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Hypercoagulability in Venous and Arterial Thrombosis

Duncan P. Thomas, MD; and Harold R. Roberts, MD
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From University of North Carolina School of Medicine, Chapel Hill, North Carolina. Grant Support: In part by National Heart, Lung, and Blood Institute grant HL 26309 (Dr. Roberts). Requests for Reprints: Harold R. Roberts, MD, Division of Hematology/Oncology, Department of Medicine, CB 7035, 932 Faculty Office Building, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035. Current Author Addresses: Drs. Thomas and Roberts: Division of Hematology/Oncology, Department of Medicine, CB 7035, 932 Faculty Office Building, University of North Carolina at Chapel Hill, Chapel Hill, NC 27599-7035.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1997;126(8):638-644. doi:10.7326/0003-4819-126-8-199704150-00009
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The term “hypercoagulability” is used to describe patients who are at increased risk for thrombosis because of inherited defects in their anticoagulant pathways or because of various predisposing causes. About one in five patients of European descent who present with venous thromboembolism have a specific genetic defect in their anticoagulant pathway. In these patients, anticoagulant prophylaxis is indicated at times of high risk, such as after surgery. Prolonged anticoagulant therapy may be required in patients with recurrent or life-threatening thromboemboli, but decisions about this are best made on an individual basis. Patients who present with arterial thrombosis usually develop their disease as a complication of atherosclerosis. However, these patients also have a form of hypercoagulability, manifested primarily by high fibrinogen levels and elevated factor VII activity. Evidence increasingly indicates that these and other hemostatic markers may help in the assessment of patients at risk for coronary heart disease.





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