As with all members of its class, propafenone has its major effect on the fast inward sodium current. The IC agents depress Vmax over a wide range of heart rates and shift the resting membrane potential in the direction of hyperpolarization. The IC agents bind slowly to the sodium channel and dissociate slowly. Therefore, they exhibit rate-dependent block. Inhibition of the sodium channel throughout the cardiac cycle will result in a decrease in the rate of ectopy and trigger ventricular tachycardia.
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