title: The effects of extended-release niacin on carotid intimal media thickness, endothelial function and inflammatory markers in patients with the metabolic syndrome.
abstract: BACKGROUND
  Niacin is an agent that significantly increases high-density lipoprotein cholesterol (HDL-C), but its effects on surrogate markers of atherosclerosis and inflammatory markers are less clear. We studied the effects of niacin on carotid intimal media thickness (IMT), brachial artery reactivity as well as markers of inflammation and the metabolic profile of patients with metabolic syndrome.
  
  
  RESULTS
  Fifty patients with the metabolic syndrome (Adult Treatment Panel (ATP) III criteria) were randomised to either extended-release niacin (1000 mg/day) or placebo. After 52 weeks of treatment, there was a change of carotid IMT of +0.009 +/- 0.003 mm in the placebo group and -0.005 +/- 0.002 mm in the niacin group (p = 0.021 between groups). Endothelial function improved by 22% in the group treated with niacin (p < 0.001), whereas no significant changes were seen in the placebo group. High sensitivity C-reactive protein decreased by 20% in the group treated with niacin for 52 weeks (p = 0.013). Niacin increased HDL-C (p < 0.001) and decreased low-density lipoprotein cholesterol and triglycerides (p < 0.001) significantly, and there were no adverse effects on fasting glucose levels after 52 weeks of treatment.
  
  
  CONCLUSIONS
  Extended-release niacin therapy effects a regression in carotid intimal medial thickness and improvement in metabolic parameters (increased HDL and reduced triglycerides). Furthermore, extended-release niacin may demonstrate an anti-atherogenic effect in the metabolic syndrome by improving endothelial function and decreasing vascular inflammation.
authors.affiliation: Institut für klinische Pharmakologie, Technische Universität Dresden, Dresden, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Thoenes
authors.forename: A
authors.initials: A
authors.lastname: Oguchi
authors.forename: S
authors.initials: S
authors.lastname: Nagamia
authors.forename: C S
authors.initials: CS
authors.lastname: Vaccari
authors.forename: R
authors.initials: R
authors.lastname: Hammoud
authors.forename: G E
authors.initials: GE
authors.lastname: Umpierrez
authors.forename: B V
authors.initials: BV
authors.lastname: Khan
mesh_terms: D000328:Adult; D050197:Atherosclerosis / Q000517:prevention & control*; D015415:Biomarkers / Q000032:analysis; D001786:Blood Glucose / Q000378:metabolism; D002339:Carotid Arteries / Q000473:pathology*; D008076:Cholesterol, HDL / Q000378:metabolism; D003692:Delayed-Action Preparations; D004311:Double-Blind Method; D004727:Endothelium / Q000473:pathology; D005260:Female; D006801:Humans; D000960:Hypolipidemic Agents / Q000627:therapeutic use*; D007249:Inflammation / Q000473:pathology; D008297:Male; D008659:Metabolic Diseases / Q000150:complications / Q000188:drug therapy* / Q000473:pathology; D008875:Middle Aged; D009525:Niacin / Q000627:therapeutic use*; D011446:Prospective Studies; D013577:Syndrome; D016896:Treatment Outcome; D017539:Tunica Intima / Q000473:pathology*
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D008076:Cholesterol, HDL; D003692:Delayed-Action Preparations; D000960:Hypolipidemic Agents; D009525:Niacin