International Journal of Clinical Practice
Volume 61 Issue 11 Page 1942-1948, November 2007

The effects of extended-release niacin on carotid intimal media
thickness, endothelial function and inflammatory markers in patients
with the metabolic syndrome

M. Thoenes11Institut für klinische Pharmakologie, Technische
Universität Dresden, Dresden, Germany, A. Oguchi22Division of
Cardiology, Emory University School of Medicine, Atlanta, GA, USA, S.
Nagamia22Division of Cardiology, Emory University School of Medicine,
Atlanta, GA, USA, C. S. Vaccari22Division of Cardiology, Emory
University School of Medicine, Atlanta, GA, USA, R. Hammoud22Division
of Cardiology, Emory University School of Medicine, Atlanta, GA, USA,
G. E. Umpierrez22Division of Cardiology, Emory University School of
Medicine, Atlanta, GA, USA, B. V. Khan22Division of Cardiology, Emory
University School of Medicine, Atlanta, GA, USA1Institut für klinische
Pharmakologie, Technische Universität Dresden, Dresden, Germany
2Division of Cardiology, Emory University School of Medicine, Atlanta,
GA, USA
Bobby V. Khan, MD, PhD,
Division of Cardiology, Emory University School of Medicine, 69 Jesse
Hill Jr Dr SE, Suite C247, Atlanta, GA 30303, USA
Tel.: + 1 404 616 4440
Fax: + 1 404 616 4400
Email: bkhan@emory.edu
Disclosures The authors have declared that they have no interests
which might be perceived as posing a conflict or bias.

Summary

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.

Methods and 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.

Conclusion: 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.