C-Reactive protein and cardiovascular risk: has the time come for screening the general population?

C-Reactive protein (CRP), an exquisitely sensitive marker of systemic inflammation, has emerged as a powerful predictor of cardiovascular diseases, in particular of coronary heart disease (CHD) (1). The availability of high-sensitivity (hs) assays has enabled the detection of even low-grade inflammatory responses that have previously been regarded as clinically not meaningful. In this issue of the Journal, Rifai and Ridker (2) propose an algorithm using CRP concentrations together with the total cholesterol:HDL-cholesterol ratio, the most powerful predictor among lipoproteins, for cardiovascular risk assessment. They suggest risk stratification based on two consecutive hs-CRP measurements and categorizing subjects according to quintiles of hs-CRP and total cholesterol:HDL-cholesterol ratio. These quintiles were derived from ongoing population-based surveys, whereas risk estimates were taken from prospective studies in men and in women. CRP fulfills most of the requirements needed to serve as a new risk factor for CHD: (a) The consistency of results from 11 prospective population-based studies in initially healthy subjects has been remarkable. (b) The association between CRP and future coronary events is strong. The combined risk ratio for CHD from metaanalysis is 2 if subjects with baseline CRP concentrations in the upper tertile of the population distribution are compared with those in …

[1]  G. Lowe,et al.  Immunoradiometric assay of circulating C-reactive protein: age-related values in the adult general population. , 2000, Clinical chemistry.

[2]  M. Pfeffer,et al.  Inflammation, pravastatin, and the risk of coronary events after myocardial infarction in patients with average cholesterol levels. Cholesterol and Recurrent Events (CARE) Investigators. , 1998, Circulation.

[3]  S. Bhakdi,et al.  Complement and atherogenesis: binding of CRP to degraded, nonoxidized LDL enhances complement activation. , 1999, Arteriosclerosis, thrombosis, and vascular biology.

[4]  S. Fichtlscherer,et al.  Elevated C-Reactive Protein Levels and Impaired Endothelial Vasoreactivity in Patients With Coronary Artery Disease , 2000, Circulation.

[5]  R J Glynn,et al.  C-reactive protein adds to the predictive value of total and HDL cholesterol in determining risk of first myocardial infarction. , 1998, Circulation.

[6]  P. Ridker,et al.  C-reactive protein and other markers of inflammation in the prediction of cardiovascular disease in women. , 2000, The New England journal of medicine.

[7]  J. Danesh,et al.  Low grade inflammation and coronary heart disease: prospective study and updated meta-analyses , 2000, BMJ : British Medical Journal.

[8]  N Rifai,et al.  Proposed cardiovascular risk assessment algorithm using high-sensitivity C-reactive protein and lipid screening. , 2001, Clinical chemistry.

[9]  W. Koenig,et al.  C-reactive protein frequently colocalizes with the terminal complement complex in the intima of early atherosclerotic lesions of human coronary arteries. , 1998, Arteriosclerosis, thrombosis, and vascular biology.

[10]  M. Pfeffer,et al.  Long-Term Effects of Pravastatin on Plasma Concentration of C-reactive Protein , 1999 .

[11]  R. Ross Atherosclerosis is an inflammatory disease , 1999 .

[12]  W. Koenig,et al.  C-Reactive Protein in the Arterial Intima: Role of C-Reactive Protein Receptor–Dependent Monocyte Recruitment in Atherogenesis , 2000, Arteriosclerosis, thrombosis, and vascular biology.

[13]  R. Tracy,et al.  Variability in the measurement of C-reactive protein in healthy subjects: implications for reference intervals and epidemiological applications. , 1997, Clinical chemistry.

[14]  N Rifai,et al.  Clinical efficacy of an automated high-sensitivity C-reactive protein assay. , 1999, Clinical chemistry.