The pathogenesis of arterial thrombosis has been conceptualized as an amplified or misdirected form of the normal hemostatic process which controls spontaneous or traumatic hemorrhage. During these events, platelets adhere to subendothelium which has been traumatically exposed in the injured vessels. Adhesion leads to platelet activation, followed by recruitment and aggregation of additional platelets. These events culminate in thrombin formation, accompanied by fibrin deposition in the interstices of the accumulated platelets. In addition, a fibrin cap develops at the periphery of the clot. This concept of thrombosis as an exaggerated form of hemostasis originated from experiments wherein the response of healthy blood vessels to injury was studied. The concept also constitutes the basis for development of current therapeutic modalities directed toward blockade and inhibition of further platelet accumulation. In sharp contrast to the hemostatic process in traumatized healthy blood vessels, thrombotic events usually occur at anatomic sites of pathological vascular damage, ie fissured or ruptured atherosclerotic plaques containing lipid-rich or necrotic cell debris which have formed a nidus for an inflammatory response consisting of monocytes/macrophages (1-3). Stenotic atherosclerotic lesions encroaching on the lumen of the vessels create high shear forces which promote additional platelet accumulation and interactions between multiple cell types in the fluid-phase and in the vessel wall (4). These prothrombotic moieties are much stronger agonists than those found in the milieu of injured healthy vessel surfaces. Time-course studies of morphology of evolving thrombi, in addition to experimental observations in vitro, invariably demonstrate participation of platelets, erythrocytes and leukocytes in addition to intact endothelial cells surrounding the lesion (5). The central core of arterial thrombi usually consists of platelets, which are admixed with erythrocytes, neutrophils and monocytes as one moves to the periphery of the coagulum. Morphologic identification of several cell types in evolving thrombi was initially interpreted as a passive, random phenomenon. However, we now know there is biochemical participation in evolving thrombi as demonstrated by in vitro studies from our own and many other laboratories (5, 6). W e consider thrombosis to represent a highly integrated group of biochemical and physical events involving reactions between multiple cell types and platelets (5, 6, 10). Shear forces, cell motion, cell contact, and strength of