title: Intermediate-density lipoproteins and progression of carotid arterial wall intima-media thickness.
abstract: BACKGROUND
  Although LDL cholesterol (LDL-C) is generally accepted to be a major risk factor for progression of atherosclerosis, the traditional measurement of LDL-C includes measurement of IDL. Little is known about the relationship between IDL and progression of atherosclerosis. Therefore, we investigated the association of plasma lipoprotein subclasses with progression of preintrusive carotid artery atherosclerosis in the Monitored Atherosclerosis Regression Study (MARS).
  
  
  RESULTS
  MARS was a randomized, double-blind, placebo-controlled serial arterial imaging trial conducted in subjects 37 to 67 years old with angiographically defined coronary artery disease. Analytical ultracentrifugation was used to determine lipoprotein subclasses, including LDL (Sf 0 to 12), IDL (Sf 12 to 20), VLDL (Sf 20 to 400), and HDL (F1.20 0 to 9) in 188 subjects. Subjects were randomized to a cholesterol-lowering diet plus placebo or lovastatin 80 mg/d. The outcome measure, the annual progression rate of the distal common carotid artery far wall intima-media thickness determined by high resolution B-mode ultrasonography, was determined at baseline and every 6 months on trial. When the major apolipoprotein B-containing lipoproteins were measured independently, IDL (r=.21, P<.005) but not VLDL (r=-.09, P=.24) or LDL (r=.09, P=.26) was associated with the progression of carotid artery intimamedia thickness.
  
  
  CONCLUSIONS
  These data provide further evidence for the role of triglyceride-rich lipoproteins in the progression of atherosclerosis and support the evidence that indicates that the risk of atherosclerosis attributable to LDL-C may in part be the result of lipoproteins in the IDL fraction (Sf 12 to 20) that is included within the traditional measurements of LDL-C.
authors.affiliation: Department of Medicine, University of Southern California School of Medicine, Los Angeles 90033, USA.
authors.forename: H N
authors.initials: HN
authors.lastname: Hodis
authors.forename: W J
authors.initials: WJ
authors.lastname: Mack
authors.forename: M
authors.initials: M
authors.lastname: Dunn
authors.forename: C
authors.initials: C
authors.lastname: Liu
authors.forename: C
authors.initials: C
authors.lastname: Liu
authors.forename: R H
authors.initials: RH
authors.lastname: Selzer
authors.forename: R M
authors.initials: RM
authors.lastname: Krauss
mesh_terms: D000328:Adult; D000368:Aged; D001161:Arteriosclerosis / Q000097:blood* / Q000453:epidemiology / Q000209:etiology / Q000473:pathology; D017536:Carotid Artery, Common / Q000000981:diagnostic imaging / Q000473:pathology*; D016893:Carotid Stenosis / Q000097:blood* / Q000453:epidemiology / Q000209:etiology / Q000473:pathology; D002791:Cholesterol, Dietary / Q000008:administration & dosage; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D018450:Disease Progression; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000473:pathology*; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D006937:Hypercholesterolemia / Q000150:complications / Q000178:diet therapy / Q000188:drug therapy; D008074:Lipoproteins / Q000097:blood*; D053419:Lipoproteins, IDL; D008079:Lipoproteins, VLDL / Q000097:blood; D008148:Lovastatin / Q000627:therapeutic use; D008297:Male; D008875:Middle Aged; D012307:Risk Factors; D014280:Triglycerides / Q000097:blood; D014463:Ultrasonography
chemical_list: D002791:Cholesterol, Dietary; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D008074:Lipoproteins; D053419:Lipoproteins, IDL; D008079:Lipoproteins, VLDL; D014280:Triglycerides; D008148:Lovastatin