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niacin/infark

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Extended-release niacin/laropiprant improves endothelial function in patients after myocardial infarction.

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Raising high-density lipoprotein cholesterol (HDL-C) is an important strategy for reducing residual cardiovascular risk. In the present study, we sought to assess the effect of extended-release niacin/laropiprant on endothelial function in patients after a myocardial infarction with target
Niacin is a well established drug used to lower cholesterol and prevent cardiovascular disease events. However, niacin also causes cutaneous flushing side effects due to release of the proresolution mediator prostaglandin D2 (PGD2). Recent randomized clinical trials have demonstrated that addition
This post hoc analysis from the Coronary Drug Project (CDP) evaluated the effects of niacin monotherapy on clinical outcomes in patients with and without the metabolic syndrome (MS). The CDP was a randomized, placebo-controlled clinical trial of lipid-modifying agents in men with previous myocardial

Benefits of niacin by glycemic status in patients with healed myocardial infarction (from the Coronary Drug Project).

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The Coronary Drug Project, conducted during 1966 to 1974, was a randomized, double-blind, placebo-controlled trial of 5 lipid-modifying agents in 8,341 men with previous myocardial infarction. Among the 5 drug treatment regimens, only niacin significantly reduced the risk of (1) cardiovascular
The purpose of this study was to examine the hypothesis that erythrocytes that are low in n-3 fatty acids and high in trans-fatty acids and nutrient intakes are associated with the risk of atherosclerosis. Fifty patients with acute nonfatal myocardial infarction were recruited to measure their
OBJECTIVE To investigate the effects on cardiovascular outcomes of drug interventions that increase high density lipoprotein levels. METHODS Meta-analysis. METHODS Therapeutic benefit of niacin, fibrates, and cholesteryl ester transfer protein (CETP) inhibitors on cardiovascular events (all cause
OBJECTIVE To review literature relating to significant changes in drug therapy recommendations in the 1999 American College of Cardiology (ACC)/American Heart Association (AHA) guidelines for treating patients with acute myocardial infarction (AMI). METHODS 1999 ACC/AHA AMI guidelines,
Diabetes, one of the major risk factors of metabolic syndrome culminates in the development of Ischemic Heart Disease (IHD). Refined diets that lack micronutrients, mainly trivalent chromium (Cr(3+)) have been identified as the contributor in the rising incidence of diabetes. We investigated the

Niacin-bound chromium enhances myocardial protection from ischemia-reperfusion injury.

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A novel niacin-bound, chromium-based energy formula (EF; InterHealth Nutraceuticals, Benicia, CA) has been developed in conjunction with D-ribose, caffeine, ashwagandha extract (containing 5% withanolides), and selected amino acids. We have assessed the efficacy of oral administration of EF (40 mg x

Number-needed-to-treat analysis of the prevention of myocardial infarction and death by antidyslipidemic therapy.

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BACKGROUND Atherosclerosis of the coronary arteries is the most common cause of death in the United States for persons over the age of 45. Dyslipidemia is one of the risk factors for the development of coronary atherosclerosis. Recent studies suggest that treating dyslipidemia in persons with
BACKGROUND Metabolic syndrome is a powerful predictor of cardiovascular events independent of overt diabetes. Dietary restriction and weight loss modify metabolic syndrome components. This study addresses whether combination pharmacologic therapy focused on dyslipidemia provides additional

Raising high-density lipoprotein cholesterol with niacin and fibrates: a comparative review.

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A growing number of trials that used fibrates and niacin alone or in combination with other lipid-altering agents have shown that both these drugs are effective for reducing total cholesterol, low-density lipoprotein cholesterol (LDL-C) and triglycerides, and for increasing high-density lipoprotein

Is HPS2-THRIVE the death knell for niacin?

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Niacin is a lipid-modifying therapy with proven efficacy for reducing cardiovascular events as monotherapy and when used in combination with other lipid-modifying medications impacts rates of atherosclerotic disease progression. Large outcome trials using niacin against a background of statin

Niacin affects cell adhesion molecules and plasminogen activator inhibitor-1 in HepG2 cells.

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BACKGROUND Beyond lipid-modifying actions, niacin lowers the risk of atherothrombotic events by lowering prothrombotic factors like fibrinogen. Plasminogen activator inhibitor type 1 (PAI-1) is a potential factor for atherogenesis and thrombosis, increased in acute myocardial infarctions and

Effect of niacin therapy on cardiovascular outcomes in patients with coronary artery disease.

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BACKGROUND Niacin or nicotinic acid (vitamin B3) raises the levels of high-density lipoprotein cholesterol (HDL) by about 30% to 35%. In patients with prior coronary disease, 7 trials have been published on clinical cardiovascular disease outcomes and the results, not surprisingly, are inconsistent.
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