title: Late sodium current: A mechanism for angina, heart failure, and arrhythmia.
abstract: The peak sodium current underlies excitability and conduction in heart muscle, but a late sodium current flowing after the peak contributes to maintaining and prolonging the action potential plateau, and also to intracellular sodium loading, which in turn increases intracellular calcium with consequent effects on arrhythmia and diastolic function. Late sodium current is pathologically increased in both genetic and acquired heart disease, making it an attractive target for therapy to treat arrhythmia, heart failure, and angina. This review provides an overview of the underlying bases for the clinical implications of late sodium current block.
authors.affiliation: Division of Cardiovascular Medicine, Department of Medicine, University of Wisconsin-Madison, Madison, WI. Electronic address: jcm@medicine.wisc.edu.
authors.forename: Jonathan C
authors.initials: JC
authors.lastname: Makielski
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000787:Angina Pectoris / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D001145:Arrhythmias, Cardiac / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D002317:Cardiovascular Agents / Q000494:pharmacology; D022062:Electrophysiologic Techniques, Cardiac / Q000379:methods; D006333:Heart Failure / Q000188:drug therapy / Q000378:metabolism / Q000503:physiopathology; D006801:Humans; D015222:Sodium Channels / Q000494:pharmacology / Q000502:physiology
chemical_list: D002317:Cardiovascular Agents; D015222:Sodium Channels
keywords: Antiarrhythmic drugs; Long-QT syndrome; Sodium current