title: Effects of lowering average of below-average cholesterol levels on the progression of carotid atherosclerosis: results of the LIPID Atherosclerosis Substudy. LIPID Trial Research Group.
abstract: BACKGROUND
  Cholesterol lowering in patients with above-average cholesterol levels has been shown to reduce the progression of atherosclerosis and lower the risk of coronary heart disease events. However, there has been uncertainty about the effects of cholesterol lowering in patients with average or below-average cholesterol levels.
  
  
  RESULTS
  In this study, 522 patients with a history of myocardial infarction or unstable angina and with baseline levels of total cholesterol between 4 and 7 mmol/L (mean, 5.7 mmol/L) were randomized to treatment with a low fat diet plus pravastatin (40 mg daily) or to a low fat diet plus placebo. Treatment with pravastatin reduced the levels of total cholesterol by 19%, LDL cholesterol by 27%, apolipoprotein B by 19%, and triglycerides by 13% (all 2P<.0001) and increased apolipoprotein A1 and HDL cholesterol levels by 4% (both 2P<.0005), in comparison with placebo. Carotid atherosclerosis was assessed from B-mode ultrasound measurements of the common carotid artery. After 4 years, mean carotid wall thickness had increased by 0.048 mm (SE=0.01) in the placebo group and declined by 0.014 mm in the pravastatin-treated group (SE=0.01) (2P for difference <.0001). The effect of treatment on wall thickness was similar in three groups classified by tertiles of total cholesterol at baseline, with mean levels of 4.8, 5.7, and 6.6 mmol/L, respectively (2P for interaction >.8).
  
  
  CONCLUSIONS
  Treatment with pravastatin reduced the development of carotid atherosclerosis among patients with coronary heart disease and a wide range of pretreatment cholesterol levels. Treatment with this agent prevented any detectable increase in carotid wall thickening over 4 years of follow-up.
authors.affiliation: Department of Medicine, University of Auckland, New Zealand. macmahon@ctru.auckland.ac.nz
authors.forename: S
authors.initials: S
authors.lastname: MacMahon
authors.forename: N
authors.initials: N
authors.lastname: Sharpe
authors.forename: G
authors.initials: G
authors.lastname: Gamble
authors.forename: H
authors.initials: H
authors.lastname: Hart
authors.forename: J
authors.initials: J
authors.lastname: Scott
authors.forename: J
authors.initials: J
authors.lastname: Simes
authors.forename: H
authors.initials: H
authors.lastname: White
mesh_terms: D000328:Adult; D000368:Aged; D000789:Angina, Unstable / Q000453:epidemiology; D000924:Anticholesteremic Agents / Q000627:therapeutic use*; D001054:Apolipoproteins A / Q000032:analysis; D001055:Apolipoproteins B / Q000032:analysis; D001161:Arteriosclerosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000517:prevention & control*; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging; D016893:Carotid Stenosis / Q000097:blood / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D015331:Cohort Studies; D018450:Disease Progression; D004311:Double-Blind Method; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D009203:Myocardial Infarction / Q000453:epidemiology; D009520:New Zealand / Q000453:epidemiology; D017035:Pravastatin / Q000627:therapeutic use*; D012307:Risk Factors; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014463:Ultrasonography
chemical_list: D000924:Anticholesteremic Agents; D001054:Apolipoproteins A; D001055:Apolipoproteins B; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D014280:Triglycerides; D002784:Cholesterol; D017035:Pravastatin