There is now widespread agreement that inflammation is a key component in the progression of atheromatous lesions. Inflammatory cells are present at all stages in the development of the atheromatous plaque, and gene knockout experiments in mice show that atheroma is largely prevented in the absence of the normal inflammatory mediators. In humans reduction of inflammation accompanies successful treatment strategies for atheroma. An increasing number of studies suggest that the acute phase protein, C-reactive protein, provides increased prognostic information over and above existing markers of atheroma severity or progression in healthy individuals and in the acute coronary syndromes. Recent advances in our knowledge of the normal variability of C-reactive protein levels and in precise and sensitive measurements strengthen the arguments for adding this marker to the repertoire of the routine laboratory assessment of cardiovascular disease.