Worldwide, cardiovascular disease (CVD) is a leading cause of death. Endothelial dysfunction is now recognized to be a key platform for the pathophysiological effects of atherosclerosis. It is now well accepted that atherosclerosis is not merely a benign and passive process, but is in fact a dynamic and progressive disease arising from a combination of endothelial damage/dysfunction, inflammation, thrombosis and coagulation leading to potential clot-related vessel occlusion. The between inflammation, thrombosis and coagulation in the pathogenesis of CVD is more than simply association, as it clear that these processes are critically influenced by one another. In this preface we present a basic overview of the evidence in support of this relationship, which will be expanded upon in sequential chapters. In addition we briefly discuss a number of novel anticoagulants which not only reduce coagulation, but have ancillary antiinflammatory properties, thus further supporting the triad of inflammation, thrombosis and coagulation in the development of CVD.