Flecainide‐induced aggravation of ventricular tachycardia

Flecainide acetate is a new class I antiarrhythmic agent which slows atrial, A‐V nodal and ventricular conduction velocity, and prolongs refractoriness of these structures (Borchard et al. , 1982; Hodess et al. , 1979). Recent studies with oral flecainide therapy suggested its high potential for suppression of ventricular tachycardia in humans (Anderson et al. , 1981; Duff et al. , 1981; Hodges et al. , 1982). Its favorable pharmacokinetics with an average plasma half‐time of about 20 hours allows in most patients twice daily dosing (Duff et al. , 1981). Usually, the drug seemed to be well tolerated and side‐effects, such as blurred vision, could be resolved with smaller but still effective doses (Duff et al. , 1981). Actually, the ideal antiarrhythmic agent which represents a high degree of effectiveness, a low level of toxicity, a wide therapeutic range, and a prolonged antiarrhythmic action does not exist (Dreifus and Ogawa, 1977). In this report we describe a patient with flecainide‐induced aggravation of ventricular tachycardia necessitating resuscitation because of severe hemodynamic deterioration.