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In the last decade, there has been a burgeoning interest in associations between concentrations of various circulating biomarkers and later coronary disease.1 Of these, the acute phase reactant, C-reactive protein, has garnered the greatest attention. This spotlight on C-reactive protein reflects the strength and consistency of the observed associations, the fact that C-reactive protein is a stable and readily measured analyte, and the focus on the link between inflammation and atherosclerosis. The findings led initially to the proposal that its measurement might provide useful predictive information on coronary disease risk.2 Later, the proposal was made that C-reactive protein might even play a contributory role in atherogenesis.2 Associations identified between C-reactive protein and incident blood pressure, diabetes, and metabolic syndrome were used in support of this, and experimental data from studies of vascular cells and tissues in vitro and from infusions of C-reactive protein provided preliminary evidence for pro-inflammatory, pro-adhesive, and pro-thrombotic actions.3 These data are exciting because it was through a similar mix of observational and experimental work that cholesterol was first identified as a potential causal factor in atherosclerosis, a link which randomized clinical trials of cholesterol-lowering drugs subsequently confirmed to be causal. If the same is true for C-reactive protein, it would represent a new therapeutic target for coronary disease prevention.More recently, however, evidence has emerged, which questions the role of C-reactive protein in both the prediction of clinical events and in the pathogenesis of atherosclerosis. A meta-analysis of the prospective cohort studies, including a very large new study, indicated that the strength of the C-reactive protein-coronary event association may be smaller than initially supposed and that C-reactive protein may offer limited predictive information, particularly after levels of traditional risk factors are taken into account.4 This is because C-reactive protein is itself … *Corresponding author. E-mail address : a.hingorani{at}ucl.ac.uk

european heart journal

Linking observational and genetic approaches to determine the role of C-reactive protein in heart disease riskThe opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.