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European Heart Journal Advance Access originally published online on June 7, 2006
European Heart Journal 2006 27(14):1640-1641; doi:10.1093/eurheartj/ehl076
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Do genetics help to better understand the underlying mechanisms of atrial fibrillation?

Dobromir Dobrev* and Ursula Ravens

Department of Pharmacology and Toxicology, Dresden University of Technology, Fetscherstr. 74, 01307 Dresden, Germany

* Corresponding author. Tel: +49 351 4586279; fax: +49 351 4586315. E-mail address: dobrev@rcs.urz.tu-dresden.de

This editorial refers to ‘Analysis of minK and eNOS genes as candidate loci for predisposition to non-valvular atrial fibrillation’{dagger} by C. Fatini et al., on page 1712

The first 10% of the full text of this article appears below.

Atrial fibrillation (AF) commonly occurs in the context of structural heart disease and is accompanied by atrial remodelling. The latter refers to any change in atrial function that promotes AF or occurs as a consequence of the arrhythmia.1 Atrial remodelling in the aged heart and during heart failure is characterized by pronounced fibrosis leading to heterogeneous slowing conduction of and prolongation of effective refractory period (ERP). In contrast, atrial remodelling induced by tachycardia is associated with shorter ERP and impaired rate adaptation. Nevertheless, atrial remodelling cannot be . . . [Full Text of this Article]


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Related articles in EHJ:

Analysis of minK and eNOS genes as candidate loci for predisposition to non-valvular atrial fibrillation
Cinzia Fatini, Elena Sticchi, Maurizio Genuardi, Francesco Sofi, Francesca Gensini, Anna Maria Gori, Meri Lenti, Antonio Michelucci, Rosanna Abbate, and Gian Franco Gensini
EHJ 2006 27: 1712-1718. [Abstract] [FREE Full Text]