title: Prevention of the angiographic progression of coronary and vein-graft atherosclerosis by gemfibrozil after coronary bypass surgery in men with low levels of HDL cholesterol. Lopid Coronary Angiography Trial (LOCAT) Study Group.
abstract: BACKGROUND
  Studies have shown that treatment of hyperlipidemia, especially lowering of plasma LDL levels, retards the progression of coronary atherosclerosis and prevents clinical cardiovascular events. No such studies have focused on subjects with low levels of HDL cholesterol.
  
  
  RESULTS
  We randomly assigned 395 post-coronary bypass men, who had an HDL cholesterol concentration < or = 1.1 mmol/L and LDL cholesterol < or = 4.5 mmol/L, to receive gemfibrozil 1200 mg/d or placebo. Coronary angiography was performed at baseline and after, on average, 32 months of therapy. Changes in coronary dimensions were assessed by computer-assisted analysis. Average on-trial serum triglyceride concentrations were 1.69+/-0.68 and 1.02+/-0.37, total cholesterol 5.48+/-0.68 and 4.83+/-0.63, LDL cholesterol 3.84+/-0.59 and 3.39+/-0.56, and HDL cholesterol 0.88+/-0.15 and 0.98+/-0.17 mmol/L in the placebo and gemfibrozil groups, respectively (mean+/-SD, each P<.001). The change in per-patient means of average diameters of native coronary segments was -0.04+/-0.11 mm in the placebo group and -0.01+/-0.10 mm in the gemfibrozil group (P=.009). The equivalent changes in minimum luminal diameters of stenoses were -0.09+/-0.18 and -0.04+/-0.15 mm, respectively (P=.002). A similar, albeit nonsignificant, trend toward treatment benefit was found in the predefined primary study end point, segments unaffected by grafts and those distal to graft insertions. In aortocoronary bypass grafts, 23 subjects (14%) assigned to placebo had new lesions in the follow-up angiogram, compared with 4 subjects (2%) assigned to gemfibrozil (P<.001).
  
  
  CONCLUSIONS
  Gemfibrozil therapy retarded the progression of coronary atherosclerosis and the formation of bypass-graft lesions after coronary bypass surgery in men with low HDL cholesterol as their main lipid abnormality.
authors.affiliation: Department of Medicine, Helsinki University Central Hospital, Finland.
authors.forename: M H
authors.initials: MH
authors.lastname: Frick
authors.forename: M
authors.initials: M
authors.lastname: Syvänne
authors.forename: M S
authors.initials: MS
authors.lastname: Nieminen
authors.forename: H
authors.initials: H
authors.lastname: Kauma
authors.forename: S
authors.initials: S
authors.lastname: Majahalme
authors.forename: V
authors.initials: V
authors.lastname: Virtanen
authors.forename: Y A
authors.initials: YA
authors.lastname: Kesäniemi
authors.forename: A
authors.initials: A
authors.lastname: Pasternack
authors.forename: M R
authors.initials: MR
authors.lastname: Taskinen
mesh_terms: D000368:Aged; D000704:Analysis of Variance; D001161:Arteriosclerosis / Q000000981:diagnostic imaging / Q000517:prevention & control*; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood*; D008078:Cholesterol, LDL / Q000097:blood*; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003324:Coronary Artery Disease / Q000000981:diagnostic imaging / Q000517:prevention & control*; D004032:Diet; D018450:Disease Progression; D015248:Gemfibrozil / Q000627:therapeutic use*; D006083:Graft Occlusion, Vascular / Q000517:prevention & control*; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D008297:Male; D008875:Middle Aged; D012016:Reference Values; D013997:Time Factors; D014280:Triglycerides / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D000960:Hypolipidemic Agents; D014280:Triglycerides; D002784:Cholesterol; D015248:Gemfibrozil