Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2: a double-blind, placebo-controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins

Taylor, Andrew; Sullenberger, LE; Hj, Lee; Jk, Lee; Grace, KA

doi:10.3810/psm.2008.12.22

Cited by 216 publications

(311 citation statements)

References 6 publications

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“…Niacin is currently the most effective HDL-C raising agent in clinical practice, by up to 30%. While early formulations had a favorable effect on outcomes [19] and progression of atherosclerotic disease [20][21][22], difficulties with tolerance due to flushing and recent reports of no benefit with extended release formulations [23] has dampened enthusiasm for this approach. An ongoing study is currently evaluating the potential efficacy of niacin in combination with blockade of epidermal prostanoid receptors, a major pathway implicated in flushing [24].…”

Section: Therapeutic Strategies For Hdlmentioning

confidence: 99%

ApoA-I Induction as a Potential Cardioprotective Strategy: Rationale for the SUSTAIN and ASSURE Studies

Nicholls

Gordon

Johannson

et al. 2012

Cardiovasc Drugs Ther

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Section: Therapeutic Strategies For Hdlmentioning

confidence: 99%

ApoA-I Induction as a Potential Cardioprotective Strategy: Rationale for the SUSTAIN and ASSURE Studies

Nicholls

Gordon

Johannson

et al. 2012

Cardiovasc Drugs Ther

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“…A 0.4% decrease in angiographically detected stenosis was noted. The benefit of Niacin was also investigated using CIMT as a surrogate of CAD risk in the ARBITER-2 study [36]. A similar cohort of patients, as investigated in the HATS study, was treated with statin, placebo or statin/niacin therapy.…”

Section: Hdl Elevation and Plaque Regressionmentioning

confidence: 99%

Atherosclerotic Plaque Regression: Fact or Fiction?

Shanmugam

Román-Rego

Ong

et al. 2010

Cardiovasc Drugs Ther

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Coronary artery disease is the major cause of death in the western world. The formation and rapid progression of atheromatous plaques can lead to serious cardiovascular events in patients with atherosclerosis. The better understanding, in recent years, of the mechanisms leading to atheromatous plaque growth and disruption and the availability of powerful HMG CoA-reductase inhibitors (statins) has permitted the consideration of plaque regression as a realistic therapeutic goal. This article reviews the existing evidence underpinning current therapeutic strategies aimed at achieving atherosclerotic plaque regression. In this review we also discuss imaging modalities for the assessment of plaque regression, predictors of regression and whether plaque regression is associated with a survival benefit.

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“…Niacin increases high-density lipoproteins (HDLs) by approximately 20-25 % and is the most effective clinically available drug for HDL cholesterol (HDL-C) elevation [9]. Clinical studies have indicated that treatment with niacin, either alone or in combination with statins, can slow or reverse the progression of atherosclerosis and reduce cardiovascular event rates and total mortality in patients with hypercholesterolemia and established atherosclerotic cardiovascular disease [10][11][12]. These beneficial effects are thought to result from the lipid-modifying effects of niacin.…”

Section: Introductionmentioning

confidence: 99%

Niacin improves ischemia-induced neovascularization in diabetic mice by enhancement of endothelial progenitor cell functions independent of changes in plasma lipids

et al. 2012

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Niacin was shown to inhibit acute vascular inflammation and improves endothelial dysfunction independent of changes in plasma lipids. Here, we investigated whether niacin can increase blood flow recovery after tissue ischemia by enhancing endothelial progenitor cell (EPC) functions in diabetic mice. Starting at 4 weeks after the onset of diabetes, vehicle or niacin (40 mg/kg/day) was administered daily by gavage to streptozotocin (STZ)-induced diabetic mice and diabetic endothelial nitric oxide synthase (eNOS)-deficient mice. Unilateral hindlimb ischemia surgery was conducted after 2 weeks of vehicle or niacin treatment. Compared to the control group, the niacin group had significantly increased ischemic/non-ischemic limb blood perfusion ratio and higher capillary density. These effects were markedly reduced in STZ-induced diabetic eNOS-deficient mice. Flow cytometry analysis showed impaired EPC-like cell (Sca-1(+)/Flk-1(+)) mobilization after ischemia surgery in diabetic mice but augmented mobilization in the mice treated with niacin. Diabetes was induced by administering STZ to FVB mice that received eGFP mouse bone marrow cells to evaluate effects of niacin on bone marrow-derived EPC homing and differentiation to endothelial cells. Differentiation of bone marrow-derived EPCs to endothelial cells in the ischemic tissue around vessels in diabetic mice that received niacin treatment, was significantly increased than that in control group. By in vitro studies, incubation with niacin in high-glucose medium reduced H(2)O(2) production, cell apoptosis, and improved high glucose-suppressed EPC functions by nitric oxide-related mechanisms. Our findings demonstrate that niacin increases blood flow recovery after tissue ischemia in diabetic mice through enhancing EPC mobilization and functions via nitric oxide-related pathways.

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Arterial Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER) 2: a double-blind, placebo-controlled study of extended-release niacin on atherosclerosis progression in secondary prevention patients treated with statins

Abstract: anti hypertensive therapy; blood pressure; hypertension.

Cited by 216 publications

References 6 publications

ApoA-I Induction as a Potential Cardioprotective Strategy: Rationale for the SUSTAIN and ASSURE Studies

ApoA-I Induction as a Potential Cardioprotective Strategy: Rationale for the SUSTAIN and ASSURE Studies

Atherosclerotic Plaque Regression: Fact or Fiction?

Niacin improves ischemia-induced neovascularization in diabetic mice by enhancement of endothelial progenitor cell functions independent of changes in plasma lipids

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