Revisiting niacin: reviewing the evidence

Vaccari, Christopher S.; Hammoud, Ramadan; Nagamia, Sameer; Ramasamy, Kanni; Dollar, Allen L.; Khan, Bobby V.

doi:10.1016/j.jacl.2007.07.008

Cited by 13 publications

(10 citation statements)

References 75 publications

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“…The immediate-release niacin (crystalline) formulation is quickly absorbed and is associated with more flushing and less hepatotoxicity. On the other hand the older long-acting niacin preparations are absorbed very slowly, resulting in reduced flushing, but significantly increasing the risk of serious, dose-related hepatotoxicity [12]. The extended-release niacin (Niaspan; Abbott Laboratories, Chicago, Illinois, USA) formulation that was introduced 10 years ago has a more balanced metabolism, resulting in less flushing and lower risk of hepatotoxic effects compared with the other formulations.…”

Section: Introductionmentioning

confidence: 99%

“…The extended-release niacin (Niaspan; Abbott Laboratories, Chicago, Illinois, USA) formulation that was introduced 10 years ago has a more balanced metabolism, resulting in less flushing and lower risk of hepatotoxic effects compared with the other formulations. Extended-release niacin is absorbed between 8-12 h. This also makes it suitable for once-daily bedtime dosing [12]. Very recently, a newly reformulated 1000 mg extended-release niacin was introduced to the market [Niaspan (film coated), Abbott Laboratories, Chicago, Illinois (USA)].…”

Section: Introductionmentioning

confidence: 99%

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Nicotinic acid: recent developments

Kamanna

Kashyap

2008

Current Opinion in Cardiology

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Nicotinic acid: recent developments

Kamanna

Kashyap

2008

Current Opinion in Cardiology

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“…The immediate-release niacin (crystalline) formulation is quickly absorbed and is associated with more fl ushing and less hepatotoxicity. The older, long-acting niacin preparations are absorbed very slowly, resulting in reduced fl ushing, but signifi cantly increasing the risk of serious dose-related hepatotoxicity [44]. The ER niacin (Niaspan; Abbott, Abbott, IL) formulation that was introduced 10 years ago has a more balanced metabolism, resulting in less fl ushing and less risk of hepatotoxic effects compared with the other formulations.…”

Section: Newer Formulations Of Niacin To Minimize Adverse Flushing Rementioning

confidence: 99%

“…ER niacin is absorbed between 8 and 12 hours after ingestion. This also makes it suitable for once-daily bedtime dosing [44]. Very recently, a newly reformulated niacin ER of 1000 mg was introduced to the market (Niaspan [fi lm coated]; Abbott, Abbott, IL).…”

Section: Newer Formulations Of Niacin To Minimize Adverse Flushing Rementioning

confidence: 99%

Niacin: An old drug rejuvenated

Kamanna¹,

Ganji²,

Kashyap³

2008

Curr Atheroscler Rep

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Niacin has long been used in the treatment of dyslipidemia and cardiovascular disease. Recent research on niacin has been focused on understanding the mechanism of action of niacin and preparation of safer niacin formulations. New findings indicate that niacin does the following: 1) it inhibits hepatic diacylglycerol acyltransferase 2, resulting in inhibition of triglyceride synthesis and decreased apolipoprotein B-containing lipoproteins; 2) it decreases the surface expression of hepatic adenosine triphosphate synthase beta-chain, leading to decreased holoparticle high-density lipoprotein catabolism and increased high-density lipoprotein levels; and 3) it increases redox potential in arterial endothelial cells, resulting in inhibition of redox-sensitive genes. Flushing, an adverse effect of niacin, results from niacin receptor GPR109A-mediated production of prostaglandin D2 and E2 via DP1 and EP2/4 receptors. DP1 receptor antagonist (laropiprant) attenuates the niacin flush. A reformulated preparation of extended-release niacin (Niaspan; Abbott, Abbott Park, IL) lowers flushing compared with an older Niaspan formulation. These advancements in niacin research have rejuvenated its use for the treatment of dyslipidemia and cardiovascular disease.

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“…Aggressive lipid management with statins has been shown to improve vascular reactivity (13). Other lipid therapies such as niacin and fibrates also may contribute (14,15). The recently released highly selective beta-1 receptor antagonist nebivolol has also been shown to improve vascular function, potentially through a nitric oxide-mediated mechanism (16).…”

mentioning

confidence: 99%

Endothelial Dysfunction Associated With Drug-Eluting Stents

Muhlestein¹

2008

Journal of the American College of Cardiology

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The advent of drug-eluting stents (DES) into the practice of interventional cardiology has had a tremendous impact. After their demonstration of a significant reduction in restenosis in randomized trials and U.S. Food and Drug Administration approval for their use in 2003, the incorporation of DES into clinical practice was rapid and extensive. However, beginning in 2004, a variety of reports began to circulate documenting an increased incidence of early, late, and very late stent thrombosis after DES implantation, especially after discontinuation of dual antiplatelet therapy (1). This was proposed to be caused by impaired endothelialization of the vessel at the site of stent deployment because of the presence of either the drug, the stent polymer, or both (2). Shortly thereafter, several studies reported another, more distant, effect of both sirolimus-coated See pages 2123 and 2130 and paclitaxel-coated stents, that of long-term endotheliumrelated vascular dysfunction detected in nonstented segments of the coronary artery (3-6). Although the precise mechanism of this distant vascular phenomenon was not known, because it was not apparent in vessels receiving bare-metal stents (BMS), it was presumed to be secondary to the presence of either the antiproliferative drug itself or its associated polymeric DES coating. Two important articles published in this issue of the Journal address these issues. One evaluates the effect on vascular function of chronic exposure to sirolimus (7). The other reports the results of a new DES, with both a different drug and a different polymeric coating, that does not seem to induce endothelial dysfunction (8). Although neither study completely answers all possible questions regarding this issue, they both contribute to our understanding of the underlying pathophysiology of the process and offer hope for a resolution of the problems with next-generation DES.In the article by Jabs et al. (7), a 7-day continuous infusion of sirolimus into Wistar rats produced a marked degree of endothelial dysfunction as well as a desensitization of the endothelium-independent vasodilator nitroglycerin, showing that the drug may play a specific role. The investigators also reported a possible mechanism, that of sirolimus increasing the production of vascular superoxide, with the result being a loss of vascular nitric oxide bioavailability. Although their rat model was one of prolonged systemic exposure to sirolimus, they proposed that these processes could contribute to the observed endothelial dysfunction noted after deployment of sirolimuscoated stents. There are several other important limitations to this study. First, it is not certain whether the sirolimus dosing in the rat study is comparable at the vascular level to that of a coronary artery containing a DES. Second, in the rat model, the presence of sirolimus adversely affected both endotheliumdependent and endothelium-independent vascular function. In the clinical studies of DES, it was only the endotheliumdependent vascular function that was ad...

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Revisiting niacin: reviewing the evidence

Cited by 13 publications

References 75 publications

Nicotinic acid: recent developments

Nicotinic acid: recent developments

Niacin: An old drug rejuvenated

Endothelial Dysfunction Associated With Drug-Eluting Stents

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