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Flecainide, a nonselective Na (+) channel blocker, is a class 1C antiarrhythmic drug, especially used for the management of supraventricular arrhythmia. Flecainide has been used extensively in the effect on providing long-term sinus rhythm (SR) restoration as well as decreasing AF symptoms.

Flecainide revealed to suppress the Nav1.5 sodium channel in the heart, leading to prolongation of the cardiac action potential. Flecainide showed to reduce Ca+ spark, wave frequency and Ca+ wave velocity in the intact rat cardiomyocyte. Besides, flecainide has shown to reduce Ca(2+) wave when I(Na) is active. It has been demonstrated that flecainide could remarkably increase the Na(+)/Ca(2+)-exchanger (NCX)-mediated Ca(2+) efflux  [1].

Flecainide has been reported to prolong ventricular repolarization, with the stronger effect at the left ventricular epicardium related to the right ventricular epicardium. Flecainide was found to produce a greater effective refractory period (ERP) lengthening at endocardium than epicardium, leading to a significant increase of ERP dispersion across the ventricular wall [2].

Flecainide has shown to dose-dependently reduce systemic pressures (32% at 0.8 μg/mL) and peripheral vascular resistance (15% at 0.8 μg/mL). In addition, at therapeutic plasma concentrations, flecainide at 0.8 μg/mL remarkably reduced the heart rate (55 beats/min) and increased QRS intervals (9.9 msec) in a rat hindlimb perfusion model [3].

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