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  • Title: Provocation of supraventricular tachycardias by an intravenous class I antiarrhythmic drug.
    Author: Brembilla-Perrot B, Terrier de la Chaise A.
    Journal: Int J Cardiol; 1992 Feb; 34(2):189-98. PubMed ID: 1737670.
    Abstract:
    Antiarrhythmic drugs may aggravate or induce ventricular arrhythmia. The induction of a supraventricular tachycardia or its facilitation has rarely been reported. The purpose of the study was to know whether the potential for supraventricular proarrhythmic effect of a class Ia intravenous antiarrhythmic drug can be exposed during electrophysiologic study. Ajmaline was chosen because of its short duration of action. The protocol of the study consisted of an electrophysiological study and programmed atrial stimulation using 1 and 2 extrastimuli on driven rhythm and atrial pacing up to second-degree atrioventricular block. Then 1 mg/kg of ajmaline was injected and atrial pacing was performed 3 minutes after its injection. Supraventricular proarrhythmic effect of ajmaline was defined as the spontaneous occurrence of a supraventricular tachycardia or the facilitation of its induction. Seventy patients among 1955 presented a proarrhythmic effect: 63 developed a supraventricular tachyarrhythmia (atrial flutter, fibrillation, tachycardia) and 7 an atrioventricular reentrant tachycardia, either spontaneously (n = 23) or during atrial pacing (n = 47). Risk factors were identified in most patients: old age, underlying heart disease, history of spontaneous supraventricular tachycardia and/or induction of a supraventricular tachycardia by 2 extrastimuli on driven rhythm in the control state (34 patients), sinus node dysfunction (22 patients). Compared with patients without proarrhythmic supraventricular effect only the history of spontaneous supraventricular tachycardia and the existence of a sinus node dysfunction were significantly more frequent (P less than 0.05) in patients with proarrhythmic effect of ajmaline. In conclusion, the supraventricular proarrhythmic effect of intravenous ajmaline exists and is related both to the electrophysiologic characteristics of the drug and to the arrhythmia substrate. The results indicate that a supraventricular tachyarrhythmia may be induced by a class I antiarrhythmic drug.
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