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Genetic Markers of Hemostatic Factors

  • Chapter
Cardiovascular Genetics for Clinicians

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 239))

  • 61 Accesses

Abstract

Thrombosis underlies most acute manifestations of coronary atherosclerotic disease, including myocardial infarction (MI) [1]. In this setting, the rupture of an atherosclerotic plaque, endothelial cell damage, or both, are the key events that trigger the thrombotic process. Plaque disruption is followed by the exposure of blood flow to tissue factor (TF), a glycoprotein elaborated by several cells infiltrating the plaque, which is accumulated especially in the lipid-rich core [2]. TF forms a high-affinity complex with coagulation factor VII [3], which initiates a cascade of enzymatic reactions resulting in the local generation of thrombin and deposition of fibrin. The evolution to occ1usive thrombus or resolving lesion is depending on a delicate equilibrium between thrombosis and endogenous thrombolysis. As part of the response to any type of endothelial wall disruption, platelet adhesion occurs through the binding of the glycoprotein (Gp) Ib/IX/V platelet receptor to von Willebrand Factor (vWF) and/or direct binding of platelets by means of their collagen receptor (Gp Ia/IIa complex). These reactions determine a conformational change in the platelet Gp IIb/IIIa integrin, from a ligand-unreceptive state to a ligand-receptive state. Ligand-receptive Gp IIb/IIIa receptors bind fibrinogen molecules, which form bridges between adjacent platelets, facilitating platelet aggregation and propagation of thrombus [4,5].

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Authors
  1. D. Girelli
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  2. O. Olivieri
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  3. R. Corrocher
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Editors and Affiliations

  1. Academic Hospital Maastricht, Maastricht, The Netherlands

    P. A. Doevendans

  2. Academic Medical Center, Amsterdam, The Netherlands

    A. A. M. Wilde

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Girelli, D., Olivieri, O., Corrocher, R. (2001). Genetic Markers of Hemostatic Factors. In: Doevendans, P.A., Wilde, A.A.M. (eds) Cardiovascular Genetics for Clinicians. Developments in Cardiovascular Medicine, vol 239. Springer, Dordrecht. https://doi.org/10.1007/978-94-010-1019-1_7

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