Atherothrombotic Disorders

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Abstract
Received February 6, 2004; revision received October 8, 2004; accepted November 23, 2004. How should we address the increasingly prevalent condition of arterial thrombophilia? Can arterial thromboses complicate hematological diseases or the use of antithrombotic drugs? What is POC testing? Is vascular regeneration a potential shield against atherothrombotic states? This report draws insights and perspective from the discipline of hematology to answer these and other clinically relevant questions. The term thrombophilia can be applied to both inherited and acquired disorders that predispose to thrombosis; the 2 forms, inherited and acquired, may coexist within the same individual. Although best characterized in the context of venous thromboembolism, the contribution of thrombophilias to arterial thrombosis is an area of intense investigation (Table). View this table: Conditions That Predispose to Thromboembolism The predisposition to venous thromboembolism among subjects with factor V Leiden (a congenital factor V resistance to cleavage by activated protein C) or with the gain-of-function G20210A variant in the prothrombin gene1,2 suggests that a fully functional system of vascular and blood-borne thromboresistance is important for venous patency. Arterial thrombosis is considered less likely to be influenced by small congenital changes in the function of hemostatic factors because it usually occurs under high shear, at sites of endothelial dysfunction/disruption or deep vessel wall injury, on a template of tissue factor–bearing cells and platelet aggregates.3 Notable exceptions, however, may concern individuals who develop arterial thromboses at a young age,4–11 are female,9,11 have no obvious predisposing illnesses or cardiovascular risk factors (hypertension, diabetes, smoking, hypercholesterolemia) other than a family history of thrombosis,12,13 or have no flow-limiting artery lesions at angiography.6,12,14 In these groups, an increasing number of reports points to a significantly higher prevalence of thrombophilic gene polymorphisms compared with controls (Table),4–14 suggesting a biologically plausible link with arterial thrombosis. …