Abstract
Atrial fibrillation (AF) is the most common cause of thromboembolic stroke. Several studies have shown an activation of the plasmatic and cellular clotting system in patients with AF.1,2 Interestingly, these changes occur within hours after initiation of AF. In order to predict the individual risk for AF-related thromboembolic events, the CHADS2-score has been developed.1 It takes into account that especially elderly patients, patients with diabetes, hypertension, heart failure, and/or previous stroke are at greatest risk. Depending on the CHADS2-score, the yearly risk of stroke may vary between 1.9% (CHADS2-score of 0) and 18.2% (CHADS2-score of 6). The pathophysiological basis of how these clinical risk factors affect cardiac thrombogenesis or predict future thromboembolic events is complex. According to the Virchow triad there are three determinants of thrombus formation: circulatory stasis, hypercoagulable state, and endothelial injury at the site of thrombus initiation. Clinical co-morbidities such as diabetes, hypertension, or heart failure influence all three factors of Virchow's triad. Increased expression of adhesion molecules at the atrial endocardium promotes the adhesion of leukocytes, leading to the formation of granulocyte–platelet conjugates at the endocardium.3 This process appears to be intensified in heart failure. Diabetes and hypertension further increase inflammatory responses. Thus, small granulocyte–platelet conjugates or larger thrombi may develop in fibrillating atria, causing silent cerebral ischaemia or manifest stroke.2,4,5 In addition to thromboembolic events, cerebral hypoperfusion induced by cardiac beat-to-beat variability is considered as an alternative pathophysiological mechanism for silent cerebral ischaemia during AF.6 Thus, it appears very reasonable to believe that AF may cause … *Corresponding author. Tel: +49 391 6713225, Fax: +49 391 6713202, Email: andreas.goette{at}medizin.uni-magdeburg.de
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