In both in vivo and in vitro experiments, it rarely happens that the lumen of straight vessels and Y-bifurcations become occluded with thrombi. However, if a stenosis is placed in the flow system, distal to which there is flow separation and vortex formation, sooner or later the vessel becomes occluded, emphasizing the importance of disturbed flow and the narrowing of blood vessels in the etiology of occlusive thrombosis in vivo. However, it is still not well understood why disturbed flows augment thrombus formation and what are the mechanisms involved in the process. Hence to investigate the exact role of disturbed flow and vortices in thrombogenesis, flow behavior and interactions of red cells and platelets in an annular vortex formed distal to a sudden tubular expansion of a 0.15 into 0.50 mm diameter glass tube (serving as a model of a stenosis) were studied under a microscope. It was found first that the annular vortex provided favorable conditions for spontaneous aggregation of normal human platelets through shear-induced collisions of particles while circulating in the orbits of the vortex. It was also found that adhesion of platelets onto a vessel wall was greatly enhanced in regions of disturbed flow. Here, wall adhesion of platelets was localized on both sides of the reattachment (stagnation) point where blood cells were carried by the flow toward the vessel wall along curved streamlines having a pronounced radial velocity component. To find out where such disturbed flows form and facilitate thrombus formation in the circulation, flow patterns in various regions of the arterial and venous systems were studied using isolated transparent arteries and veins prepared from dogs and humans postmortem, and by means of flow visualization and high speed cinemicrographic techniques. It was found that formation of recirculation flows similar to those observed downstream of a tubular expansion, where formation of platelet aggregates and enhanced wall adhesion of platelets occurred, certainly occur at some sites in vivo such as downstream of venous valves, in the carotid sinus, and distal to an anastomotic junction of end-to-end anastomosed vessels all of which are well known to be preferred sites for thrombus formation in the human cardiovascular system.