title: Measurement of C-reactive protein for the targeting of statin therapy in the primary prevention of acute coronary events.
abstract: BACKGROUND
  Elevated levels of C-reactive protein, even in the absence of hyperlipidemia, are associated with an increased risk of coronary events. Statin therapy reduces the level of C-reactive protein independently of its effect on lipid levels. We hypothesized that statins might prevent coronary events in persons with elevated C-reactive protein levels who did not have overt hyperlipidemia.
  
  
  METHODS
  The level of C-reactive protein was measured at base line and after one year in 5742 participants in a five-year randomized trial of lovastatin for the primary prevention of acute coronary events.
  
  
  RESULTS
  The rates of coronary events increased significantly with increases in the base-line levels of C-reactive protein. Lovastatin therapy reduced the C-reactive protein level by 14.8 percent (P<0.001), an effect not explained by lovastatin-induced changes in the lipid profile. As expected, lovastatin was effective in preventing coronary events in participants whose base-line ratio of total cholesterol to high-density lipoprotein (HDL) cholesterol was higher than the median ratio, regardless of the level of C-reactive protein (number needed to treat for five years to prevent 1 event, 47; P=0.005). However, lovastatin was also effective among those with a ratio of total to HDL cholesterol that was lower than the median and a C-reactive protein level higher than the median (number needed to treat, 43; P=0.02). In contrast, lovastatin was ineffective among participants with a ratio of total to HDL cholesterol and a C-reactive protein level that were both lower than the median (number needed to treat, 983; P=0.80).
  
  
  CONCLUSIONS
  Statin therapy may be effective in the primary prevention of coronary events among subjects with relatively low lipid levels but with elevated levels of C-reactive protein.
authors: Center for Cardiovascular Disease Prevention, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02215, USA. pridker@partners.org
authors: P M
authors: PM
authors: Ridker
authors: N
authors: N
authors: Rifai
authors: M
authors: M
authors: Clearfield
authors: J R
authors: JR
authors: Downs
authors: S E
authors: SE
authors: Weis
authors: J S
authors: JS
authors: Miles
authors: A M
authors: AM
authors: Gotto
mesh_terms: D000208:Acute Disease; D000924:Anticholesteremic Agents / Q000494:pharmacology / Q000627:therapeutic use*; D002097:C-Reactive Protein / Q000032:analysis*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000517:prevention & control*; D004311:Double-Blind Method; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000494:pharmacology / Q000627:therapeutic use*; D008148:Lovastatin / Q000494:pharmacology / Q000627:therapeutic use*; D011322:Primary Prevention; D016016:Proportional Hazards Models; D012306:Risk; D012307:Risk Factors
chemical_list: D000924:Anticholesteremic Agents; D008076:Cholesterol, HDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D002097:C-Reactive Protein; D002784:Cholesterol; D008148:Lovastatin