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Calcium‐mediated cellular triggered activity in atrial fibrillation
Author(s) -
Dobrev Dobromir,
Wehrens Xander H. T.
Publication year - 2017
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jp273048
Subject(s) - ryanodine receptor 2 , ryanodine receptor , atrial fibrillation , calcium , endoplasmic reticulum , medicine , calcium in biology , cardiac arrhythmia , calcium signaling , pathogenesis , intracellular , cardiology , biology , microbiology and biotechnology
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 Ca 2+ 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 Ca 2+ 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 Ca 2+ 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.