title: Apolipoprotein-E polymorphism and response to pravastatin in men with coronary artery disease (REGRESS).
abstract: OBJECTIVE
  [corrected] The influence ofApoE polymorphism on the efficacy of statins in lowering plasma lipids and lipoproteins and improving angiographic parameters was assessed.
  
  
  METHODS
  ApoE genotypes were studied in a group (n = 815) of well-characterised male coronary artery disease (CAD) patients who participated in the lipid-lowering regression study 'Regression Growth Evaluation Statin Study (REGRESS)'.
  
  
  RESULTS
  There was a significant interaction between treatment (placebo/pravastatin) and APOE genotype when lipid levels were considered, APOE2 + carriers exhibited the largest improvement of HDL levels (+0.15 mmol/l) and LDL/HDL ratios (-0.60) compared with APOE3 + (+ 0.06 mmol/l, -0.043, respectively) and APOE4 + carriers (+ 0.07 mmol/l, -0.040). In contrast,APOE2 + allele carriers had the least effect in terms of angiographic parameters, although the difference was not statistically significant.
  
  
  CONCLUSIONS
  The effects of statins in subjects with different ApoE genotypes were different with regard to the lipoprotein profile, but not with regard to angiographic parameters.
authors.affiliation: Department of Pharmacoepidemiology and Pharmacotherapy, Utrecht Institute for Pharmaceutical Sciences (UIPS), Utrecht University, Utrecht, The Netherlands. A.H.Maitland-vanderZee@pharm.uu.nl
authors.forename: Anke-Hilse
authors.initials: AH
authors.lastname: Maitland-van der Zee
authors.forename: J Wouter
authors.initials: JW
authors.lastname: Jukema
authors.forename: Aeilko H
authors.initials: AH
authors.lastname: Zwinderman
authors.forename: D Michael
authors.initials: DM
authors.lastname: Hallman
authors.forename: Anthonius
authors.initials: A
authors.lastname: De Boer
authors.forename: John J P
authors.initials: JJ
authors.lastname: Kastelein
authors.forename: Peter
authors.initials: P
authors.lastname: De Knijff
mesh_terms: D000368:Aged; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D053329:Apolipoprotein E2 / Q000235:genetics; D053318:Apolipoprotein E3 / Q000235:genetics; D053327:Apolipoprotein E4 / Q000235:genetics*; D001057:Apolipoproteins E / Q000235:genetics*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy* / Q000235:genetics*; D006580:Genetic Carrier Screening; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic / Q000235:genetics*; D017035:Pravastatin / Q000627:therapeutic use*; D012044:Regression Analysis; D013223:Statistics as Topic; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood
chemical_list: D000924:Anticholesteremic Agents; D053329:Apolipoprotein E2; D053318:Apolipoprotein E3; D053327:Apolipoprotein E4; D001057:Apolipoproteins E; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D014280:Triglycerides; D002784:Cholesterol; D017035:Pravastatin