Several
antiarrhythmic drugs are prone to cause QT interval prolongation and
torsades de pointes (TDP). Predisposing risk factors include congenital
channelopathies, severe
bradycardia, drugs, and
hypokalemia. Individual genetic variation and
drug metabolism exaggerate susceptibility to adverse reactions. These proarrhythmic effects create a deficit in the repolarization reserve and prolong action potential duration, resulting in early afterdepolarizations, which promote a reentry circuit.
Flecainide, a class IC
drug, also exhibits inhibitory actions on the K(+) channels, causing QT interval prolongation. We identified six cases of
flecainide-induced TDP in the literature. Most patients had other predisposing factors.
Bradycardia was present in all cases. Our case demonstrates two arrhythmias caused by
flecainide:
atrial flutter with 1:1 atrioventricular conduction and TDP. Both arrhythmias developed in the absence of
hypokalemia, with the use of other drugs that prolong QT interval, or
genetic predisposition. Therefore, this is purely a
drug effect. This case report illustrates a rare but serious proarrhythmic property of
flecainide observed particularly in women.