Lack of clinically significant beta-blocking effect of propafenone

Abstract

To study possible beta-blocking effects of propafenone, a class 1c antiarrhythmic agent, electrocardiographic variables were studied at rest and during exercise. Forty-two patients with symptomatic ventricular arrhythmias were included. In 31 patients, exercise electrocardiograms before and after propafenone were available for study. The mean dose of propafenone was 603 mg for all 42 patients, 585 mg for patients undergoing exercise testing (range 450-1200). At rest, the PR interval, duration of P wave and QRS complex changed significantly without any change in the resting heart rate and QTc interval. During exercise there were no changes after propafenone in peak heart rate, PR interval, QTc interval, duration of exercise, or blood pressure. We conclude that, while class I effects are evident both at rest and after exercise, no clinically significant beta-blocking effects of propafenone could be demonstrated either at rest or during exercise.

P wave duration in paroxysmal and persistent atrial fibrillation

“…Propafenone is an IC class agent which blocs the fast sodium channels, slowing down the conduction velocity in the working myocardium. According to literature data there is no direct relationship between the dose of propafenone and the duration of the P wave, however the same study confirms a weak correlation between the treatment with propafenone and the elongation of the P wave duration [26]. Our data do not confirm this finding.…”

Pharmacokinetic and pharmacodynamic interaction between mexiletine and propafenone in human beings*1

“…These results are in agreement with those of others who reported no reduction in the maximal heart rate during exercise after propafenone administration at doses required to control ventricular arrhythmias. 49 However, Lee et al 50 clearly established the β-blocking properties of propafenone, especially in poor metabolizers.…”

Exercise-induced left bundle branch block and propafenone administration

“…Sodium channel blockade is probably responsible for the important QRS prolongation during exercise in patients taking propafenone [1]. Rate-dependent conduction slowing by the sinus tachycardia of exercise may be responsible for some cases of proarrhythmia caused by class IC drugs [2].…”