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Updated: Mar 7, 2026

Isolation of Human Atrial Myocytes for Simultaneous Measurements of Ca2+ Transients and Membrane Currents
Published on: July 3, 2013
Calcium-mediated cellular triggered activity in atrial fibrillation
Dobromir Dobrev1,2, Xander H T Wehrens2,3
1Institute for Pharmacology, West German Heart and Vascular Centre, University Duisburg-Essen, Essen, Germany.
Atrial fibrillation (AF) mechanisms are unclear, but altered intracellular calcium handling, particularly ryanodine receptor type 2 (RyR2) dysfunction, causes triggered activity. This review explores calcium
Area of Science:
- Cardiology
- Molecular Biology
- Electrophysiology
Background:
- Atrial fibrillation (AF) is a common cardiac arrhythmia with incompletely understood mechanisms.
- Intracellular calcium (Ca2+) handling alterations are increasingly implicated in AF pathogenesis.
Purpose of the Study:
- To review the mechanisms and role of calcium-mediated cellular triggered activity in AF.
- To address current controversies regarding calcium handling in AF.
Main Methods:
- Review of studies in animal models and human atrial samples.
- Focus on ryanodine receptor type 2 (RyR2) dysfunction and sarcoplasmic reticulum (SR) Ca2+ leak.
Main Results:
- RyR2 dysfunction and spontaneous Ca2+ release from SR contribute to proarrhythmic activity in AF.
- Molecular mechanisms of RyR2 dysfunction vary with AF stage and model.
Conclusions:
- Calcium-mediated triggered activity is a significant factor in AF.
- Further research is needed to clarify the precise mechanisms and therapeutic targets related to calcium handling in AF.
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