Use of Niacin, Statins, and Resins in Patients With Combined Hyperlipidemia

Brown, B. Greg; Zambón, Alberto; Poulin, Drew; Rocha, Anita; Maher, Vincent; Davis, Joseph; Albers, John J.; Brunzell, John D.

doi:10.1016/s0002-9149(98)00039-3

Cited by 54 publications

(22 citation statements)

References 18 publications

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“…HDL-C correlated signifi cantly with a change in severity of proximal stenosis, as did apo B, apo A-I, and LDL-C. Clinical events occurred in 19% of patients who received placebo-colestipol therapy, compared with 4.2% of those who received niacin-colestipol therapy and 6.5% of those receiving colestipol plus statin. In a small follow-up study in subgroups with high and low levels of triglycerides treated with the same combinations of agents as in the original study, persons with high triglyceride and low HDL-C levels showed reduced severity of coronary stenosis with intensive combination therapy [ 70 ].…”

Section: Combination Therapy With Multiple Agentssupporting

confidence: 87%

When high is low: Raising low levels of high-density lipoprotein cholesterol

Tóth

2008

Curr Cardiol Rep

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Low serum levels of high-density lipoprotein cholesterol (HDL-C) are highly prevalent and are recognized as an independent risk factor for cardiovascular morbidity (myocardial infarction, stroke, peripheral arterial disease, and restenosis after coronary stenting) and mortality. HDL plays an important role in modulating atherogenesis, although its functions are varied and complex and the mechanisms for its antiatherogenic effects have not been completely elucidated. The inverse relationship between HDL-C and cardiovascular risk is well established, and epidemiologic studies and clinical trials have provided ample evidence that higher levels of HDL-C are vasculoprotective. Although considerable interest exists in the development of novel approaches to raise serum HDL-C and to augment HDL functionality, this article discusses currently available therapies to raise suboptimal levels of this important lipoprotein.

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Section: Combination Therapy With Multiple Agentssupporting

confidence: 87%

When high is low: Raising low levels of high-density lipoprotein cholesterol

Tóth

2008

Curr Cardiol Rep

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“…When combined with colestipol, a bile-acid sequestrant, in the FATS (Familial Pharmacotherapy and Effects on HDL-C Table 3 Pharmacotherapy and Effects on HDL-C (155) 15%-35% AIM-HIGH (156); HPS2-THRIVE (157) Fibrates PPAR␣ agonism resulting in ABCA1 up-regulation and synthesis, and ApoA-I transcription (122,(162)(163)(164)(165)(166)(167) Helsinki Heart Study (168), VA-HIT (169), BIP (171), FIELD (173) 10%-15% ACCORD (188) Thiazolidinediones PPAR␥ agonism resulting in cellular differentiation in vascular tissue and adipocytes (190) PROACTIVE (193), CHICAGO (194), PERISCOPE (195), RECORD (197) 5%-10% - Atherosclerosis Treatment Study), HDL-C increased by 43%, with angiographic atherosclerotic regression in 39% and a 73% reduction in CHD rates over a 2.5-year follow-up period (139). After 10 years of niacin combined with both colestipol and lovastatin, there was an 18.5% absolute risk reduction in all-cause mortality (140). The CLAS (Cholesterol-Lowering Atherosclerosis Study) also evaluated the effect of combining colestipol with niacin in 162 men who had prior coronary artery bypass graft surgery, and demonstrated an HDL-C increase by 37%, with angiographic regression of atherosclerosis of 16% at 2 years and 18% at 4 years (141,142).…”

Section: Pharmacological Interventionsmentioning

confidence: 99%

High-Density Lipoprotein and Coronary Heart Disease

Natarajan

Ray

Cannon

2010

Journal of the American College of Cardiology

184

129

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Coronary heart disease remains a major cause of worldwide morbidity and mortality despite therapeutic advances that control many risk factors such as low-density lipoprotein cholesterol to levels lower than previously possible. Population studies have consistently demonstrated an inverse association between high-density lipoprotein cholesterol (HDL-C) levels with the risk of coronary heart disease. As a result, HDL-C is gaining increasing interest as a therapeutic target. In this review, we explore the protective mechanisms of HDL and how current and future therapies harness these beneficial properties. We offer a biological framework to understand treatment strategies as well as their resultant successes and failures to guide management and future directions. At present, raising HDL-C level holds great promise, on the basis of epidemiology and initial trials, but we await the outcomes of the many large clinical outcomes trials currently under way to define the clinical role of older and novel therapies to raise HDL-C level.

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“…At the end of the trial period, patients in the treatment group had a 26% relative risk reduction in all-cause mortality (21.9% versus 29.7%; p < 0.05) and a 36% relative risk reduction in cardiovascular mortality [Brown et al 1990[Brown et al , 1998 apoB, apolipoprotein B; CHD, coronary heart disease; CI, confidence interval; CV, cardiovascular; HDL-C, high-density lipoprotein cholesterol; LDL-C, low-density lipoprotein cholesterol; MI, myocardial infarction; TIA, transitory ischemic attack.…”

Section: Adipose Tissuementioning

confidence: 99%

The facts behind niacin

Hochholzer

Berg

Giugliano

2011

Therapeutic Advances in Cardiovascular Disease

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Although low-density lipoprotein cholesterol (LDL-C) lowering represents the mainstay of current lipid treatment, high-density lipoprotein cholesterol (HDL-C) has generated increasing interest as a secondary therapeutic target because of strong evidence that serum HDL-C concentration is inversely associated with coronary heart disease risk. Niacin is a lipid-altering drug that has been used to lower cholesterol since the 1950s. In addition to its LDL-C-lowering effects, niacin is the most effective agent currently available for raising HDL-C. Despite its long history as a lipid-altering drug, only limited data are available regarding its clinical benefit alone and in combination with other agents, and the majority of studies investigating its impact on clinical outcomes are from the pre-statin area. Several studies have demonstrated a beneficial effect of treatment with niacin in combination with statin therapy on surrogate cardiovascular markers (e.g. carotid intima-media thickness). However, the clinical significance of these surrogate markers has been questioned. Two large randomized trials will address whether niacinstatin combination therapy is an appropriate therapeutic alternative to statin monotherapy.

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Use of Niacin, Statins, and Resins in Patients With Combined Hyperlipidemia

Cited by 54 publications

References 18 publications

When high is low: Raising low levels of high-density lipoprotein cholesterol

When high is low: Raising low levels of high-density lipoprotein cholesterol

High-Density Lipoprotein and Coronary Heart Disease

The facts behind niacin

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