<unk> 's Class 1a activity is similar to that of quinidine in that it targets sodium channels to inhibit conduction.<unk>  depresses the increase in sodium permeability of the cardiac myocyte during Phase 0 of the cardiac action potential, in turn decreasing the inward sodium current. This results in an increased threshold for excitation and a decreased upstroke velocity.<unk>  prolongs the PR interval by lengthening both the QRS and P wave duration. This effect is particularly well suited in the treatment of ventricular tachycardia as it slows the action potential propagation through the atria to the ventricles.<unk>  does not act as a blocking agent for beta or alpha adrenergic receptors, but does have a significant negative inotropic effect on the ventricular myocardium. As a result, the use of<unk>  may reduce contractile force up to 42% at low doses and up to 100% in higher doses leading to heart failure. Levites proposed a possible secondary mode of action for<unk> , against reentrant arrhythmias after an ischemic insult.<unk>  decreases the inhomogeneity between infarcted and normal myocardium refractory periods; in addition to lengthening the refractory period. This decreases the chance of re-entry depolarization, because signals are more likely to encounter tissue in a refractory state which cannot be excited. This provides a possible treatment for atrial and ventricular fibrillation, as it restores pacemaker control of the tissue to the SA and AV nodes.
Disopyramide
Pizotifen
Lumasiran
Pilocarpine
Mitratapide
Trospium chloride
Cisapride
Ketotifen