<unk>  works by blocking the Nav1.5 sodium channel in the heart, slowing the upstroke of the cardiac action potential. This thereby slows conduction of the electrical impulse within the heart, i.e. it "reduces excitability". The greatest effect is on the His-Purkinje system and ventricular myocardium. The effect of<unk>  on the ventricular myocardium causes decreased contractility of the muscle, which leads to a decrease in the ejection fraction. The effect of<unk>  on the sodium channels of the heart increases as the heart rate increases; This is known as use-dependence and is why that<unk>  is useful to break a tachyarrhythmia.<unk>  also inhibits ryanodine receptor 2 (RyR2), a major regulator of sarcoplasmic release of stored calcium ions. It can reduce calcium sparks and thus arrhythmogenic calcium waves in the heart. While<unk>  therapy has been shown to suppress ventricular arrhythmias in patients with catecholaminergic polymorphic ventricular tachycardia (CPVT) and mouse models of this disease, the relative contribution from the inhibition of sodium channels and of RyR2 in this effect on CPVT is unclear.
Flecainide
Tocainide
Procainamide
Acecainide
Amiodarone
Ibutilide
Verapamil
Dofetilide