Afterdepolarization is commonly a consequence of myocardial infarction, cardiac hypertrophy, or heart failure.
Early afterdepolarizations can result in torsades de pointes, tachycardia, and other arrhythmias.
[3] EADs can be triggered by hypokalemia and drugs that prolong the QT interval, including class Ia and III antiarrhythmic agents, as well as catecholamines.
There, they typically follow an action potential and are mediated by voltage gated sodium or chloride channels.
Purkinje fibers which survive myocardial infarction remain partially depolarized due to its high concentration of cations.