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Blood, 26 February 2009, Vol. 113, No. 9, pp. 2070-2078. Prepublished online as a Blood First Edition Paper on October 17, 2008; DOI 10.1182/blood-2008-07-167411. This Article Full Text Full Text (PDF) All Versions of this Article: blood-2008-07-167411v1 113/9/2070    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 Undas, A. Articles by Mann, K. G. Search for Related Content PubMed PubMed Citation Articles by Undas, A. Articles by Mann, K. G. Related Collections Thrombosis and Hemostasis Related Article in Blood Online Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  THROMBOSIS AND HEMOSTASIS Systemic blood coagulation activation in acute coronary syndromes Anetta Undas1, Konstanty Szudrzyski2, Kathleen E. Brummel-Ziedins3, Wiesawa Tracz1, Krzysztof Zmudka1, and Kenneth G. Mann3 1 Institute of Cardiology and 2 Department of Medicine, Jagiellonian University School of Medicine, Krakow, Poland; and 3 Department of Biochemistry, University of Vermont, Burlington We evaluated systemic alterations to the blood coagulation system that occur during a coronary thrombotic event. Peripheral blood coagulation in patients with acute coronary thrombosis was compared with that in people with stable coronary artery disease (CAD). Blood coagulation and platelet activation at the microvascular injury site were assessed using immunochemistry in 28 non-anticoagulated patients with acute myocardial infarction (AMI) versus 28 stable CAD patients matched for age, sex, risk factors, and medications. AMI was associated with increased maximum rates of thrombin-antithrombin complex generation (by 93.8%; P < .001), thrombin B-chain formation (by 57.1%; P < .001), prothrombin consumption (by 27.9%; P = .012), fibrinogen consumption (by 27.0%; P = .02), factor (f) Va light chain generation (by 44.2%; P = .003), and accelerated fVa inactivation (by 76.1%; P < .001), and with enhanced release of platelet-derived soluble CD40 ligand (by 44.4%; P < .001). FVa heavy chain availability was similar in both groups because of enhanced formation and activated protein C (APC)–mediated destruction. The velocity of coagulant reactions in AMI patients showed positive correlations with interleukin-6. Heparin treatment led to dampening of coagulant reactions with profiles similar to those for stable CAD. AMI-induced systemic activation of blood coagulation markedly modifies the pattern of coagulant reactions at the site of injury in peripheral vessels compared with that in stable CAD patients. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? Related Article in Blood Online: Supercharged blood coagulation Sriram Krishnaswamy Blood 2009 113: 1873-1874. [Full Text] [PDF] This article has been cited by other articles: S. Krishnaswamy Supercharged blood coagulation Blood, February 26, 2009; 113(9): 1873 - 1874. [Full Text] [PDF]

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