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(Circulation. 2008;117:1449-1459.)
© 2008 American Heart Association, Inc.

Basic Science for Clinicians

Von Willebrand Factor in Cardiovascular Disease

Focus on Acute Coronary Syndromes

Alexander O. Spiel, MD; James C. Gilbert, MD; Bernd Jilma, MD

From the Department of Clinical Pharmacology, Medical University of Vienna, Vienna, Austria (A.O.S., B.J.), and Archemix Corp, Cambridge, Mass (J.C.G.).

Correspondence to Bernd Jilma, MD, Department of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel 18-20, 1090 Vienna, Austria. E-mail Bernd.Jilma{at}meduniwien.ac.at

von Willebrand factor (VWF) plays a pivotal role in platelet adhesion and aggregation at sites of high shear rates (eg, in coronary arteries that have stenotic or ruptured atherosclerotic plaque lesions). Numerous studies have investigated the relationship between VWF plasma levels and thromboembolic cardiovascular events. In contrast to the rather weak association in the general population, in patients with preexisting vascular disease, VWF is significantly predictive for adverse cardiac events, including death. Likewise, VWF typically rises during the course of acute coronary syndrome, and the extent of this VWF release is an independent predictor of adverse clinical outcome in these patients. Various lines of evidence indicate that VWF is not only a marker but also actually an important effector in the pathogenesis of myocardial infarction. This central role of VWF in thrombogenesis has made it a promising target for research into new antiplatelet therapies that specifically inhibit VWF. This review focuses on the role of VWF in acute coronary syndrome and further outlines the relevance of therapeutic interventions targeting VWF for acute coronary syndrome patients.

Key Words: coronary disease • myocardial infarction • platelets • thrombosis • von Willebrand factor

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