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Blood, 1 March 2004, Vol. 103, No. 5, pp. 1728-1734. Prepublished online as a Blood First Edition Paper on November 13, 2003; DOI 10.1182/blood-2003-08-2886. This Article Full Text (PDF) All Versions of this Article: 2003-08-2886v1 103/5/1728    most recent Alert me when this article is cited Alert me if a correction is posted 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 Kerlin, B. A Articles by Weiler, H. Search for Related Content PubMed PubMed Citation Articles by Kerlin, B. A Articles by Weiler, H. Related Collections Related Article in Blood Online Social Bookmarking                   What's this? Submitted August 27, 2003 Accepted October 21, 2003 Cause-effect relation between hyperfibrinogenemia and vascular disease Bryce A Kerlin, Brian C Cooley, Berend H Isermann, Irene Hernandez, Rashmi Sood, Mark Zogg, Sara B Hendrickson, Michael W Mosesson, Susan T Lord, and Hartmut Weiler* Blood Research Institute, Blood Center of SE Wisconsin, Milwaukee, WI, USA; Medical College of Wisconsin, Milwaukee, WI, USA University of North Carolina at Chapel Hill, Chapel Hill, NC, USA * Corresponding author; email: hweiler{at}bcsew.edu. Elevated plasma levels of fibrinogen are associated with the presence of cardiovascular disease, but it is controversial whether elevated fibrinogen causally imparts an increased risk, and as such is a true modifier of cardiovascular disease, or is merely associated with disease. By investigating a transgenic mouse model of hyperfibrinogemia, we show that elevated plasma fibrinogen concentration (1) elicits augmented fibrin deposition in specific organs, (2) interacts with an independent modifier of hemostatic activity to regulate fibrin turnover/deposition, (3) exacerbates neointimal hyperplasia in an experimental model of stasis-induced vascular remodeling, yet (4) may suppress thrombin generation in response to a procoagulant challenge. These findings provide direct experimental evidence that hyperfibrinogenemia is more than a by-product of cardiovascular disease, and may function independently or interactively to modulate the severity and/or progression of vascular disease. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Hyperfibrinogenemia and vascular disease: does it matter? William P. Fay Blood 2004 103: 1569-1570. [Full Text] [PDF] This article has been cited by other articles: S. 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