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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. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2006-07-038166v1 109/5/1998    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Chion, C. K. N. K. Articles by Rosendaal, F. R. Search for Related Content PubMed PubMed Citation Articles by Chion, C. K. N. K. Articles by Rosendaal, F. R. Related Collections Hemostasis, Thrombosis, and Vascular Biology Clinical Trials and Observations Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  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. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: J. Thachil The role for adjunctive treatment to plasma exchange in thrombotic thrombocytopenic purpura Nephrol. Dial. Transplant., April 10, 2008; (2008) gfn173v1. [Full Text] [PDF] A. O. Spiel, J. C. Gilbert, and B. Jilma Von Willebrand Factor in Cardiovascular Disease: Focus on Acute Coronary Syndromes Circulation, March 18, 2008; 117(11): 1449 - 1459. [Abstract] [Full Text] [PDF] T. A. J. McKinnon, A. C. K. Chion, A. J. Millington, D. A. Lane, and M. A. Laffan N-linked glycosylation of VWF modulates its interaction with ADAMTS13 Blood, March 15, 2008; 111(6): 3042 - 3049. [Abstract] [Full Text] [PDF]

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