Afterdepolarizations and triggered activity

Abstract

One of the possible cellular mechanisms for certain types of ventricular arrhythmias is afterdepolarizations. There are two types of afterdepolarization. The delayed afterdepolarization (DAD) arises from the resting potential after full repolarization of an action potential and it may reach threshold for activation. It is favored by cellular Ca overload, and rapid preceding activation rates. The inward current generating the DAD is caused by one of two mechanisms: a Ca-dependent opening of non-specific cation channels, or Ca activation of a rheogenic Na/Ca exchange. The early afterdepolarization (EAD) arises on the shoulder of a preceding action potential plateau and it is favored by slow preceding activation rate and prolonged action potentials. Ca channels are usually responsible for the inward current for EAD's, and cellular Ca overload is not related. These afterdepolarizations have characteristics that suggest their etiological role in certain arrhythmias found in heart failure.