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Cardiovascular Research Advance Access originally published online on June 17, 2009
Cardiovascular Research 2009 84(1):15-23; 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 connexin40 in atrial fibrillation

Sevasti-Maria Chaldoupi1, Peter Loh1, Richard N.W. Hauer1, Jacques M.T. de Bakker1,2,3 and Harold V.M. van Rijen4,*

1 Department of Cardiology, 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
4 Department of Medical Physiology, Division Heart and Lungs, University Medical Center Utrecht, Alexander Numan Building, Yalelaan 50, 3584 CM Utrecht, The Netherlands

* Corresponding author. Tel: +31 30 253900; fax: +31 30 2539036. E-mail address: h.v.m.vanrijen{at}umcutrecht.nl

Connexin40 (Cx40) is a 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 of 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 remodelling that favours the reoccurrence or perpetuation of AF. This electrical remodelling 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 AF, 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.

KEYWORDS Connexins; Atrial fibrillation

Time for primary review: 21 days


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