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Cardiovascular Research Advance Access [Accepted Manuscript] published online on June 17, 2009
Cardiovascular Research, doi:10.1093/cvr/cvp203
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2009. For permissions please email: journals.permissions@oxfordjournals.org.

The Role of Connexin 40 in Atrial Fibrillation

Sevasti-Maria Chaldoupi1, Peter Loh1, Richard N.W. Hauer1, Jacques M.T. de Bakker1,2,3 and Harold V.M. van Rijen1

1 Division Heart and Lungs, University Medical Center Utrecht, The Netherlands
2 Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
3 Heart Failure Center, Academic Medical Center University of Amsterdam, The Netherlands

Correspondence: H.V.M. van Rijen, Division Heart & Lungs. University Medical Center Utrecht, The Netherlands. Address: Alexander Numan Building, Yalelaan 50, 3584 CM, Utrecht, The Netherlands. Tel: 0031-30253908. E-mail: h.v.m.vanrijen{at}umcutrecht.nl

Connexin40 (Cx40) is the major gap junction protein in the atrial myocardium. In the heart, gap junctions are responsible for cell-to-cell conduction of the action potential. In several cardiac diseases, the expression of connexins is changed and is associated with increased propensity for arrhythmias. Atrial fibrillation (AF) is the most common arrhythmia in man with a diverse clinical presentation, different underlying mechanisms and difficult treatment. The vulnerability to arrhythmias of the heart is determined by the combined presence of an arrhythmogenic substrate and initiating triggers. The arrhythmogenic substrate is formed by reduced effective refractory period, enhanced spatial dispersion of refractoriness or abnormal atrial impulse conduction. Initiating triggers for AF most frequently originate from firing foci in the pulmonary veins and/or superior caval vein. Prolonged episodes of AF result in electrical and structural remodeling that favors the reoccurrence or perpetuation of AF. This electrical remodeling embodies changes in Cx40 expression and distribution, both in the atrial myocardium itself and in the thoracic veins. In addition, Cx40 gene mutations or polymorphisms give an inherited predisposition to AF. This review focuses on the role of Cx40 in atrial fibrillation, showing that abnormal Cx40 expression is correlated with both trigger formation from the thoracic veins as well as enhanced vulnerability of the atrial myocardium to AF.

Time for primary review: 21 Days


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