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Hazards of Heparin Therapy

Arch Surg. 1976;111(5):614-615. doi:10.1001/archsurg.1976.01360230114031.
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To the Editor.—Ariyan and Stansel's recent observation on delayed bleeding after vascular surgery with the use of heparin sodium (Arch Surg 111:120-121, 1976) is not only of considerable practical, clinical significance, but also tends to confirm a basic theoretical concept, namely, that fibrin deposition is not a static but a dynamic process. The explanation for this concept, which also explains how heparin therapy promotes the "spontaneous" disappearance of thrombi, is simple. Thrombin clotting activity is readily inhibited by heparin; thrombin esterase activity is not.1 Thrombin esterase activates plasminogen.

It should be recalled that thrombin and plasminogen are integral components of a clot; in fact, both are firmly bound to fibrin. Treatment with heparin, leaving thrombin esterase activity unaffected, is expected to result in a fibrin-associated localized fibrinolysis in thrombi and in fibrin deposited at the site of a vascular anastomosis. However, it interferes with the thrombin clotting activity, thus


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