The genesis of an atherosclerotic plaque depends on interplay of cellular components of the immune system such as monocytes, cytokines, and cell adhesion molecules with lipids, platelets and endothelial cells. Thus, inflammation may play a pivotal role in the propagation of coronary artery disease. Several reports have linked inflammation and cardiovascular risk, particularly a novel acute inflammatory peptide, C-reactive protein (CRP), with future risk of coronary events independent of the traditional coronary artery disease risk factors. To this end, many studies suggest that CRP may be used as a marker of sub-clinical atherosclerosis and cardiovascular risk. Specifically, CRP has been positively linked to future cardiovascular events in healthy women, healthy men, elderly patients, and high-risk individuals. In addition, reports have shown associations between CRP and peripheral vascular disease and stroke. Furthermore, preliminary data suggest that the relative efficacy of secondary preventive therapies such as statin drugs and aspirin may depend on the individual patient's baseline CRP level.