Inflammation plays a role in vascular injury and repair. The inflammatory acute phase protein C-reactive protein (CRP) has emerged as a powerful predictor of cardiovascular events. CRP serum levels display rapid rise following infection or tissue damage. CRP is a pentraxin regulated mainly by IL-6. Several studies established correlation between CRP levels and cardiovascular disease risk and the long term clinical outcome after acute coronary syndrome. Such correlation has yet to be proven regarding CRP and atherosclerosis. A growing body of evidence supports a role for CRP in the cardiovascular pathogenesis. CRP binds to LDL, VLDL and oxidized LDL, promoting complement activation. CRP induces tissue factor secretion from monocytes, enhances the expression of adhesion molecules and inhibits production of nitric oxide and prostacycline by human endothelial cells. The in-vitro studies which utilize recombinant CRP are criticized by studies in which preservatives and contaminants rather than CRP are responsible for the biological effects. Nevertheless, transgenic mice expressing human CRP have been shown to have an increased thrombotic risk. This data supports an active role of CRP in the evolvement of vascular damage rather than being just a marker, but its role in the development of atherosclerosis is not yet clear. There is no evidence to lowering vascular risk by reducing CRP levels but weight loss, exercise, statins and smoking secession all decrease CRP blood levels.