Circulating concentrations of C reactive protein (CRP), a hepatic derived inflammatory marker that is secreted in response to specific cytokines, have been shown to predict the risk of coronary heart disease (CHD) and diabetes in large epidemiological studies.^1,,² These data highlight the concept that inflammation is a central component of the pathogenesis of atherosclerosis. The plaque composition of unstable coronary lesions includes an abundance of inflammatory molecules and cells at the shoulder region and these may act to erode the collagen cap separating the atheromatous material of the plaque from blood. The strength of the prospective data linking CRP to CHD are such that a recent American Heart Association/Centers for Disease Control and Prevention consensus report suggested that high sensitivity CRP assays may be employed in helping predict CHD risk.¹

The recognition of the contribution of inflammation to atherosclerosis has focused attention on the impact of treatments on inflammatory markers. Treatments with proven effects on cardiovascular mortality, such as the lipid lowering 3-hydroxy-3-methylglutaryl coenzyme A (HMG-Co A) reductase inhibitors (statins) and also the insulin sensitising peroxisome proliferator activated receptor γ activators (thiazolidinediones), exhibit anti-inflammatory effects providing indirect support for the inflammation hypothesis.¹ For example, recent trials suggest a …