title: Effects of oral niacin on endothelial dysfunction in patients with coronary artery disease: results of the randomized, double-blind, placebo-controlled INEF study.
abstract: High-density-lipoproteins-cholesterol (HDL-C) is invertedly related to the incidence of cardiovascular events. Recent studies suggest that HDL-C directly improves endothelial function. Nicotinic acid (niacin) effectively raises serum HDL-C. We therefore hypothesized that treatment with niacin improves endothelial dysfunction in patients with coronary artery disease (CAD). One hundred seven patients with CAD were randomly assigned to double-blinded treatment for 12 weeks with extended-release (ER)-niacin 1000 mg/day (N) or placebo (C), respectively. Flow-mediated dilation (FMD) of the brachial artery, nitroglycerin-mediated endothelium-independent dilation (NMD) and serum lipid concentrations were measured before and after treatment. Triglycerides (P=0.013), low-density-lipoprotein-cholesterol (LDL-C) (P=0.013) and HDL-C (P<0.0001) were altered by N compared to C. Niacin treatment was without effect on FMD or NMD, respectively, compared to placebo. However, post-hoc subgroup analysis revealed an improvement in FMD in patients with low HDL-C at baseline (absolute change in FMD (mean+/-S.D.) N: +3.25+/-3.88%, C: +1.03+/-2.71% in low tertile HDL-C <or=45 mg/dl. P=0.047). The present findings indicate that ER-niacin treatment improves endothelial dysfunction in patients with CAD and low HDL-C, but not with normal HDL-C.
authors.affiliation: Department of Medicine II, Johannes Gutenberg-University Mainz, Mainz, Germany. warnholt@uni-mainz.de
authors.forename: Ascan
authors.initials: A
authors.lastname: Warnholtz
authors.forename: Philipp
authors.initials: P
authors.lastname: Wild
authors.forename: Mir Abolfazl
authors.initials: MA
authors.lastname: Ostad
authors.forename: Veronika
authors.initials: V
authors.lastname: Elsner
authors.forename: Fabian
authors.initials: F
authors.lastname: Stieber
authors.forename: Reinhard
authors.initials: R
authors.lastname: Schinzel
authors.forename: Ulrich
authors.initials: U
authors.lastname: Walter
authors.forename: Dirk
authors.initials: D
authors.lastname: Peetz
authors.forename: Karl
authors.initials: K
authors.lastname: Lackner
authors.forename: Stefan
authors.initials: S
authors.lastname: Blankenberg
authors.forename: Thomas
authors.initials: T
authors.lastname: Munzel
mesh_terms: D000284:Administration, Oral; D000368:Aged; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000187:drug effects; D001916:Brachial Artery / Q000000981:diagnostic imaging / Q000187:drug effects* / Q000503:physiopathology; D015815:Cell Adhesion Molecules / Q000097:blood; D008076:Cholesterol, HDL / Q000097:blood; D008078:Cholesterol, LDL / Q000097:blood; D003324:Coronary Artery Disease / Q000097:blood / Q000188:drug therapy* / Q000503:physiopathology; D003692:Delayed-Action Preparations; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000187:drug effects* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008840:Microfilament Proteins / Q000097:blood; D008875:Middle Aged; D009525:Niacin / Q000008:administration & dosage*; D005996:Nitroglycerin / Q000008:administration & dosage; D010750:Phosphoproteins / Q000097:blood; D010766:Phosphorylation; D011446:Prospective Studies; D016896:Treatment Outcome; D014280:Triglycerides / Q000097:blood; D014463:Ultrasonography; D014664:Vasodilation / Q000187:drug effects*; D014665:Vasodilator Agents / Q000008:administration & dosage*; D000098662:Vasodilator-Stimulated Phosphoprotein
chemical_list: D015415:Biomarkers; D001786:Blood Glucose; D015815:Cell Adhesion Molecules; D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D003692:Delayed-Action Preparations; D008840:Microfilament Proteins; D010750:Phosphoproteins; D014280:Triglycerides; D014665:Vasodilator Agents; D000098662:Vasodilator-Stimulated Phosphoprotein; D009525:Niacin; D005996:Nitroglycerin