title: Targets of statin therapy: LDL cholesterol, non-HDL cholesterol, and apolipoprotein B in type 2 diabetes in the Collaborative Atorvastatin Diabetes Study (CARDS).
abstract: BACKGROUND
  LDL can vary considerably in its cholesterol content; thus, lowering LDL cholesterol (LDLC) as a goal of statin treatment implies the existence of considerable variation in the extent to which statin treatment removes circulating LDL particles. This consideration is particularly applicable in diabetes mellitus, in which LDL is frequently depleted of cholesterol.
  
  
  METHODS
  Type 2 diabetes patients randomly allocated to 10 mg/day atorvastatin (n = 1154) or to placebo (n = 1196) for 1 year were studied to compare spontaneous and statin-induced apolipoprotein B (apo B) concentrations (a measure of LDL particle concentration) at LDLC and non-HDL cholesterol (non-HDLC) concentrations proposed as statin targets in type 2 diabetes.
  
  
  RESULTS
  Patients treated with atorvastatin produced lower serum apo B concentrations at any given LDLC concentration than patients on placebo. An LDLC concentration of 1.8 mmol/L (70 mg/dL) during atorvastatin treatment was equivalent to a non-HDLC concentration of 2.59 mmol/L (100 mg/dL) or an apo B concentration of 0.8 g/L. At the more conservative LDLC targets of 2.59 mmol/L (100 mg/dL) and 3.37 mmol/L (130 mg/dL) for non-HDLC, however, the apo B concentration exceeded the 0.9-g/L value anticipated in the recent Consensus Statement from the American Diabetes Association and the American College of Cardiology.
  
  
  CONCLUSIONS
  The apo B concentration provides a more consistent goal for statin treatment than the LDLC or non-HDLC concentration.
authors.affiliation: University of Manchester Cardiovascular Research Group, Manchester, UK.
authors.forename: Valentine
authors.initials: V
authors.lastname: Charlton-Menys
authors.forename: D John
authors.initials: DJ
authors.lastname: Betteridge
authors.forename: Helen
authors.initials: H
authors.lastname: Colhoun
authors.forename: John
authors.initials: J
authors.lastname: Fuller
authors.forename: Michael
authors.initials: M
authors.lastname: France
authors.forename: Graham A
authors.initials: GA
authors.lastname: Hitman
authors.forename: Shona J
authors.initials: SJ
authors.lastname: Livingstone
authors.forename: H Andrew W
authors.initials: HA
authors.lastname: Neil
authors.forename: Connie B
authors.initials: CB
authors.lastname: Newman
authors.forename: Michael
authors.initials: M
authors.lastname: Szarek
authors.forename: David A
authors.initials: DA
authors.lastname: DeMicco
authors.forename: Paul N
authors.initials: PN
authors.lastname: Durrington
mesh_terms: D000328:Adult; D000368:Aged; D001055:Apolipoproteins B / Q000097:blood*; D000069059:Atorvastatin; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D003924:Diabetes Mellitus, Type 2 / Q000097:blood* / Q000188:drug therapy* / Q000201:enzymology; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D006903:Hydroxymethylglutaryl CoA Reductases / Q000378:metabolism*; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011758:Pyrroles / Q000627:therapeutic use*
chemical_list: D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin; D006903:Hydroxymethylglutaryl CoA Reductases