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Blood, 1 March 2007, Vol. 109, No. 5, pp. 1998-2000.
Prepublished online as a Blood First Edition Paper on October 19, 2006; DOI 10.1182/blood-2006-07-038166.
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HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
Brief Report
ADAMTS13 and von Willebrand factor and the risk of myocardial infarction in men
Chan K. N. K. Chion1,
Carine J. M. Doggen2,
James T. B. Crawley1,
David A. Lane1, and
Frits R. Rosendaal2,3
1 Department of Haematology, Imperial College London, Hammersmith Hospital Campus, London, United Kingdom;
2 Department of Clinical Epidemiology and Hemostasis, Leiden University Medical Center, Leiden, The Netherlands;
3 Thrombosis Research Center, Leiden University Medical Center, Leiden, The Netherlands
Von Willebrand factor (VWF) mediates the tethering/adhesion of platelets at sites of vascular injury. This function depends on its multimeric size, which is controlled by ADAMTS13. We measured plasma ADAMTS13 and VWF antigen levels by enzyme-linked immunosorbent assay (ELISA) in a large population-based case-control study (Study of Myocardial Infarctions Leiden [SMILE]), consisting of 560 men with a first myocardial infarction (MI) and 646 control subjects. Although ABO blood groups influenced VWF levels, they had no influence on ADAMTS13. Furthermore, there was no relationship between plasma ADAMTS13 and VWF levels. Similar to VWF, the estimated risk of MI was increased for every quartile of ADAMTS13 when compared to the lowest quartile (odds ratio, 1.5-1.6). If confirmed, the association of ADAMTS13 with MI may suggest an unexpected mechanistic action of ADAMTS13.

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