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