Abstract
Unlike the brief action potentials (APs) in skeletal myocytes or neurons, the human cardiac AP takes 100s of milliseconds to repolarize the cell. This slow repolarization is essential for proper excitation–contraction coupling in cardiac muscle, and precise control of AP duration contributes to electrical stability. Under various pathological conditions, often when the AP duration is prolonged, repolarization can transiently fail with a sudden transient depolarization of membrane potential (Fig. 1). If such an early afterdepolarization (EAD) reaches threshold, it can trigger a premature AP and thereby initiate potentially fatal ventricular arrhythmias such as torsades de pointes (TdP) and ventricular fibrillation (Cranefield and Aronson, 1991). Thus, understanding the causes of EADs and how one might block them is of significant clinical importance.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
