title: Prognostic utility of apoB/AI, total cholesterol/HDL, non-HDL cholesterol, or hs-CRP as predictors of clinical risk in patients receiving statin therapy after acute coronary syndromes: results from PROVE IT-TIMI 22.
abstract: OBJECTIVE
  The purpose of this study was to compare the prognostic utility of apoB/AI, total cholesterol/HDL (TC/HDL) ratio, non-HDL cholesterol (non-HDL-C), or hs-CRP as predictors of clinical risk among patients receiving statin therapy after acute coronary syndromes (ACS).
  
  
  RESULTS
  Patients with ACS were randomized in the PROVE IT-TIMI 22 trial to either pravastatin 40 mg or atorvastatin 80 mg. Cox regression models adjusting for confounders were used to assess the relationship between on-treatment lipids or hs-CRP and risk of death or acute coronary events. At 4 months a 1 SD increment in apoB/AI (HR 1.10, 95% CI 1.01 to 1.20), TC/HDL (HR 1.12, 95% CI 1.01 to 1.24), and non-HDL-C (HR 1.20, 95% CI 1.07 to 1.35) predicted events to a similar extent as LDL-C (HR 1.20, 95% CI 1.07 to 1.35) with neither apoB/AI, TC/HDL, nor non-HDL-C improving risk prediction models which included LDL-C. In contrast, the addition of hs-CRP significantly improved risk prediction models irrespective of the lipid parameters included, with a 29% to 30% increased risk observed per 1 SD increment in log CRP.
  
  
  CONCLUSIONS
  In the present study of ACS patients receiving statin therapy, on-treatment apoB/AI, TC/HDL, and non-HDL-C offered similar prognostic information to LDL-C. However, the addition of hs-CRP to lipid-based measurements significantly improved risk prediction. On treatment CRP measurement may therefore offer additive prognostic information to lipids in ACS patients.
authors.affiliation: TIMI Study Group, Cardiovascular Division and the Department of Medicine, Brigham and Women's Hospital/Harvard Medical School, Boston, MA 02115, USA.
authors.forename: Kausik K
authors.initials: KK
authors.lastname: Ray
authors.forename: Christopher P
authors.initials: CP
authors.lastname: Cannon
authors.forename: Richard
authors.initials: R
authors.lastname: Cairns
authors.forename: David A
authors.initials: DA
authors.lastname: Morrow
authors.forename: Paul M
authors.initials: PM
authors.lastname: Ridker
authors.forename: Eugene
authors.initials: E
authors.lastname: Braunwald
mesh_terms: D054058:Acute Coronary Syndrome / Q000097:blood / Q000188:drug therapy* / Q000401:mortality; D016632:Apolipoprotein A-I / Q000097:blood*; D001055:Apolipoproteins B / Q000097:blood*; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D003327:Coronary Disease / Q000097:blood / Q000209:etiology / Q000401:mortality / Q000517:prevention & control*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D017035:Pravastatin / Q000627:therapeutic use*; D011237:Predictive Value of Tests; D016016:Proportional Hazards Models; D011758:Pyrroles / Q000627:therapeutic use*; D012008:Recurrence; D018570:Risk Assessment; D013997:Time Factors; D016896:Treatment Outcome
chemical_list: C505693:APOA1 protein, human; D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D015415:Biomarkers; D008076:Cholesterol, HDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin; D017035:Pravastatin