title: Effect of atorvastatin on circulating hsCRP concentrations: a sub-study of the achieve cholesterol targets fast with atorvastatin stratified titration (ACTFAST) study.
abstract: BACKGROUND
  Elevated C-reactive protein (CRP) concentration is a risk factor for cardiovascular events that may add prognostic information. Statin treatment is associated with significant reductions in CRP concentrations, which appear to be unrelated to the magnitude of LDL-cholesterol reduction. We investigated the effect of atorvastatin, across its dose range, on high sensitivity (hs)CRP in subjects at high cardiovascular risk.
  
  
  METHODS
  ACTFAST was a 12 week, prospective, multicenter, open-label trial in which high-risk subjects were assigned a starting dose of atorvastatin (10, 20, 40 or 80 mg/d) based on LDL-C and status of statin use at screening (1345 statin-free [SF] and 772 previously statin-treated [ST]).
  
  
  RESULTS
  At baseline, ST subjects had significantly lower hsCRP levels than SF subjects (ST group 2.31, 95% CI 2.15, 2.48 mg/L vs. SF group 3.16, 95% CI 2.98, 3.34 mg/L, p<0.05). In the SF group, atorvastatin 10 to 80 mg significantly (p<0.01) reduced hsCRP levels in a dose dependent-manner. In ST group, additional hsCRP reductions were observed over the statin used at baseline, which were not dose-dependent. Atorvastatin significantly decreased hsCRP concentrations in subjects with or without diabetes or the metabolic syndrome.
  
  
  CONCLUSIONS
  Atorvastatin treatment at different doses, particularly 80 mg, significantly reduced hsCRP serum concentrations. This reduction was observed in both SF and ST groups and was independent of the presence of metabolic syndrome and/or diabetes. The beneficial effect of atorvastatin was evident at 6 weeks, supporting the practice of early introduction of higher doses of atorvastatin in high-risk patients.
authors.affiliation: Department of Medical and Surgical Critical Care, University of Florence, Azienda Ospedaliero-Universitaria Careggi Hospital, Firenze, Italy.
authors.forename: G F
authors.initials: GF
authors.lastname: Gensini
authors.forename: A M
authors.initials: AM
authors.lastname: Gori
authors.forename: B
authors.initials: B
authors.lastname: Dilaghi
authors.forename: C
authors.initials: C
authors.lastname: Rostagno
authors.forename: A
authors.initials: A
authors.lastname: Gaw
authors.forename: L M
authors.initials: LM
authors.lastname: Blanco-Colio
authors.forename: E
authors.initials: E
authors.lastname: de Teresa
authors.forename: J
authors.initials: J
authors.lastname: Egido
authors.forename: C
authors.initials: C
authors.lastname: Farsang
authors.forename: L A
authors.initials: LA
authors.lastname: Leiter
authors.forename: P
authors.initials: P
authors.lastname: Martineau
authors.forename: A
authors.initials: A
authors.lastname: Nozza
authors.forename: A
authors.initials: A
authors.lastname: Langer
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000008:administration & dosage*; D000069059:Atorvastatin; D002097:C-Reactive Protein / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood; D003324:Coronary Artery Disease / Q000453:epidemiology / Q000517:prevention & control*; D003924:Diabetes Mellitus, Type 2 / Q000453:epidemiology; D004305:Dose-Response Relationship, Drug; D050171:Dyslipidemias / Q000188:drug therapy* / Q000453:epidemiology; D005260:Female; D006538:Heptanoic Acids / Q000008:administration & dosage*; D006801:Humans; D008297:Male; D024821:Metabolic Syndrome / Q000453:epidemiology; D008875:Middle Aged; D011446:Prospective Studies; D011758:Pyrroles / Q000008:administration & dosage*; D012307:Risk Factors
chemical_list: D000924:Anticholesteremic Agents; D006538:Heptanoic Acids; D011758:Pyrroles; D002097:C-Reactive Protein; D002784:Cholesterol; D000069059:Atorvastatin