Calcium-mediated cellular triggered activity in atrial fibrillation.
Although atrial fibrillation (AF) is the most commonly encountered cardiac arrhythmia, the basic mechanisms underlying this disorder remain incompletely understood. During the past decade or so, it has become clear that alterations in intracellular Ca2+handling may play a role in the pathogenesis of AF. Studies in small and large animal models, as well as atrial samples from patients with different forms of AF, have implicated ryanodine receptor type 2 (RyR2) dysfunction and enhanced spontaneous Ca2+release events from the sarcoplasmic reticulum (SR) as a potential cause of proarrhythmic cellular ectopic (triggered) activity in AF. The molecular mechanisms leading to RyR2 dysfunction and SR Ca2+leak depend on the clinical stage of AF or specific animal model studied. This review focuses on the mechanisms and role of calcium-mediated cellular triggered activity in AF, and addresses some of the current controversies in the field.
Institute for Pharmacology, West German Heart and Vascular Centre, University Duisburg-Essen, Essen, Germany.|Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX, USA.
Dobromir
D
Dobrev
Cardiovascular Research Institute, Baylor College of Medicine, Houston, TX, USA.|Departments of Molecular Physiology & Biophysics, Pediatrics (Cardiology), Medicine (Cardiology), Baylor College of Medicine, Houston, TX, USA.
Xander H T
0000-0001-5044-672X
XHT
Wehrens
D000818:Animals; D001281:Atrial Fibrillation / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D006325:Heart Atria / Q000378:metabolism; D006801:Humans; D032383:Myocytes, Cardiac / Q000378:metabolism; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium
arrhythmia; atrial fibrillation; calcium; ryanodine receptor; triggered activity