Effects of High-Dose Modified-Release Nicotinic Acid on Atherosclerosis and Vascular Function

Lee, Justin; Robson, Matthew D.; Yu, Ly-Mee; Shirodaria, C; Cunnington, Colin; Kylintireas, I; Digby, Janet E.; Bannister, Thomas D.; Handa, Ashok; Wiesmann, Frank; Durrington, Paul N.; Channon, Keith M.; Neubauer, Stefan; Choudhury, Robin P.

doi:10.1016/j.jacc.2009.06.036

Cited by 233 publications

(116 citation statements)

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“…In patients with CAD, the addition of niacin significantly improved endothelial function in patients with low HDLcholesterol levels [217,218]. In statin-treated patients with low HDL-cholesterol and CVD (65% T2D with CAD), 12 months of niacin treatment, when compared with placebo, significantly reduced carotid atherosclerosis, but did not alter either aortic distensibility or brachial artery FMD [219]. Statin-treated T2D with LDL-cholesterol <2.5mmol/L and ED were randomized to niacin (nicotinic acid prolonged release) or no additional therapy [220].…”

Section: Combination Therapiesmentioning

confidence: 97%

Endothelial Dysfunction in Diabetes: Pathogenesis, Significance, and Treatment

2013

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■ AbstractType 2 diabetes (T2D) markedly increases the risk of cardiovascular disease. Endothelial dysfunction (ED), an early indicator of diabetic vascular disease, is common in T2D and independently predicts cardiovascular risk. Although the precise pathogenic mechanisms for ED in T2D remain unclear, at inception they probably involve uncoupling of both endothelial nitric oxide synthase activity and mitochondrial oxidative phosphorylation, as well as the activation of vascular nicotinamide adenine dinucleotide phosphate oxidase. The major contributing factors include dyslipoproteinemia, oxidative stress, and inflammation. Therapeutic interventions are designed to target these pathophysiological factors that underlie ED. Therapeutic interventions, including lifestyle changes, antiglycemic agents and lipid-regulating therapies, aim to correct hyperglycemia and atherogenic dyslipidemia and to improve ED. However, high residual cardiovascular risk is seen in both research and clinical practice settings. Well-designed studies of endothelial function in appropriately selected volunteers afford a good opportunity to test new therapeutic interventions, paving the way for clinical trials and utilization in the care of the diabetic patient. However, based on the results from a recent clinical trial, niacin should not be added to a statin in individuals with low high-density lipoprotein cholesterol and very well controlled low-density lipoprotein cholesterol.

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Section: Combination Therapiesmentioning

confidence: 97%

Endothelial Dysfunction in Diabetes: Pathogenesis, Significance, and Treatment

2013

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“…However, a recent study clearly showed that HDL isolated from subjects with T2DM after 3 months of treatment with niacin displayed an improved ability to stimulate NO production, to reduce reactive oxygen species, and to promote EPC-mediated endothelial repair in vitro when compared to HDL isolated at baseline (Sorrentino et al 2010), further strengthening the concept that plasma HDL-C and its change may not be a reliable indicator of HDL function. Recent studies analyzed the effect of niacin treatment in patients with established CAD on top of the existing statin therapy; two of them failed to detect any significant improvement of FMD, while in one case FMD was significantly increased only in the subgroup of patients with a low baseline HDL-C level (Lee et al 2009;Philpott et al 2013;Warnholtz et al 2009). …”

Section: Niacinmentioning

confidence: 99%

Effects of Established Hypolipidemic Drugs on HDL Concentration, Subclass Distribution, and Function

Gomaraschi

Adorni

Banach

et al. 2014

Handbook of Experimental Pharmacology

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“…Magnetic resonance imaging enables characterization of plaque burden and composition, with early studies reporting the favorable effects of statins 82 and niacin. 83 However, this technique is limited to imaging larger arteries and at this point in time evaluation of the effect of novel therapies on coronary atherosclerosis is not possible. The ability to combine these non-invasive techniques with molecular targeted agents will enable study of the effects of therapies on specific factors in atherosclerotic plaque that is involved in rupture.…”

Section: Non-invasive Imagingmentioning

confidence: 99%