Effects of Extended-Release Niacin on Lipoprotein Particle Size, Distribution, and Inflammatory Markers in Patients With Coronary Artery Disease

Kuvin, Jeffrey T.; Dave, Devang M.; Sliney, Kathleen A.; Mooney, Paula; Patel, Ayan R.; Kimmelstiel, Carey; Karas, Richard H.

doi:10.1016/j.amjcard.2006.04.011

Cited by 123 publications

(94 citation statements)

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“…The reduction in Lp-PLA 2 mass after 12 weeks of treatment was 27%, 35% and 36% in the fenofibrate, simvastatin and combined treatment group, respectively [71]. Kuvin et al [74] randomized patients with CAD to extended release niacin versus placebo (on top of pre-existing lipid-lowering regimen) and reported a 20% reduction in Lp-PLA 2 with niacin.…”

Section: Other Agentsmentioning

confidence: 99%

“…Statins [70][71][72], fenofibrate [38,70,71,73], niacin [74], ezetimide [70] and orlistat [73] have been shown to decrease Lp-PLA 2 levels to varying degrees, but none are as potent as direct Lp-PLA 2 inhibition. Atorvastatin reduced Lp-PLA 2 by 20% and had the strongest effect when compared to fluvastatin, pravastatin, lovastatin and simvastatin [72].…”

Section: Other Agentsmentioning

confidence: 99%

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Lp-PLA2- a novel risk factor for high-risk coronary and carotid artery disease

Epps

Wilensky

2010

Journal of Internal Medicine

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Section: Other Agentsmentioning

confidence: 99%

Section: Other Agentsmentioning

confidence: 99%

Lp-PLA2- a novel risk factor for high-risk coronary and carotid artery disease

Epps

Wilensky

2010

Journal of Internal Medicine

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“…For example, statins ( 41,42 ), niacin ( 43 ), and CETP inhibitors ( 44 ) tend to increase the concentration of large, apoA-Icontaining HDLs. Fibrates, on the other hand, tend to increase levels of smaller HDL particles that contain both apoA-I and apoA-II ( 45 ).…”

Section: Hdls and Cholesterol Effluxmentioning

confidence: 99%

Cardioprotective functions of HDLs

Rye

Barter

2014

Journal of Lipid Research

253

170

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This article is available online at http://www.jlr.org inverse predictors of the risk of having a cardiovascular event ( 1-5 ); moreover, a low concentration of HDL cholesterol remains predictive of increased cardiovascular risk, even when low density lipoprotein (LDL) cholesterol has been reduced to very low levels by treatment with statins ( 6 ); ii ) HDLs have several well-documented functions with the potential to protect against cardiovascular disease ( 7,8 ); iii ) interventions that increase the concentration of HDLs inhibit the development and progression of atherosclerosis in several animal models ( 9-12 ); and iv ) in "proofof-concept" studies in humans, intravenous infusions of reconstituted HDLs (rHDLs) consisting of apoA-I complexed with phospholipids promote regression of coronary atheroma as assessed by intravascular ultrasound ( 13,14 ).However, interventions that increase the concentration of HDL cholesterol in humans have not yet been shown to translate into a reduction in clinical cardiovascular events. Indeed, recent human clinical trials investigating the effects of raising the level of HDL cholesterol by treatment with cholesteryl ester transfer protein (CETP) inhibitors or with niacin failed to demonstrate any clinical cardiovascular benefi t ( 15-17 ) (http://www.thrivestudy. org), and in one case, the treatment caused harm ( 15 ). A reasonable assumption that has been made from these studies is that the cholesterol content of HDLs is not the factor that protects. Thus, if HDLs do have direct cardioprotective properties, it follows from the human population studies that, while the concentration of HDL cholesterol is generally an excellent marker of the HDL functions that do protect, it does not invariably refl ect their cardioprotective functions. This is consistent with the fi nding in a recent Mendelian randomization study that some genetic mechanisms that raise the concentration of HDL cholesterol appear not to lower the risk of myocardial infarction ( 18 ). The authors of this analysis concluded that, while The proposition that high density lipoproteins (HDLs) protect against the development of cardiovascular diseases is based on a number of robust and consistent observations: i ) numerous human population studies have shown that the plasma concentrations of both HDL cholesterol and the major HDL apolipoprotein, apoA-I, are independent, Abbreviations: CETP, cholesteryl ester transfer protein; HO-1, heme oxygenase-1; PON-1, paraoxonase-1; rHDL, reconstituted HDL; SR-B1, scavenger receptor-B1; VCAM-1, vascular cell adhesion molecule-1.

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“…Several studies have confirmed this observation in patients with different types of dyslipidemia treated with 2, 3, or 4 g/day of regular or ER niacin (Johansson and Carlson 1990;Knopp et al 1998;Morgan et al 2003;Wahlberg et al 1990) and in patients with coronary artery disease (Kuvin et al 2006). A very recent study showed that also 1 g/day of ER niacin increases large HDL particles in dyslipidemic patients, with a concomitant significant increase in mean HDL size (Franceschini et al 2013).…”

Section: Niacinmentioning

confidence: 51%

“…In 2002, Kuvin et al demonstrated that a 3-month treatment with niacin improved FMD in patients with CAD and low HDL-C and that this improvement could be related to the HDL ability to increase eNOS protein abundance in vitro (Kuvin et al 2002). Some years later, the same authors also showed that in statin treated patients with established CAD, the addition of niacin caused a reduction of the plasma levels of inflammatory biomarkers as CRP and lipoproteinassociated phospholipase A2 (Kuvin et al 2006); unfortunately, likely due to the small number of participants, correlation analyses between changes of endothelial function parameters and the increase of HDL-C or other lipid variables were not performed (Kuvin et al 2006). Later on, the ability of niacin to improve FMD and reduce inflammatory biomarkers as CRP was confirmed in subjects with isolated low HDL-C (Benjo et al 2006), with the metabolic syndrome (Thoenes et al 2007), and in patients after myocardial infarction (Bregar et al 2013); the relationship between increase of HDL-C and changes of FMD was analyzed only in the latter case, and no correlation was found with any lipid parameter.…”

Section: Niacinmentioning

confidence: 80%