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Thrombosis and the hypercoagulable state

O D Ratnoff

    Circulation
    |November 1, 1984
    PubMed

    Our understanding of thrombosis remains anchored to Virchow's view that the evolution of a thrombus is fostered by vascular damage, by retarded blood flow, and by alterations in the blood itself that increases its likelihood to clot. The last of these forces, the so-called hypercoagulable state, has been defined in many ways. For example, some evidence exists that increased titers of clotting factors or increased numbers of circulating platelets may be correlated with a thrombotic tendency. A more exciting way that clotting factors might contribute to thrombosis is that under certain conditions the titer of their activated forms might reach critical levels in the circulation. Another possibility is that a thrombotic tendency may be caused by qualitative alterations in clotting factors or platelets. The firmest evidence that alterations in blood clotting may be related to thrombosis is the undoubted high incidence of recurrent thromboembolism in patients with familial deficiencies of antithrombin III or protein C, an inhibitor of antihemophilic factor (factor VIII) and proaccelerin (factor V). Impaired fibrinolytic mechanisms may also predispose to thrombosis. Not yet explained is the fact that patients with lifelong hemostatic alterations in peripheral blood sustain only a handful of thrombotic episodes.

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