Efficacy of controlled-release niacin in treatment of metabolic syndrome: Correlation to surrogate markers of atherosclerosis, vascular reactivity, and inflammation

Vaccari, Christopher S.; Nagamia, Sameer; Thoenes, Martin; Oguchi, Asahiko; Hammoud, Ramadan; Khan, Bobby V.

doi:10.1016/j.jacl.2007.10.002

Cited by 15 publications

(9 citation statements)

References 27 publications

(27 reference statements)

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“…The median hsCRP reduction of 23% in the present study is consistent with improved vascular reactivity reported for niacin34 and statin 35 treatment. The greater decrease in CRP may reflect its hepatic origin compared to TNFα and IL-6 which reflect inflammation elsewhere, particularly adipose tissue.…”

Section: Discussionsupporting

confidence: 90%

The SLIM study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

Knopp

Retzlaff

Fish

et al. 2009

Journal of Clinical Lipidology

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Background-The combination of niacin and statin has proven value in hyperlipidemia management and heart disease prevention. However, the efficacy of the non-prescription time-release niacin, Slo-Niacin®, is little studied alone and not at all with atorvastatin. We gave Slo-Niacin® and atorvastatin, singly and together to determine efficacy on the combined abnormalities of triglyceride, LDL and HDL.

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Section: Discussionsupporting

confidence: 90%

The SLIM study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

Knopp

Retzlaff

Fish

et al. 2009

Journal of Clinical Lipidology

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“…In subjects with the metabolic syndrome, Vaccari et al, Westphal et al, and Thoenes et al demonstrated a significant increases in HDL-C, but Westphal et al failed to show corresponding improvements in flow mediated dilation, while Vaccari et al and Thoenes et al treated subjects with niacin for 52 weeks. 16-18 In subjects with coronary artery disease already on statin therapy, Kuvin et al showed a significant increase in HDL-C and corresponding improvement in FMD, while Andrews et al were unable to show increased FMD despite increasing their subjects’ HDL-C by >25%. 7,19 Warnholtz et al were only able to demonstrate improved FMD in the tertile of subjects who began with HDL-C < 45.…”

Section: Discussionmentioning

confidence: 99%

“…21,22 All of these authors used niacin dosing equivalent to or below our chosen 1500mg, but 3 chose to treat for longer than 12 weeks. 16,18,19,23 Furthermore recently, a meta-analysis was published in JACC, which concluded that while niacin reduces cardiovascular disease events, this reduction was not directly related to patients’ changes in HDL-C. 24,25 …”

Section: Discussionmentioning

confidence: 99%

Effect of Extended-Release Niacin on Serum Lipids and on Endothelial Function in Adults With Sickle Cell Anemia and Low High-Density Lipoprotein Cholesterol Levels

Scoffone

Krajewski

Zorca

et al. 2013

The American Journal of Cardiology

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Through bound apolipoprotein A-I (apoA-I), high density lipoprotein cholesterol (HDL-C) activates endothelial nitric oxide synthase, inducing vasodilation. Because patients with sickle cell disease (SCD)have low apoA-I andendothelial dysfunction,we conducted a randomized, double-blinded, placebo-controlled trial to test whether extended-release niacin (niacin-ER) increases apoA-I-containing HDL-C, and improves vascular function in SCD. Twenty-seven SCD patientswith HDL-C <39 mg/dL or apoA-I <99 mg/dL were randomized to 12 weeks of niacin-ER, increased in 500mg increments to a maximum of 1500mg daily, or placebo. The primary outcome was the absolute change in HDL-C after 12 weeks, with endothelial function assessed before and at the end of treatment. Niacin-ER-treated patients trended to greater increase in HDL-C compared with placebo treatment at 12 weeks (5.1±7.7 vs. 0.9±3.8 mg/dL, one-tailed p=0.07), associated with significantly greater, improvements in the ratios of low-density lipoprotein to HDL-C (1.24 vs. 1.95, p = 0.003), and apolipoprotein B to apoA-I (0.46 vs. 0.58, p = 0.03) compared with placebo-treated patients. No improvements were detected in three independent vascular physiology assays of endothelial function. Thus, the relatively small changes in HDL-C achieved by the dose of niacin-ER used in our study are not associated with improved vascular function in patients with SCD with initially low levels of apoA-I or HDL-C.

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“…After careful assessment of full-texts, seven articles were found to fulfill the inclusion criteria and were selected for meta-analysis. [15][16][17][18][19][20][21] Reasons for rejecting the other 12 articles were: not measuring FMD, [29][30][31][32][33][34] not having a randomized design, 35 not including an appropriate control group, 36 FMD not being measured in the brachial artery, 37 insufficient data on baseline and/or endpoint FMD values, 22,38 and not being in the English language. 39 A summary of the study selection process is illustrated in Figure 1.…”

Section: Flow Of Included Studiesmentioning

confidence: 99%

Effect of niacin on endothelial function: A systematic review and meta-analysis of randomized controlled trials

Sahebkar

2014

Vasc Med

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Endothelial dysfunction is an independent predictor of incident atherosclerotic cardiovascular disease (ACVD). Niacin possesses high-density lipoprotein (HDL)-elevating, antioxidant and anti-inflammatory properties, all potentially contributing to the amelioration of endothelial function. However, controversies exist among trials reporting the effects of niacin on endothelium-dependent flow-mediated dilation (FMD) as a reliable surrogate of endothelial function. The objective of this study was to assess the effect of niacin on brachial artery FMD using a meta-analysis of available evidence. MEDLINE and Scopus databases were searched for randomized controlled trials investigating the impact of niacin therapy on brachial artery FMD. Meta-analysis of eligible studies was conducted using a random-effects model. Pooled effects were measured by weighted mean difference (WMD) and 95% confidence intervals (CIs). Quality assessment, and subgroup, meta-regression and sensitivity analyses were conducted using standard methods. Among 596 citations, 19 full-text articles were read and seven were found to be eligible for inclusion. Eligible studies involved 441 subjects comprising 228 in the niacin and 213 in the control groups. Niacin therapy significantly improved FMD (WMD: 1.98%; 95% CI: 0.91-3.05%; p = 0.0003) and this effect was robust in the sensitivity analysis. The effect size was greater in the subgroup of studies administering higher doses of niacin (≥ 2000 mg/day) as well as those studies administering niacin for primary prevention of ACVD. Metaregression indicated no association between niacin-induced changes in FMD and changes in plasma HDL-cholesterol, lowdensity lipoprotein-cholesterol or triglycerides. None of the included studies could find any significant effect of niacin on nitroglycerin-mediated dilation. In conclusion, treatment with niacin improves endothelial function.

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Efficacy of controlled-release niacin in treatment of metabolic syndrome: Correlation to surrogate markers of atherosclerosis, vascular reactivity, and inflammation

Cited by 15 publications

References 27 publications

The SLIM study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

The SLIM study: Slo-Niacin® and Atorvastatin Treatment of Lipoproteins and Inflammatory Markers in Combined Hyperlipidemia

Effect of Extended-Release Niacin on Serum Lipids and on Endothelial Function in Adults With Sickle Cell Anemia and Low High-Density Lipoprotein Cholesterol Levels

Effect of niacin on endothelial function: A systematic review and meta-analysis of randomized controlled trials

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