Association between beta2-glycoprotein I plasma levels and the risk of myocardial infarction in older men
Laat de, Bas and Groot de, Philip G. and Derksen, Ronald H.W.M. and Urbanus, Rolf T. and Mertens, Koen and Rosendaal, Frits R. and Doggen, Carine J.M. (2009) Association between beta2-glycoprotein I plasma levels and the risk of myocardial infarction in older men. Blood, 114 (17). pp. 3656-3661. ISSN 0006-4971
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| Abstract: | von Willebrand factor (VWF) serves as adhesive surface for platelets to adhere to the vessel wall. We have recently found that beta2-glycoprotein I is able to inhibit platelet binding to VWF, indicating a role in the pathophysiology of arterial thrombosis. In the present study, we investigated whether differences in beta2-glycoprotein I plasma levels influence the risk of myocardial infarction. We have measured beta2-glycoprotein I and VWF antigen levels in 539 men with a first myocardial infarction and in 611 control subjects. Although we did not find a profound effect of beta2-glycoprotein I plasma levels on myocardial infarction in the overall population, we found a dose-dependent protective effect of increasing beta2-glycoprotein I plasma levels on myocardial infarction in men 60 years and older. In this age group, we found an odds ratio of 0.41 (95% confidence interval, 0.22-0.74) for high beta2-glycoprotein I levels compared with low levels. High plasma levels of beta2-glycoprotein I remained protective for myocardial infarction despite high levels of VWF. To conclude, high circulating levels of beta2-glycoprotein I appeared to be associated with a reduced risk of myocardial infarction in elderly men. In vivo experiments are needed to investigate the exact contribution of beta2-glycoprotein I on the pathophysiology of myocardial infarction |
| Item Type: | Article |
| Copyright: | © 2009 by The American Society of Hematology |
| Faculty: | Management and Governance (SMG) |
| Research Group: | |
| Link to this item: | http://purl.utwente.nl/publications/76786 |
| Official URL: | http://dx.doi.org/10.1182/blood-2009-03-212910 |
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