Flecainide-induced aggravation of ventricular tachycardia

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Abstract
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.