteen patients received intravenous
flecainide (2 mg/kg
body weight over 15 minutes) during an initial electrophysiologic study. Nine patients were restudied during oral
flecainide administration (200 to 400 mg/day). After intravenous or oral
flecainide therapy, reentrant SVT was noninducible in 6 patients with AV reentrance and in the 3 with AV nodal reentrance. In these 9 patients, intravenous
flecainide prevented induction of reentrant SVT by depressing conduction over the retrograde limb of the reentry circuits. In the 6 patients with inducible sustained AV reentrant SVT before and after
flecainide therapy, the cycle length of
tachycardia increased significantly, mainly as the result of an increase in ventriculoatrial conduction time. There was concordance between the intravenous and the oral effects of
flecainide on the mechanism of the SVT. Twelve patients continued oral
flecainide treatment for a mean of 16 months (range 5 to 28).
Tachycardia recurred in 3 of 4 patients whose
arrhythmia remained inducible after
flecainide therapy and in 1 of 8 patients whose SVT was suppressed. It is concluded that
flecainide is an effective and convenient antiarrhythmic agent to treat patients who have AV nodal or AV reentrant SVT.