Atrial action potential prolongation (AAPP)

Atrial action potential prolongation is a physiological phenomenon characterized by an increase in the duration of the repolarization phase in atrial cardiac myocytes. This effect is a key therapeutic objective in the treatment of supraventricular tachyarrhythmias, such as atrial fibrillation and atrial flutter, because it extends the effective refractory period (ERP) of the tissue (Source: StatPearls, Antiarrhythmic Class III Drugs, 2023). By lengthening the time during which the heart cells cannot be re-excited, this process helps to terminate re-entrant circuits and prevent the rapid, disorganized electrical activity typical of these conditions. While not a single molecular entity, this prolongation is typically achieved through the pharmacological inhibition of various potassium ion channels, including the rapid delayed rectifier (IKr) and the atrium-specific ultra-rapid delayed rectifier (IKur) (Source: Journal of Cardiovascular Pharmacology, Atrial-selective drugs for treatment of atrial fibrillation, 2015). However, a major challenge in inducing this effect is the risk of non-selective prolongation in the ventricles, which can lead to life-threatening arrhythmias like Torsades de Pointes (Source: Circulation, Atrial-Selective Sodium Channel Block as a Strategy for Suppressing Atrial Fibrillation, 2011).

Other names

Atrial APD prolongationProlongation of atrial refractory periodClass III antiarrhythmic effectAtrial repolarization delay

Inhibition of repolarizing potassium currents (such as the rapid delayed rectifier IKr, the slow delayed rectifier IKs, or the ultra-rapid delayed rectifier IKur) to extend the duration of the action potential and the effective refractory period in atrial myocytes.