Ion channels as novel therapeutic targets in heart failure.
Electrophysiological remodeling in heart failure (HF) is characterized by major changes in ion channel function and expression that alter the electrical phenotype and predispose to the development of lethal ventricular tachyarrhythmias. In this article, we provide a review of our current understanding of HF-induced ion channel dysfunction by highlighting changes in potassium and sodium currents, pumps, and exchangers as well as calcium handling proteins. We further relate these changes in ion channel function to abnormalities in impulse generation, conduction, and repolarization with a view towards identifying potentially novel targets for anti-arrhythmic therapy for this public health epidemic.
Akar
Fadi G
FG
Division of Cardiology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA.
Tomaselli
Gordon F
GF
D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use; D001145:Arrhythmias, Cardiac / Q000150:complications / Q000188:drug therapy / Q000378:metabolism; D001693:Biological Transport, Active / Q000187:drug effects / Q000502:physiology; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism*; D006801:Humans; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism*; D017136:Ion Transport / Q000187:drug effects / Q000502:physiology; D020257:Ventricular Remodeling / Q000187:drug effects / Q000502:physiology
D000889:Anti-Arrhythmia Agents; D007473:Ion Channels