Key result
A review of heart failure-induced ion channel dysfunction highlights changes in currents and proteins as potentially novel targets for anti-arrhythmic therapy.
This review highlights the role of ion channel dysfunction in heart failure-induced electrophysiological remodeling and identifies potential novel targets for anti-arrhythmic therapy.
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.
No takes yet. Share an insight, caveat, or question.
Akar et al. (2005) conducted a review in Heart failure. Ion channel targets was evaluated. A review of heart failure-induced ion channel dysfunction highlights changes in currents and proteins as potentially novel targets for anti-arrhythmic therapy.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: