Acute coronary syndromes are multifactorial and occur in response to inflammation, plaque rupture and subsequent thrombosis, progressive mechanical obstruction, and dynamic obstruction. Among potential biomarkers, much interest has focused on biomarkers of inflammation. The process that leads to eventual plaque erosion or rupture involves a number of inflammatory mechanisms, including endothelial dysfunction, leukocyte migration, extracellular matrix degradation, and platelet activation. We discuss herein blood levels of adhesion molecules, matrix metalloproteases, monocyte chemoattractant protein-1, and tissue factor and interferon-gamma production of circulating T cell in patients with acute coronary syndromes. These biomarkers are associated with not only formation and progression of atherosclerotic plaque but also incidence of coronary event.