NDLI: Rosuvastatin to prevent vascular events in men and women with elevated C-reactive protein.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Glynn, Robert J. Macfadyen, Jean G. Shepherd, James Lorenzatti, Alberto J. Koenig, Wolfgang Willerson, James T. Libby, Peter Genest, Jacques Nordestgaard, Børge G. Danielson, Eleanor Fonseca, Francisco A. H. Ridker, Paul M. Gotto, Antonio M. Kastelein, John J. P.
Description	Author Affiliation: Ridker PM ( Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02215, USA. pridker@partners.org)
Abstract	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.)
ISSN	00284793
Issue Number	21
Volume Number	359
e-ISSN	15334406
Journal	New England Journal of Medicine
Language	English
Publisher	Massachusetts Medical Society (United States)
Publisher Date	2008-11-20
Publisher Place	United States
Access Restriction	Subscribed
Subject Keyword	C-Reactive Protein Metabolism Cardiovascular Diseases Prevention & Control Fluorobenzenes Therapeutic Use Hydroxymethylglutaryl-CoA Reductase Inhibitors Pyrimidines Sulfonamides Aged Biological Markers Blood Mortality Cholesterol, LDL Diabetes Mellitus Chemically Induced Double-Blind Method Female Adverse Effects Follow-Up Studies Hemoglobin A, Glycosylated Humans Kaplan-Meier Estimate Male Middle Aged Muscular Diseases Myocardial Infarction Epidemiology Proportional Hazards Models Rosuvastatin Calcium Stroke Journal Article Multicenter Study Randomized Controlled Trial Research Support, Non-U.S. Gov't Medicine
Content Type	Text
Resource Type	Article
Subject	Medicine

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