Arrhythmogenic effects of antiarrhythmic drugs in patients with an old myocardial infarction and asymptomatic ventricular ectopic activity as studied by programmed electrical stimulation.

In 22 patients with a previous myocardial infarction and documented Lown class II to IV asymptomatic ventricular arrhythmias, the arrhythmogenic effect of mexiletine (18 patients) and propafenone (10 patients) has been assessed by programmed electrical stimulation. Ventricular arrhythmias induced during the basal study were: repetitive ventricular responses (RVR) (11/22, 50%), nonsustained ventricular tachycardia (VT) (3/22, 14%), sustained VT (7/22, 32%) and ventricular fibrillation (VF) (1/22, 4%). The induction of sustained VT or VF increased to 50% after mexiletine and to 80% following propafenone. An arrhythmogenic effect was found in 7/11 patients (64%) without VT at the control study (P = 0.004). One patient of this group spontaneously developed sustained VT both after mexiletine and propafenone. Only 1/8 patients (13%) with sustained VT/VF at the basal study had RVR after drug administration. The R-R interval of sustained VT at the basal state tended to be faster than that after the drugs (260 +/- 60 ms vs 293 +/- 56 and 332 +/- 77 ms for mexiletine and propafenone, respectively) (P = 0.052). Statistical significance was only reached in the propafenone group (P = 0.03). Facilitation of VT induction after antiarrhythmic drugs is most likely due to a modest lengthening of refractoriness in contrast with a more evident reduction in conduction velocity within the reentry pathway. Our study illustrates that treating asymptomatic ventricular ectopic activity in patients with an old myocardial infarction may be dangerous and that antiarrhythmic drugs show a significant arrhythmogenic potential at least in the laboratory setting.