CRP is an acute-phase protein that is produced primarily in the liver but may also be produced in atherosclerotic plaques. CRP is a calcium-dependent ligand-binding pentameric protein that activates the complement system, induces adhesion molecule expression, enhances macrophage phagocytosis, and may well play a direct role in the pathogenesis of atherosclerosis.
Sensitive and reproducible hsCRP assays are now available. Increased hsCRP is an independent predictor of cardiovascular disease (CVD), and hsCRP concentrations are often increased in obese and diabetic patients. hsCRP is now incorporated into CVD risk scores for both men and women. Statins inhibit cholesterol production, and treatment with statins, especially rosuvastatin and atorvastatin, has been shown to reduce LDL-C and hsCRP concentrations. In the recent JUPITER trial, 17 802 individuals (men older than 50 and women older than 60 years) with LDL-C concentrations <3.37 mmol/L (130 mg/dL) and hsCRP concentrations >2 mg/L were randomized to rosuvastatin 20 mg/day or placebo. The trial was stopped early in favor of the rosuvastatin arm and demonstrated significant reductions in heart disease, stroke, and total mortality associated with rosuvastatin treatment.
The case patient described here was a 72-year-old woman with a history of hypertension and current cigarette smoking, as well as a positive family history of premature heart disease. She had a body mass index of 23 kg/m2, and her laboratory values were: LDL-C 69 mmol/L (104 mg/dL), HDL-C 2.12 mmol/L (82 mg/dL), and hsCRP 7.7 and 7.2 mg/L. Despite excellent lipid values, 4 months after her examination the patient suffered a myocardial infarction and was documented to have significant coronary heart disease requiring angioplasty and stent placement. Ridker has made a compelling case for the use of hsCRP in patient risk stratification and selection for aggressive lifestyle and risk-factor modification and statin therapy for the prevention of CVD in middle-aged and elderly people.
Author Contributions: All authors confirmed they have contributed to the intellectual content of this paper and have met the following 3 requirements: (a) significant contributions to the conception and design, acquisition of data, or analysis and interpretation of data; (b) drafting or revising the article for intellectual content; and (c) final approval of the published article.
Authors’ Disclosures of Potential Conflicts of Interest: Upon manuscript submission, all authors completed the Disclosures of Potential Conflict of Interest form. Potential conflicts of interest:
Employment or Leadership: None declared.
Consultant or Advisory Role: E.J. Schaefer has received consulting fees and/or lecture fees from Abbott, AstraZeneca, Boston Heart Laboratory, Merck, Merck Schering, Pfizer, Roche, Schering, and Unilever.
Stock Ownership: None declared.
Honoraria: None declared.
Research Funding: E.J. Schaefer has received investigator-initiated research grant support from the National Heart Lung and Blood Institute, and the US Department of Agriculture Research Service as well as Abbott, AstraZeneca, Merck-Schering, Novartis, Pfizer, Roche, Schering, and Unilever.
Expert Testimony: None declared.
Role of Sponsor: The funding organizations played no role in the design of study, choice of enrolled patients, review and interpretation of data, preparation or approval of manuscript.
- © 2009 The American Association for Clinical Chemistry