Hypercoagulability

Excerpt

Hypercoagulability or thrombophilia is the increased tendency of blood to thrombose. A normal and healthy response to bleeding for maintaining hemostasis involves the formation of a stable clot, and the process is called coagulation. Hypercoagulability describes the pathologic state of exaggerated coagulation or coagulation in the absence of bleeding. Different constituents of the blood interact to create a thrombus. Arterial thrombosis, such as in myocardial infarction and stroke, is different from venous thromboses, such as deep venous thrombosis (DVT) and pulmonary embolism (PE). Pathophysiology and treatment differ for arterial and venous thrombosis, but risk factors overlap. Thromboembolism describes the migration of a local thrombus to distant areas leading to luminal obstruction. Different hypercoagulable states and thrombophilic diseases cause hypercoagulability. As early as 1906 Wasserman et al., described the antiphospholipid syndrome. In 1965 Egeberg et al., discovered antithrombin III deficiency. During the 1980s protein C (Griffin, 1981) and protein S (Comp, 1984) deficiencies were introduced. Dahlbäck discovered activated protein C resistance in 1993, which is commonly caused by the factor V Leiden mutation.