Calcium handling abnormalities in atrial fibrillation as a target for innovative therapeutics.
Atrial electrical and structural alterations (remodeling) have emerged as key elements in the development of the atrial fibrillation (AF) substrate. Evidence points to abnormalities in intracellular Ca (calcium) handling as crucial links in AF-initiating focal activity and in perpetuation by rapidly firing foci and reentry. This review focuses on the molecular basis of altered Ca handling in AF, with the goal of providing new insights into molecular effective antiarrhythmic therapy.
Dobrev
Dobromir
D
Department of Pharmacology and Toxicology, Dresden University of Technology, Dresden, Germany. dobrev@rcs.urz.tu-dresden.de
Nattel
Stanley
S
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D000889:Anti-Arrhythmia Agents / Q000009:adverse effects / Q000145:classification / Q000627:therapeutic use*; D001281:Atrial Fibrillation / Q000188:drug therapy* / Q000503:physiopathology / Q000517:prevention & control; D016275:Atrial Function; D002118:Calcium / Q000378:metabolism*; D020746:Calcium Channels, L-Type / Q000187:drug effects; D000075202:Contraindications; D006339:Heart Rate / Q000187:drug effects; D006801:Humans; D008955:Models, Cardiovascular; D032383:Myocytes, Cardiac / Q000187:drug effects; D010138:Pacemaker, Artificial; D019831:Sodium-Calcium Exchanger / Q000037:antagonists & inhibitors; D013748:Tetracaine / Q000627:therapeutic use
D000889:Anti-Arrhythmia Agents; D020746:Calcium Channels, L-Type; D019831:Sodium-Calcium Exchanger; C110374:sodium-calcium exchanger 1; D013748:Tetracaine; D002118:Calcium