title: Niacin improves lipid profile but not endothelial function in patients with coronary artery disease on high dose statin therapy.
abstract: OBJECTIVE
  To determine the effect of extended release (ER) niacin on endothelial and vascular function assessed by brachial flow-mediated dilatation (FMD), peak hyperemic velocity (VTiRH) and pulse arterial tonometry (PAT) in patients with established coronary artery disease (CAD), already treated with high dose statins. Endothelial dysfunction is common in patients with established coronary artery disease (CAD) and has prognostic implications. Niacin has proven clinical benefit in patients with CAD, but its additive effect in patients on statin therapy is being evaluated. The effect of niacin on endothelial function, in the presence of optimal LDL cholesterol is unclear.
  
  
  RESULTS
  Sixty-six patients with CAD (mean age 57.9 ± 8.5 yrs) received ER niacin (1500 mg per day) and placebo in a randomized crossover fashion for 3 months of each therapy. All patients received atorvastatin 80 mg per day. FMD, VTiRH and PAT measurements were performed at baseline and after each treatment period. Treatment with niacin improved dyslipidemia parameters (LDL placebo 1.52 ± 0.51 vs. niacin 1.30 ± 0.43; p = 0.004; HDL placebo 0.95 ± 0.16 vs. niacin 1.11 ± 0.22; p < 0.001). However, there was no observed improvement in endothelial function as assessed by FMD (placebo 6.1 ± 4.9 vs. niacin 6.6 ± 4.8%; p = 0.48), VTiRH (placebo 75 ± 28 vs. niacin 78 ± 26 cm; p = 0.23) or PAT (placebo 1.8 ± 0.42 vs. niacin 1.79 ± 0.5; p = 0.43).
  
  
  CONCLUSIONS
  Niacin as add-on treatment to high dose statins in patients with established CAD significantly improves lipid profile. However, these changes were not associated with improved endothelial or microvascular function. Registered clinical trial with clinicaltrials.gov: NCT00150722.
authors.affiliation: Department of Cardiology, Lyell McEwin Hospital, Elizabeth Vale, Adelaide, South Australia 5000, Australia. aphilp02@gmail.com
authors.forename: Andrew C
authors.initials: AC
authors.lastname: Philpott
authors.forename: Jaroslav
authors.initials: J
authors.lastname: Hubacek
authors.forename: Yichun C
authors.initials: YC
authors.lastname: Sun
authors.forename: Darlene
authors.initials: D
authors.lastname: Hillard
authors.forename: Todd J
authors.initials: TJ
authors.lastname: Anderson
mesh_terms: D000368:Aged; D000069059:Atorvastatin; D003324:Coronary Artery Disease / Q000188:drug therapy*; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006538:Heptanoic Acids / Q000627:therapeutic use*; D006801:Humans; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors / Q000627:therapeutic use*; D052456:Hypoalphalipoproteinemias / Q000188:drug therapy; D000960:Hypolipidemic Agents / Q000627:therapeutic use; D008055:Lipids / Q000097:blood; D008297:Male; D008875:Middle Aged; D009525:Niacin / Q000008:administration & dosage*; D011758:Pyrroles / Q000627:therapeutic use*
chemical_list: D006538:Heptanoic Acids; D019161:Hydroxymethylglutaryl-CoA Reductase Inhibitors; D000960:Hypolipidemic Agents; D008055:Lipids; D011758:Pyrroles; D009525:Niacin; D000069059:Atorvastatin