Is it important to measure or reduce C-reactive protein in people at risk of cardiovascular disease?

Systemic and local vascular inflammation is implicated in atherogenesis. High-sensitivity (hs) assays detecting low concentrations of C-reactive protein (CRP) in healthy individuals have delineated associations of this inflammation marker with cardiovascular events years later. A 160 309-person participant level meta-analysis of 54 prospective studies found the relationship between log-CRP concentration and cardiovascular disease (CVD) events to be linear, with a 2.5-fold risk difference in individuals at opposite extremes of the CRP distribution.1In vitro studies and animal experiments point to potentially atherogenic actions of CRP,2 and statins lower both CRP and low-density lipoprotein cholesterol (LDL-C).3 The Justification for the Use of statins in Primary prevention: an Intervention Trial Evaluating Rosuvastatin (JUPITER),4 designed to ‘assess the effect of rosuvastatin on first ever cardiovascular events in apparently healthy men and women who do not qualify for statin therapy due to low levels of LDL-C, but who are at increased cardiovascular risk due to elevated levels of hs-CRP’, was halted because of ‘unequivocal evidence of a reduction in cardiovascular morbidity and mortality among patients who received CRESTOR (rosuvastatin) when compared to placebo’ (http://clinicaltrials.gov/ct2/show/NCT00239681). Consequently, the US Food and Drug Administration approved an amended license for rosuvastatin for the primary prevention of CVD events in men and women over 50 and 60 years, respectively, with one other risk factor and a CRP concentration of >2 mg/L.