Coagulation abnormalities and cardiovascular disease

    Research output: Contribution to journalArticle

    16 Citations (Scopus)

    Abstract

    In patients with excessive venous thrombosis, genetic defects predisposing to thrombosis can be found in 60-80%. Increased plasma levels of coagulation proteins such as fibrinogen and plasminogen activator inhibitor-1 (PAI-1) are associated with an increased risk of myocardial infarction. However, despite the presence of polymorphisms that regulate plasma levels of factor VIII, PAI-1, and fibrinogen the association between common polymorphisms of these coagulation protein and ischemic cardiac disease remains ambiguous. Up to 10% of the population have defects that predispose them to excessive venous thrombosis. In spite of the essential role of thrombosis in coronary ischemic syndrome, no convincing evidence has implicated the two most common venous hypercoagulable states in ischemic heart disease. Pathogenic polymorphisms in the platelet fibrinogen and collagen receptors remain an area of intense research interest. Finally, it has been shown that lipoproteins can act as mediators of coagulation processes.

    Original languageEnglish (US)
    Pages (from-to)443-448
    Number of pages6
    JournalCurrent Opinion in Lipidology
    Volume10
    Issue number5
    DOIs
    StatePublished - 1999

    Fingerprint

    Plasminogen Activator Inhibitor 1
    Coagulation
    Polymorphism
    Venous Thrombosis
    Fibrinogen
    Cardiovascular Diseases
    Fibrinogen Receptors
    Collagen Receptors
    Coronary Thrombosis
    Factor VIII
    Lipoproteins
    Myocardial Ischemia
    Plasmas
    Heart Diseases
    Defects
    Proteins
    Thrombosis
    Blood Platelets
    Myocardial Infarction
    Platelets

    ASJC Scopus subject areas

    • Biochemistry, Genetics and Molecular Biology(all)

    Cite this

    Coagulation abnormalities and cardiovascular disease. / Deloughery, Thomas.

    In: Current Opinion in Lipidology, Vol. 10, No. 5, 1999, p. 443-448.

    Research output: Contribution to journalArticle

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