It becomes increasingly evident that blood platelets do not only exert important functions in hemostasis and thrombus formation but are also involved in atherosclerotic vascular disease. The intact, nonactivated endothelium normally prevents platelet adhesion to the arterial wall. Inflamed endothelial cells become adhesive for platelets. During the adhesion process, platelets become activated and release potent inflammatory and mitogenic substances into the local microenvironment, thereby altering chemotactic, adhesive, and proteolytic properties of endothelial cells and supporting leukocytes recruitment into inflamed vascular wall. Activation of platelets, endothelial cells and leukocytes result in the formation of increased levels of microparticles, highly proinflammatory and proatherosclerotic bodies distributing substantial amounts of immunologically active substances between cells promoting inflammation. The evolving inflammatory reactions are instrumental in the initiation of atherosclerotic plaques and their destabilization. Atherosclerotic plaque develops in response to a localized inflammatory reaction in the vessel wall. Inflammation is crucial at all stages of atherosclerosis, when the endothelial cells and platelets are activated and express cytokines and adhesion molecules leading to monocyte/lymphocyte recruitment and infiltration into subendothelium. The purpose of this review is to bring together the current information concerning the role of activated platelets and activated endothelial cells in the development and progression of inflammation and atherosclerosis. The part one of this review focuses on multicellular adhesive interaction in the vasculature, with particular attention to the interplay between adhesive receptors of endothelial cells and platelets. This review summarizes also the present understanding of the role of microvesicles derived from blood cells in the progression of inflammation.