Atrioventricular re-entrant

Flecainide slows conduction in all cardiac cells including the anomalous pathways responsible for the Wolff-Parkinson-White (WPW) syndrome. Together with encainide and moricizine, it underwent clinical trials to establish if suppression of asymptomatic premature beats with antiarrhythmic drugs would reduce the risk of death from arrhythmia after myocardial infarction. The study was terminated after preliminary analysis of 1727 patients revealed that mortality in the groups treated with flecainide or encainide was 7.7% compared with 3.0% in controls. The most likely explanation for the result was the induction of lethal ventricular arrhythmias possibly due to ischaemia by flecainide and encainide, i.e. a proarrhythmic effect. In the light of these findings the indications for flecainide are restricted to patients with no evidence of structural heart disease. The most common indication, indeed where it is the drug of choice, is atrioventricular re-entrant tachycardia, such as AV nodal tachycardia or in the tachycardias associated with the WPW syndrome or similar conditions with anomalous pathways. This should be as a prelude to definitive treatment with radiofrequency ablation. Flecainide may also be useful in patients with paroxysmal atrial fibrillation. 

Ajmaline occasionally causes cardiac dysrh5dhmias (SEDA-17, 219). Of 1995 patients who were given ajmaline 1 mg/kg intravenously during an electrophysiological study, 63 developed a supraventricular tachydysrhythmia (atrial flutter, fibrillation, or tachycardia), and seven an atrioventricular re-entrant tachycardia (2). Those most at risk were older patients, those with underlying cardiac disease, and those with a history of dysrhythmias or sinus node dysfunction. 

In patients with electrically inducible atrioventricular re-entrant tachycardia intravenous dofetilide 1.5-15 micrograms/kg had no effect on tachycardia inducibility at two lower doses but prevented the re-induction of tachycardia at three higher doses in 11 of 31 patients (40). 

In a randomized, placebo-controlled, crossover study in 15 men, mean age 34 (range 18-63) years, with Wolff-Parkinson-White syndrome and atrial fibrillation or atrioventricular re-entrant tachycardia induced electro-physiologically, six of ten patients who were given dofetilide converted to sinus rhythm, compared with one of five who were given placebo (47). There were no dysrhythmias. 

Qther cardiac dysrhjdhmias that have been reported have included episodes of junctional rhjdhm with bundle branch block, spontaneous atrioventricular re-entrant tachycardia, and sustained supraventricular tachycardia (40). 

Cobbe SM, Campbell RW, Camm AJ, Nathan AW, Rowland E, Bloch-Thomsen PE, Moller M, Jordaens L. Effects of intravenous dofetilide on induction of atrioventricular re-entrant tachycardia. Heart 2001 86(5) 522-6. 

This occurs in otherwise healthy individuals, who possess an anomalous (accessory) atrioventricular pathway they often experience attacks of paroxj mal AV re-entrant tachycardia or atrial fibrillation. Drugs that both suppress the initiating ectopic beats and delay conduction through the accessory pathway are used to prevent attacks e.g. flecainide, sotalol or amiodarone. Verapamil and digoxin may increase conduction through the anomalous pathway and should not be used. Electrical conversion may be needed to restore sinus rhythm when the ventricular rate is very rapid. Radiofrequency ablation of aberrant pathways will almost certainly provide a cure. 

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