Class III Antiarrhythmic Drugs

These antiarrhythmic drugsAntiarrhythmic drugs (AADs) prolong the cardiac action potential durationAction potential duration (APD) and refractoriness at concentrations at which intracardiac conductionConduction velocity is not significantly affected. This effect is the result of the blockade of several outward-repolarizing K+ currents and less frequently, to the activation the late inward Na+ current during the plateau phase of the action potential. This prolongation of APD and refractoriness, combined with the maintenance of normal conduction velocity, leads to an increase in the wavelength of the cardiac impulse, close the excitable gap in the re-entrant circuit and may suppress re-entrant arrhythmias. However, some of these drugs exhibit reverse-use dependence (i.e, their ability to prolong APD and refractoriness diminishes at fast cardiac frequencies, while increases at slower heart rates) and they have the potential to prolong the QT interval of the electrocardiogram and induce a polymorphic ventricular tachycardia termed torsades de pointes. In this chapter, we analyse the electrophysiological and pharmacological characteristics as well as the clinical uses of amiodarone, dofetilide, dronedarone, ibutilide and sotalol.