title: Doses of rosuvastatin, atorvastatin and simvastatin that induce equal reductions in LDL-C and non-HDL-C: Results from the VOYAGER meta-analysis.
abstract: BACKGROUND
  Achieving the greatest reduction in atherogenic lipoproteins requires the optimum dose and potency of statin. Using data from the VOYAGER meta-analysis, we determined doses of rosuvastatin, atorvastatin and simvastatin that induce equal reductions in low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non-HDL-C).
  
  
  METHODS
  Least squares mean percentage change in LDL-C and non-HDL-C was calculated using 38,052 patient exposures to rosuvastatin 5-40 mg, atorvastatin 10-80 mg and simvastatin 10-80 mg. Equipotent doses were estimated by linear interpolation between actual adjacent doses.
  
  
  RESULTS
  Rosuvastatin 5 mg reduced LDL-C by 39% and non-HDL-C by 35%. Equivalent reductions in LDL-C required atorvastatin 15 mg or simvastatin 39 mg. Equivalent reductions in non-HDL-C required atorvastatin 14 mg or simvastatin 42 mg. Rosuvastatin 10 mg reduced LDL-C by 44% and non-HDL-C by 40%. Equivalent reductions in LDL-C required atorvastatin 29 mg or simvastatin 72 mg. Equivalent reductions in non-HDL-C required atorvastatin 27 mg or simvastatin 77 mg. Rosuvastatin 20 mg reduced LDL-C by 50% and non-HDL-C by 45%. Equivalent reductions in LDL-C and non-HDL-C required atorvastatin 70 mg and atorvastatin 62 mg, respectively, and were not achieved with the maximum 80 mg dose of simvastatin. Rosuvastatin 40 mg reduced LDL-C by 55% and non-HDL-C by 50%. Comparable reductions were not achieved with the maximum 80 mg doses of atorvastatin or simvastatin.
  
  
  CONCLUSIONS
  Regarding reductions in LDL-C and non-HDL-C, each rosuvastatin dose is equivalent to doses 3-3.5 times higher for atorvastatin and 7-8 times higher for simvastatin.
authors.affiliation: AstraZeneca, Mölndal, Sweden Department of Molecular and Clinical Medicine, Sahlgrenska Academy, University of Gothenburg, Sweden Bjorn.W.Karlson@astrazeneca.com.
authors.forename: Björn W
authors.initials: BW
authors.lastname: Karlson
authors.affiliation: School of Healthcare Science, Manchester Metropolitan University, UK.
authors.forename: Michael K
authors.initials: MK
authors.lastname: Palmer
authors.affiliation: South Australian Health and Medical Research Institute, University of Adelaide, Australia.
authors.forename: Stephen J
authors.initials: SJ
authors.lastname: Nicholls
authors.affiliation: Danderyd Hospital, Karolinska Institute, Sweden.
authors.forename: Pia
authors.initials: P
authors.lastname: Lundman
authors.affiliation: University of New South Wales, Australia.
authors.forename: Philip J
authors.initials: PJ
authors.lastname: Barter
mesh_terms: D050197:Atherosclerosis / Q000097:blood / Q000188:drug therapy*; D000069059:Atorvastatin / Q000627:therapeutic use*; D008076:Cholesterol, HDL / Q000097:blood* / Q000187:drug effects; D008078:Cholesterol, LDL; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use; D000068718:Rosuvastatin Calcium / Q000627:therapeutic use*; D019821:Simvastatin / Q000627:therapeutic use*
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000068718:Rosuvastatin Calcium; D000069059:Atorvastatin; D019821:Simvastatin
keywords: Rosuvastatin; atorvastatin; low-density lipoprotein cholesterol; non-high-density lipoprotein cholesterol; simvastatin