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Electrophysiological mechanism for the antiarrhythmic action of propafenone: a comparison with mexiletine

1 The antiarrhythmic potency of propafenone was evaluated in the guinea‐pig isolated heart; arrhythmias were induced with (a) digitalis intoxication and (b) hypoxia followed by reoxygenation. 2 Propafenone, 0.5 μm, was found to be the minimal but effective antiarrhythmic concentration. The antiarrhythmic activity of propafenone developed slower than that of 10 μm mexiletine, which was the lowest effective concentration under the same experimental conditions. 3 The electrophysiological effects of propafenone were then studied on sheep cardiac Purkinje fibres (manifesting oscillatory afterpotentials and triggered automaticity induced by barium or strophanthidin) and compared with those of 10 μm mexiletine. 4 Both 0.5 μm propafenone and 10 μm mexiletine consistently blocked triggered activity in sheep Purkinje fibres. The onset of the effect of propafenone was slower than that of mexiletine. 5 Unlike mexiletine, propafenone did not reduce the amplitude of oscillatory afterpotentials. 6 In contrast, propafenone significantly reduced in barium‐ and strophanthidin‐treated preparations. 7 It is concluded that the antiarrhythmic action of propafenone on digitalis‐ and reoxygenation‐induced arrhythmias is probably due to an electrophysiological mechanism different from that of mexiletine. Mexiletine, by reducing the amplitude of oscillatory afterpotentials, prevents the attainment of the threshold; propafenone, by reducing the excitability of the cell, increases the threshold and consequently an oscillatory afterpotential of the same amplitude will not generate arrhythmias.