Survival and turnover measurements of platelets, fibrinogen and plasminogen have been studied in eight patients with arterial and twelve patients with venous thromboembolism, and six patients with advanced, stable atherosclerotic peripheral vascular disease. Venous thrombosis is characterized by combined and equivalent consumption of platelets, fibrinogen and plasminogen. This process, the result of activation of the coagulation system, is completely reversed by heparin or warfarin anticoagulation but remains unaltered by dipyridamole. The removal of circulating plasminogen is directly reflected as fibrinogen-fibrin related antigen in the blood and is regulated by the rate of fibrin formation as evidenced by the reversal of fibrinogen and plasminogen consumption to normal following heparin therapy. In contrast, arterial thromboembolism involves selective platelet consumption presumably in the formation of platelet thrombus on non-endothelialized end-arterial surfaces. This process is interrupted by dipyridamole inhibition of platelet function but not by heparin anticoagulation. Although acetylsalicylic acid itself has little capacity to correct platelet consumption, it has a potentiating effect on dipyridamole. Stable, severe, widespread arteriosclerotic disease only minimally increases platelet consumption and produces no change in fibrinogen and plasminogen kinetics from normal. The minimal decrease in platelet survival in these patients is not corrected by dipyridamole therapy. The results of these studies demonstrate the potential usefulness of platelet and fibrinogen kinetic measurements in the differentiation of ongoing venous and arterial thromboembolism and in identifying potentially effective antithrombotic therapy. * Presented at the International Conference on “Platelets in Thrombosis: Their Clinical Significance and the Evaluation of Potential Drugs” in Titisee, Germany, October, 1973.