European Heart Journal Advance Access originally published online on August 7, 2006
European Heart Journal 2006 27(17):2034-2035; doi:10.1093/eurheartj/ehl019
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© The European Society of Cardiology 2006. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Inhibition of angiotensin II type 1 receptors reduces atrial stunning and spontaneous echo contrast after electrical cardioversion of atrial fibrillation
1 Division of Cardiology, University Hospital Magdeburg, Leipzigerstr. 44, 39120 Magdeburg, Germany
2 Department of Physiology, University Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands
* Corresponding author. Tel: +49 391 6713225; fax: +49 391 673202. E-mail address: andreas.goette@medizin.uni-magdeburg.de
This editorial refers to Pre-treatment with Irbesartan attenuates left atrial stunning after electrical cardioversion of atrial fibrillation
by N. Dagres et al., on page 2062
| The first 10% of the full text of this article appears below. |
Atrial fibrillation (AF) is known to be an important risk factor for thrombo-embolism.1,2 AF has been shown to induce a prolonged mechanical dysfunction of the atria, which becomes apparent after successful conversion of AF to normal sinus rhythm.14 The reduced mechanical function after termination of AF has been termed atrial stunning. Atrial stunning has been described after electrical (DC shock, overdrive pacing, catheter ablation), pharmacological, and spontaneous cardioversion of AF, which demonstrates that AF itself, rather than the mode of conversion, induces mechanical dysfunction. Pathophysiologically, the transient dysfunction of the atria appears to be due to abnormalities in cellular calcium handling and reduced calcium transient through L-type calcium channels.1,3 Furthermore, destruction of contractile proteins by calcium-dependent proteases such
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EHJ 2006 27: 2062-2068.[Abstract] [FREE Full Text]