Abstract
During the last decades Ca2+ has been found to play a crucial role in cardiac arrhythmias associated with heart failure and a number of congenital arrhythmia syndromes. Recent studies demonstrated that altered atrial Ca2+ cycling may promote the initiation and maintenance of atrial fibrillation, the most common clinical arrhythmia that contributes significantly to population morbidity and mortality. This article describes physiological Ca2+ cycling mechanisms in atrial cardiomyocytes and relates them to fundamental cellular proarrhythmic mechanisms involving Ca2+ signaling abnormalities in the atrium during atrial fibrillation.
Keywords
- Calcium
- Atrial arrhythmias
- Remodeling
- Ion channels
- Reentry
- Triggered activity
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Acknowledgements
The author’s research is supported by the Deutsche Forschungsgemeinschaft (Do769/1-1-3, to DD), the German Federal Ministry of Education and Research (BMBF; Atrial Fibrillation Competence Network [01Gi0204] and German Center of Cardiovascular Research, both to DD), the European Union through the European Network for Translational Research in Atrial Fibrillation, (EUTRAF, FP7-HEALTH-2010, large-scale integrating project, Proposal No. 261057 to DD), the Canadian Institutes of Health Research (MOP44365, to SN) and the European-North American Atrial Fibrillation Research Alliance (ENAFRA) grant of Fondation Leducq (07CVD03, to DD and SN).
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Voigt, N., Nattel, S., Dobrev, D. (2012). Proarrhythmic Atrial Calcium Cycling in the Diseased Heart. In: Islam, M. (eds) Calcium Signaling. Advances in Experimental Medicine and Biology, vol 740. Springer, Dordrecht. https://doi.org/10.1007/978-94-007-2888-2_53
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