The role that inflammation plays on the vasculature has become fundamental in our understanding of the different steps underlying the development of coronary heart disease (CHD).1 Immunological-related inflammatory processes accompany all stages of atherosclerosis development, from the early formation of lesions in the arteries to the rupture of the atherosclerotic plaques, which leads to dramatic consequences such as myocardial infarction and stroke. In this light, the search of markers of inflammation that could help to predict and even to treat cardiovascular diseases has been the subject of intense investigation.

C reactive protein (CRP, so named because it was originally found to react with the C-polysaccharide of the bacterium Streptococcus pneumoniae) is a plasma protein produced mainly by the liver. As part of the acute-phase response proteins, CRP production is rapidly induced in response to infections and other inflammatory conditions and its expression is triggered by cytokines such as interleukin-6 (IL-6), which is released in the blood by macrophages.2 The best characterised biological function of CRP is the clearance of necrotic or apoptotic cells which occur by the binding to phosphocoline residues present on the surface of damaged cells and the activation of the complement system. These features have made CRP a useful systemic marker for inflammation and tissue damage in routine clinical measurements.

What placed CRP at the centre of cardiovascular research were the initial observations that a small rise in the baseline level of CRP concentration correlated significantly with increased risk of future cardiovascular events. In addition to this, the presence of CRP in atherosclerotic plaques3 and its …