Propafenone is an orally active
sodium channel blocking agent with
beta-adrenoceptor antagonist and weak
calcium antagonist activity. The pharmacokinetic profile of
propafenone is complex, characterised as typically nonlinear, saturable, stereoselective and dependent on both dose and
debrisoquin metaboliser phenotype; individualised dosage titration is required. Both placebo- and
drug-controlled studies have confirmed the efficacy of
propafenone in the treatment of premature ventricular complexes, ventricular couplets and
nonsustained ventricular tachycardia; in a large meta-analysis,
propafenone together with
amiodarone,
flecainide and
encainide were significantly more effective in the control of ventricular ectopy than other antiarrhythmic agents. However, the use of
propafenone in these indications, like that of other antiarrhythmic agents, is likely to be limited to patients with a favourable risk-to-benefit ratio.
Propafenone has also demonstrated efficacy in the treatment of malignant ventricular arrhythmias (
ventricular fibrillation and sustained
ventricular tachycardia); preliminary mortality data obtained with
propafenone have been encouraging in this patient group. In addition,
propafenone has a favourable noncardiac tolerability profile and
beta-adrenoceptor antagonist activity, which may offer advantages in some specific patient groups. The area of research concerning
propafenone which has shown the greatest expansion over the past 5 years is in the treatment of supraventricular arrhythmias.
Propafenone has marked efficacy in patients with
Wolff-Parkinson-White syndrome and has been recommended as a first-line prophylactic agent in those with rapid anterograde conduction.
Propafenone is also effective in the conversion of
atrial fibrillation to sinus rhythm, although comparative studies are required to determine advantages over more established agents.
Propafenone use has been successfully extended to children with limited data demonstrating consistent efficacy in the control of
junctional ectopic tachycardia. As with all antiarrhythmic agents,
propafenone has the potential to induce arrhythmias. Comparative studies are required to assess in more detail the cardiac tolerability profile of
propafenone against other class Ic agents. In conclusion,
propafenone offers a broad spectrum of activity in the treatment of
cardiac arrhythmias, although its use in patients with potentially malignant arrhythmias will remain limited for the present. Due to its unique pharmacodynamic profile,
propafenone deserves consideration as an individual agent.