The goal of anticoagulant therapy is to prevent thrombosis, but to preserve hemostasis. We would like to give the highest intensity of therapy possible without undue risk of hemorrhage. Therefore, if we could establish criteria for the critical level of hypoagulability below which hemorrhagic tendency will be too high to be accepted, this would give us a sound basis for evaluating different methods and for selecting techniques which are sensitive in signaling the crossing of the critical border into the area of high hemorrhagic risk.
Hemostasis proceeds through 3 main stages (Fig. 1). The initial reaction of platelet adhesion and reversible aggregation is independent of coagulation.
The second reaction, however, of irreversible aggregation and viscous metamorphosis, which produces impermeability of the platelet plug and arrest of bleeding, requires thrombin. We have found that thrombin for this process is provided by clotting factors which are adsorbed on the platelet surface and