title: Change in alpha1 HDL concentration predicts progression in coronary artery stenosis.
abstract: OBJECTIVE
  We examined the effects of simvastatin-niacin and antioxidant vitamins on changes in high-density lipoprotein (HDL) subpopulations and alterations in coronary artery stenosis, as assessed by angiography.
  
  
  RESULTS
  Lipids, lipoproteins, and HDL particles were measured on and off treatment in 123 subjects of the HDL-Atherosclerosis Treatment Study. Patients were assigned to 4 treatment groups, simvastatin-niacin, simvastatin-niacin-antioxidant vitamins, antioxidant vitamins, and placebo. Subjects were followed for 3 years on treatment and then for 2 months off treatment. Simvastatin-niacin significantly increased the 2 large apoA-I-containing HDL subpopulations, alpha1 and prealpha1, and significantly decreased the 2 smallest particles, prebeta1 and alpha3, compared with values obtained from the same patients off treatment. Adding antioxidant vitamins to the lipid-modifying agents blunted these effects (not significant). A significant negative correlation (r=-0.235; P<0.01) between the changes in alpha1 HDL particle concentration and coronary artery stenosis was noted. Subjects in the third tertile (157% increase in alpha1) had no progression of stenosis in the 3-year follow-up period, whereas subjects in the first tertile (15% decrease in alpha1) had an average of 2.1% increase in stenosis.
  
  
  CONCLUSIONS
  Simvastatin-niacin therapy significantly increased the large apoA-I-containing alpha1 HDL particles. This increase was significantly associated with less progression of coronary stenosis even after adjusting for traditional risk factors.
authors.affiliation: Lipid Metabolism Laboratory, Jean Mayer USDA Human Nutrition Center on Aging at Tufts University and Division of Endocrinology, Metabolism, Diabetes, and Molecular Medicine, New England Medical Center, Boston, Mass 02111, USA. bela.asztalos@tufts.edu
authors.forename: Bela F
authors.initials: BF
authors.lastname: Asztalos
authors.forename: Marcelo
authors.initials: M
authors.lastname: Batista
authors.forename: Katalin V
authors.initials: KV
authors.lastname: Horvath
authors.forename: Caitlin E
authors.initials: CE
authors.lastname: Cox
authors.forename: Gerard E
authors.initials: GE
authors.lastname: Dallal
authors.forename: Josh S
authors.initials: JS
authors.lastname: Morse
authors.forename: Greg B
authors.initials: GB
authors.lastname: Brown
authors.forename: Ernst J
authors.initials: EJ
authors.lastname: Schaefer
mesh_terms: D000368:Aged; D000975:Antioxidants / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D016632:Apolipoprotein A-I / Q000097:blood; D016633:Apolipoprotein A-II / Q000097:blood; D023921:Coronary Stenosis / Q000097:blood* / Q000000981:diagnostic imaging / Q000188:drug therapy; D018450:Disease Progression; D004587:Electrophoresis, Agar Gel; D005260:Female; D006801:Humans; D008055:Lipids / Q000097:blood; D008075:Lipoproteins, HDL / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009525:Niacin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D010316:Particle Size; D011859:Radiography; D019821:Simvastatin / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use; D016896:Treatment Outcome; D014815:Vitamins / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000975:Antioxidants; D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D008055:Lipids; D008075:Lipoproteins, HDL; D014815:Vitamins; D009525:Niacin; D019821:Simvastatin