title: Statin therapy, lipid levels, C-reactive protein and the survival of patients with angiographically severe coronary artery disease.
abstract: OBJECTIVE
  The joint predictive value of lipid and C-reactive protein (CRP) levels, as well as a possible interaction between statin therapy and CRP, were evaluated for survival after angiographic diagnosis of coronary artery disease (CAD).
  
  
  BACKGROUND
  Hyperlipidemia increases risk of CAD and myocardial infarction. For first myocardial infarction, the combination of lipid and CRP levels may be prognostically more powerful. Although lipid levels are often measured at angiography to guide therapy, their prognostic value is unclear.
  
  
  METHODS
  Blood samples were collected from a prospective cohort of 985 patients diagnosed angiographically with severe CAD (stenosis > or =70%) and tested for total cholesterol (TC), low-density lipoprotein (LDL), high-density lipoprotein (HDL), and CRP levels. Key risk factors, including initiation of statin therapy, were recorded, and subjects were followed for an average of 3.0 years (range: 1.8 to 4.3 years) to assess survival.
  
  
  RESULTS
  Mortality was confirmed for 109 subjects (11%). In multiple variable Cox regression, levels of TC, LDL, HDL and the TC:HDL ratio did not predict survival, but statin therapy was protective (adjusted hazard ratio [HR] = 0.49, p = 0.04). C-reactive protein levels, age, left ventricular ejection fraction and diabetes were also independently predictive. Statins primarily benefited subjects with elevated CRP by eliminating the increased mortality across increasing CRP tertiles (statins: HR = 0.97 per tertile, p-trend = 0.94; no statins: HR = 1.8 per tertile, p-trend < 0.0001).
  
  
  CONCLUSIONS
  Lipid levels drawn at angiography were not predictive of survival in this population, but initiation of statin therapy was associated with improved survival regardless of the lipid levels. The benefit of statin therapy occurred primarily in patients with elevated CRP.
authors.affiliation: Cardiovascular Department, LDS Hospital and University of Utah, Salt Lake City 84143, USA.
authors.forename: B D
authors.initials: BD
authors.lastname: Horne
authors.forename: J B
authors.initials: JB
authors.lastname: Muhlestein
authors.forename: J F
authors.initials: JF
authors.lastname: Carlquist
authors.forename: T L
authors.initials: TL
authors.lastname: Bair
authors.forename: T E
authors.initials: TE
authors.lastname: Madsen
authors.forename: N I
authors.initials: NI
authors.lastname: Hart
authors.forename: J L
authors.initials: JL
authors.lastname: Anderson
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use; D002097:C-Reactive Protein / Q000032:analysis*; D003327:Coronary Disease / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000401:mortality* / Q000503:physiopathology; D005260:Female; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D011237:Predictive Value of Tests; D011446:Prospective Studies; D011859:Radiography; D012307:Risk Factors; D013318:Stroke Volume; D016277:Ventricular Function, Left
chemical_list: D000924:Anticholesteremic Agents; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D008074:Lipoproteins; D002097:C-Reactive Protein