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Previous Volume 359:2195-2207 November 20, 2008 Number 21 Next

	Full Text PDF PDA Full Text PowerPoint Slide Set Supplementary Material Editorial by Hlatky, M. A. Editorial by Kritek, P. Letters Add to Personal Archive Add to Citation Manager Notify a Friend E-mail When Cited E-mail When Letters Appear PubMed Citation

Editor's note: We invite readers to submit comments on the JUPITER trial in a new interactive feature, Clinical Directions – The JUPITER Trial: Will You Change Your Practice? Commenting closes November 26, 2008.

Background Increased levels of the inflammatory biomarker high-sensitivity C-reactive protein predict cardiovascular events. Since statins lower levels of high-sensitivity C-reactive protein as well as cholesterol, we hypothesized that people with elevated high-sensitivity C-reactive protein levels but without hyperlipidemia might benefit from statin treatment.

Methods We randomly assigned 17,802 apparently healthy men and women with low-density lipoprotein (LDL) cholesterol levels of less than 130 mg per deciliter (3.4 mmol per liter) and high-sensitivity C-reactive protein levels of 2.0 mg per liter or higher to rosuvastatin, 20 mg daily, or placebo and followed them for the occurrence of the combined primary end point of myocardial infarction, stroke, arterial revascularization, hospitalization for unstable angina, or death from cardiovascular causes.

Results The trial was stopped after a median follow-up of 1.9 years (maximum, 5.0). Rosuvastatin reduced LDL cholesterol levels by 50% and high-sensitivity C-reactive protein levels by 37%. The rates of the primary end point were 0.77 and 1.36 per 100 person-years of follow-up in the rosuvastatin and placebo groups, respectively (hazard ratio for rosuvastatin, 0.56; 95% confidence interval [CI], 0.46 to 0.69; P<0.00001), with corresponding rates of 0.17 and 0.37 for myocardial infarction (hazard ratio, 0.46; 95% CI, 0.30 to 0.70; P=0.0002), 0.18 and 0.34 for stroke (hazard ratio, 0.52; 95% CI, 0.34 to 0.79; P=0.002), 0.41 and 0.77 for revascularization or unstable angina (hazard ratio, 0.53; 95% CI, 0.40 to 0.70; P<0.00001), 0.45 and 0.85 for the combined end point of myocardial infarction, stroke, or death from cardiovascular causes (hazard ratio, 0.53; 95% CI, 0.40 to 0.69; P<0.00001), and 1.00 and 1.25 for death from any cause (hazard ratio, 0.80; 95% CI, 0.67 to 0.97; P=0.02). Consistent effects were observed in all subgroups evaluated. The rosuvastatin group did not have a significant increase in myopathy or cancer but did have a higher incidence of physician-reported diabetes.

Conclusions In this trial of apparently healthy persons without hyperlipidemia but with elevated high-sensitivity C-reactive protein levels, rosuvastatin significantly reduced the incidence of major cardiovascular events. (ClinicalTrials.gov number, NCT00239681 [ClinicalTrials.gov] .)

Source Information

From the Center for Cardiovascular Disease Prevention (P.M.R., E.D., J.G.M., R.J.G.) and Division of Cardiovascular Medicine (P.M.R., P.L.), Brigham and Women's Hospital, Harvard Medical School, Boston; Universidade Federal de São Paulo, São Paulo (F.A.H.F.); McGill University Health Center, Montreal (J.G.); Weill Cornell Medical College of Cornell University, New York (A.M.G.); Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam (J.J.P.K.); University of Ulm Medical Center, Ulm, Germany (W.K.); Hospital Cordoba, Cordoba, Argentina (A.J.L.); Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark (B.G.N.); University of Glasgow, Glasgow, Scotland (J.S.); and St. Luke's Episcopal Hospital–Texas Heart Institute, Houston (J.T.W.).

This article (10.1056/NEJMoa0807646) was published at www.nejm.org on November 9, 2008.

Address reprint requests to Dr. Ridker at the Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, Boston, MA 02215, or at pridker{at}partners.org.

Full Text of this Article

Related Letters:

Rosuvastatin in Patients with Elevated C-Reactive Protein
Gibbons R. J., Fugh-Berman A., Chan P. S., Nallamothu B. K., Hayward R. A., Jenny-Avital E. R., Mak K.-H., Chan E. S.-Y., Pierard L. A., Davis C. E., Koller M. T., Bucher H. C., Steyerberg E. W., Ridker P. M, Glynn R. J.
Extract | Full Text | PDF  
N Engl J Med 2009; 360:1038-1042, Mar 5, 2009. Correspondence

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