Flecainide is class Ic Na + channel blocker that is used to restore sinus rhythm and to prevent the arrhythmia recurrence in patients with atrial fibrillation. Antiarrhythmic effect of flecainide is attribut- ed to prolonged atrial effective refractory period and depressed car- diac action potential upstroke. Nevertheless, flecainide has been reported to produce arrhythmogenic responses in ventricular myo- cardium. In this regard, the Cardiac Arrhythmia Suppression Trial (CAST) has shown that flecainide therapy is associated with marked- ly increased risk of sudden arrhythmic death in patients with healed myocardial infarction, an effect possibly accounted for by the drug- induced anisotropic conduction slowing in the peri-infarct zone. Based on these findings, indications for flecainide therapy are cur- rently limited to the atrial fibrillation control in patients with no structural heart disease. Although flecainide-induced conduction abnormalities are unlikely to occur in the absence of myocardial ischemia or fibrosis, there is in- creasing evidence to suggest that flecainide may promote arrhythmo- genic responses in patients with structurally normal hearts. Flecainide administration has been reported to induce torsade de pointes, a poten- tially life-threatening polymorphic ventricular tachycardia, in patients with no coronary artery disease or severe heart failure (1,2). This kind of arrhythmia is thought to be attributed to the prolonged QT interval and increased spatial dispersion of ventricular repolarization. However, the contribution of these factors to flecainide-induced proarrhythmia is often overlooked, because flecainide (along with other class Ic Na + channel blockers) is generally regarded asanagentproducingonly little or no effect on ventricular repolarization.