The endothelium and atrial fibrillation. The prothrombotic state revisited.
Atrial fibrillation (AF) is the commonest sustained cardiac arrhythmia, which confers a high risk of mortality and morbidity from stroke and thromboembolism. The precise mechanisms by which AF causes thromboembolism and subsequent cerebrovascular events have attracted much research interest, and are yet to be fully elucidated. Nonetheless, it is well recognised that AF fulfils Virchow's triad for thrombogenesis, with abnormal flow conditions with loss of atrial contractility and an irregularly irregular cardiac output, (i. e. flow abnormalities), as well as structural heart disease with endocardial damage (i. e. abnormal vessel wall) and abnormalities in platelet and haemostatic variables (i. e. abnormal blood constituents). This review is to summarise the evidence so far for the role of coagulation and fibrinolytic components, platelets and inflammation (that is blood constituents) in the generation of the prothrombotic state in AF, with particular focus on the endothelium and AF.
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Haemostasis, Thrombosis, and Vascular Biology Unit, University Department of Medicine, City Hospital, Birmingham, Great Britain.
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D001281:Atrial Fibrillation / Q000150:complications / Q000503:physiopathology*; D006152:Cyclic GMP / Q000097:blood; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005342:Fibrinolysis; D006487:Hemostasis / Q000502:physiology; D006801:Humans; D009569:Nitric Oxide / Q000097:blood; D020521:Stroke / Q000209:etiology / Q000401:mortality; D013923:Thromboembolism / Q000209:etiology / Q000401:mortality; D013925:Thromboplastin / Q000502:physiology; D014841:von Willebrand Factor / Q000378:metabolism
D014841:von Willebrand Factor; D009569:Nitric Oxide; D013925:Thromboplastin; D006152:Cyclic GMP