The chemical and pharmacologic properties, pharmacokinetics, drug interactions, clinical efficacy, adverse effects, and dosage of
propafenone are reviewed.
Propafenone is a class IC antiarrhythmic agent that is structurally similar to the beta blockers but that has only weak beta-blocking and
calcium-channel-blocking activity. It is well absorbed after
oral administration, but systemic bioavailability is only 12% after a 300-mg dose. Among extensive metabolizers (greater than 90% of the United States population), bioavailability seems to vary nonlinearly with dose and increases substantially with food; these effects are not seen in poor metabolizers. Elimination is primarily hepatic, with a mean elimination half-life after
oral administration of 5.5 hours in extensive metabolizers and 17.2 hours in poor metabolizers. The relationship between plasma
propafenone concentration and clinical response varies considerably among individual patients; therefore, plasma concentrations have limited usefulness in predicting efficacy or electrophysiologic effects.
Propafenone is effective in treating
ventricular tachycardia and in suppressing premature ventricular complexes (PVCs). It is less effective in the treatment of refractory
ventricular tachycardia. Concurrent administration of
digoxin,
warfarin, or
metoprolol with
propafenone has been shown to increase the serum concentrations of those three drugs, while
cimetidine slightly increases the
propafenone concentrations. Additive pharmacologic effect can occur when
lidocaine,
procainamide, and
quinidine are combined with
propafenone. Overall, 21% to 32% of patients experience adverse effects, with 3% to 7% of these serious enough to warrant discontinuing
therapy. The most common adverse effects are
dizziness or
lightheadedness,
metallic taste, and
nausea and
vomiting; the most serious adverse effects are proarrhythmic events.(ABSTRACT TRUNCATED AT 250 WORDS)