Both the electrophysiological and antiarrhythmic effects of some antiarrhythmic agents may differ markedly depending on their route of administration.
Flecainide acetate, a new class 1 agent, was therefore administered both intravenously and orally to 13 patients with recurrent
paroxysmal tachycardia to assess whether the acute response to intravenous
flecainide accurately predicts the response to oral
therapy. Eight patients had atrioventricular re-entrant
tachycardia (AVRT) and five patients intra AV nodal re-entrant
tachycardia (AVNRT). When administered by either route,
flecainide markedly prolonged both the anterograde and retrograde conduction intervals during constant rate pacing and the anterograde and retrograde Wenckebach cycle lengths during incremental pacing. Five of the 13 patients developed complete retrograde block after both routes of administration of the
drug. All 13 patients received intravenous
flecainide during
tachycardia with successful reversion to sinus rhythm in all cases.
Tachycardia could be reinitiated in five of the patients with AVRT after intravenous
flecainide and in one further patient after
oral administration. It was not possible to reinitiate
tachycardia in any of the five patients with AVNRT after either intravenous or oral
flecainide. The size of the
tachycardia initiation windows, by either atrial or ventricular premature stimuli, were significantly reduced by both intravenous and oral
flecainide. In those patients in whom
tachycardia could be reinitiated,
tachycardia cycle length was significantly increased, and to a similar degree, by both routes of administration of the
drug. This increase in cycle length was predominantly due to prolongation in retrograde conduction. It is concluded that
flecainide acetate is a potent antiarrhythmic agent for use in patients with junctional
tachycardia. The
intravenous administration of
flecainide reliably predicts the subsequent response to oral
therapy.