European Heart Journal Advance Access published online on August 22, 2007
European Heart Journal, doi:10.1093/eurheartj/ehm170
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© The European Society of Cardiology 2007. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
D-dimers in atrial fibrillation: a further step in risk stratification of thrombo-embolism?
1 Department of Cardiology, Saint-Antoine University and Medical School, Assistance Publique-Hôpitaux de Paris, 184, rue du faubourg St-Antoine, 75571 Paris Cedex 12, France
2 Université Pierre et Marie Curie, Paris, France
* Corresponding author. Tel: +33 1 49 28 28 86; fax: + 33 1 49 28 28 84. E-mail address: ariel.cohen@sat.aphp.fr
This editorial refers to Prediction of left atrial appendage thrombi in nonvalvular atrial fibrillation by S. Habara et al., doi:10.1093/eurheartj/ehm356
| The first 10% of the full text of this article appears below. |
Plasma fibrin D-dimers (hereafter D-dimers) are generated when the endogenous fibrinolytic system degrades fibrin, as in venous thrombo-embolism (VTE) and they consist of two identical subunits derived from two fibrin molecules. Unlike fibrinogen degradation products, which are derived from fibrinogen and fibrin, D-dimers are a specific cross-linked fibrin derivative.1 Because 2–3% of plasma fibrinogen is degraded to fibrin, small amounts are detectable in the plasma of healthy individuals.1 D-dimer levels may be increased in any condition involving the formation and degradation of fibrin, such as VTE, pulmonary embolism, infections, cancer, surgery, cardiac or renal failure, acute coronary syndromes, acute non-lacunar stroke, pregnancy, and sickle cell crises. D-dimer levels increase
D-dimers in atrial fibrillation
Markers of thrombo-embolism in atrial fibrillation
D-dimers and transeosophageal echocardiography-detected risk markers in atrial fibrillation