title: LDL cholesterol goals and cardiovascular risk during statin treatment: the IDEAL study.
abstract: OBJECTIVE
  We assessed the proportion of patients treated with either simvastatin 20 or 40 mg or atorvastatin 80 mg who achieved low-density lipoprotein cholesterol (LDL-C) goals of 2.5 or 2.0 mmol/l in the Incremental Decrease in End Points Through Aggressive Lipid Lowering (IDEAL) study. We explored how lipoprotein components related to cardiovascular disease (CVD) outcomes in these groups.
  
  
  RESULTS
  For subjects who reached on-treatment LDL-C goals, Cox regression models were used to assess the ability of lipoprotein components to predict CVD events. Treatment with simvastatin or atorvastatin resulted in 40 per cent and 80 per cent of patients, respectively, reaching the 2.5 mmol/l goal and 12 per cent and 52 per cent, respectively, reaching the 2.0 mmol/l goal, after 1 year (all p < 0.001 between groups). Adjusting for baseline LDL-C levels, hazard ratio (HR) for those reaching 2.0-2.5 mmol/l LDL-C versus those reaching <2.0 mmol/l was 1.16 (95% confidence interval [CI], 1.02-1.33, p = 0.023). An increase of the apolipoprotein B/A1 (apoB/A1) ratio by 1 standard deviation in participants who reached 2.0 mmol/l showed a HR for CVD of 1.14 (95% CI, 1.04-1.25, p = 0.004).
  
  
  CONCLUSIONS
  More CVD patients treated with atorvastatin than simvastatin achieved either LDL-C goal and those reaching the 2.0 mmol/l goal exhibited significantly less CVD than those only reaching 2.5 mmol/l. In those reaching the 2.0 mmol/l goal, the apoB/A1 ratio still bears a relation to CVD outcome. The use of apoB/A1 ratio may provide additional predictive value to that of LDL-C.
authors: Department of Internal Medicine, University Hospital, Linköping, Sweden. anders.olsson@liu.se
authors: Anders G
authors: AG
authors: Olsson
authors: Christina
authors: C
authors: Lindahl
authors: Ingar
authors: I
authors: Holme
authors: Rana
authors: R
authors: Fayyad
authors: Ole
authors: O
authors: Faergeman
authors: John J P
authors: JJ
authors: Kastelein
authors: Matti J
authors: MJ
authors: Tikkanen
authors: Mogens Lytken
authors: ML
authors: Larsen
authors: Terje R
authors: TR
authors: Pedersen
mesh_terms: D000368:Aged; D016632:Apolipoprotein A-I / Q000097:blood; D001055:Apolipoproteins B / Q000097:blood; D000069059:Atorvastatin; D015415:Biomarkers / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood*; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000097:blood / Q000188:drug therapy* / Q000517:prevention & control; D016016:Proportional Hazards Models; D011446:Prospective Studies; D011758:Pyrroles / Q000627:therapeutic use*; D018570:Risk Assessment; D012307:Risk Factors; D055502:Secondary Prevention; D019821:Simvastatin / Q000627:therapeutic use*; D016896:Treatment Outcome
chemical_list: C505693:APOA1 protein, human; D016632:Apolipoprotein A-I; D001055:Apolipoproteins B; D015415:Biomarkers; D008078:Cholesterol, LDL; D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D011758:Pyrroles; D000069059:Atorvastatin; D019821:Simvastatin