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The Benefits of Niacin in Atherosclerosis

Wednesday, December 3rd, 2008

(excerpts selected from the full text)

by S. Tavintharan, MD, and Moti L. Kashyap, MD

Cholesterol Research Center, Department of Veterans Affairs
Healthcare System, University of California, Irvine,
5901 East Seventh Street (11/111-I)
Long Beach, CA 90822, USA.
E-mail: moti.kashyap@med.va.gov
Current Atherosclerosis Reports 2001, 3:74–82
Current Science Inc. ISSN 1523-3804
Copyright © 2001 by Current Science Inc.

Niacin favorably alters all major lipid subfractions at pharmacologic doses. Alone or in combination, it promotes regression of coronary artery disease, decreases coronary events, stroke, and total mortality.

Major recent progress in niacin is in four areas. Firstly, recent data indicate that it increases high-density lipoprotein (HDL) and lowers triglycerides and low-density lipoprotein (LDL) by mechanisms different from statins, fibrates, and bile-sequestrants, giving rationale for combination therapy to achieve synergistic effects for complete lipid goal achievement.

Secondly, new data on an extended-release preparation of niacin given once nightly indicates that it is as effective and has greater tolerability than immediate-release niacin.

Thirdly, preliminary data with a single tablet formulation extended-release niacin and an HMG CoA reductase inhibitor (lovastatin) shows it to be safe and very effective, especially for raising HDL.

Finally, emerging evidence indicates that niacin can be used effectively and safely in patients with type 2 diabetes mellitus, who often have low HDL levels.

Introduction
Niacin, an essential B vitamin, has favorable effects on all major lipid subfractions at pharmacologic doses [1•]. Reports of its use in lipid-lowering therapy have been available since 1955 [2]. Although it is a potent lipid modifying agent, its usefulness in the past has been limited by adverse events. Nevertheless, there is renewed interest on the back of convincing data from clinical trials [3–9] and the development and availability of newer formulations of this agent. Tables 1 and 2 highlight the key facts of these clinical trials, which indicate that this agent significantly reduces atherosclerotic cardiovascular disease complications and total mortality.

The Veteran Affairs HDL Intervention Trial (VA-HIT) [10•] showed for the first time that increasing high-density lipoprotein (HDL) cholesterol and decreasing triglycerides (TG) (even without altering low-density lipoprotein [LDL] cholesterol) with gemfibrozil significantly reduced the risk of recurrent major cardiovascular events. The Bezafibrate Infarction Prevention (BIP) study [11] showed similar benefits, significantly in the subgroup with TG greater than 200 mg/dL.

With evidence showing extended-release niacin gives a twofold greater HDL cholesterol increase when compared with gemfibrozil [12•], there is strong rationale for the use of niacin for targeting increases in HDL cholesterol to prevent or reduce progression of atherosclerotic disease.

Efficacy and Toxicity of Niacin
The benefits of niacin in atherosclerosis are not surprising, looking at the broad-spectrum effects on the lipid profile.

Lowering of total cholesterol (TC), LDL cholesterol, very low-density lipoprotein (VLDL) cholesterol, TG, small dense LDL, apolipoprotein (apo) B, and lipoprotein (a) [Lp(a)] are achieved with niacin. In addition, it is also the most potent agent to raise HDL cholesterol, thus favorably reducing the ratios of total cholesterol to HDL cholesterol, and LDL cholesterol to HDL cholesterol, and apo B to apo A1.

The magnitude of cholesterol modification depends on patients’ baseline lipid levels and on the dose and preparation of niacin. On average it lowers LDL cholesterol by 15% to 30%, TG by 20% to 40%, Lp(a) by 30% to 40%, and raises HDL cholesterol by 15% to 30%.

Evidence suggests that antiatherogenic properties for LPAI particles (HDL cholesterol subfraction containing apo AI without apo AII) are greater than LP-AI +AII particles (HDL cholesterol subfraction containing apo AI with apo AII particles) [1•].

Niacin, apart from being the most potent agent in raising HDL cholesterol, has also been shown to improve HDL cholesterol quality by selectively increasing LPAI compared with LP-AI + AII particle concentration in patients with low HDL cholesterol levels [13].

Besides quantitative changes in LDL cholesterol levels, niacin mediates the generation of the more buoyant, less dense LDL particles. Data from observational studies by Austin et al. [14] show that small dense LDL particles are associated with a threefold risk of myocardial infarction (MI), and this is not related to LDL cholesterol levels [15].

The importance of reduction of this LDL subfraction thus assumes greater significance. Hydroxy methyl glutaryl (HMG) CoA reductase inhibitors (statins), which powerfully lower LDL cholesterol, do not decrease small dense LDL concentration [16], whereas fibrates like niacin do [17].

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Tags: cholesterol, Enduracin, HDL, inflammatory markers, LDL, Lipoprotein, lipoprotein-associated phospholipase, niacin
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Effects of Extended-Release Niacin on Lipoprotein Particle Size, Distribution, and Inflammatory Markers in Patients With Coronary Artery Disease .

Thursday, October 9th, 2008

The American Journal of Cardiology , Volume 98 , Issue 6 , Pages 743 - 745
J . Kuvin , D . Dave , K . Sliney , P . Mooney , A . Patel , C . Kimmelstiel , R . Karas

In this study, niacin was added to existing therapy for 3 months in 54 subjects with stable coronary artery disease. Average total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglyceride levels were similar between groups.
Three months of niacin treatment increased total HDL by 7.5% and decreased triglycerides by 15% compared with baseline values (p <0.005 for each), whereas total cholesterol and LDL levels remained unchanged. Addition of niacin resulted in a 32% increase in large-particle HDL (p <0.001), an 8% decrease in small-particle HDL (p = 0.0032), an 82% increase in large-particle LDL (p = 0.09), and a 12% decrease in small-particle LDL (p = 0.008).

Niacin decreased lipoprotein-associated phospholipase A2 and C-reactive protein levels (20% and 15%, respectively, p <0.05 for the 2 comparisons). No significant changes from baseline were seen in any tested parameter in subjects who received placebo.

In conclusion, addition of niacin to existing medical regimens for patients with coronary artery disease and already well-controlled LDL levels favorably improves the distribution of lipoprotein particle sizes and inflammatory markers in a manner that would be expected to confer atheroprotection…
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