Combination niacin and statin therapy in primary and secondary prevention of cardiovascular disease

University of Rochester School of Medicine and Dentistry, Rochester, New York, USA.
Clinical Cardiology (Impact Factor: 2.59). 07/2005; 28(7):317-20. DOI: 10.1002/clc.4960280703
Source: PubMed


Statin monotherapy may not be sufficient to reach serum lipid goals in many patients, especially in those with combined lipid abnormalities. Statins cause only a modest increase in high-density lipoprotein cholesterol (HDL)--an established independent protective factor for coronary heart disease (CHD)--and a modest decrease in triglycerides (TG). Niacin is an effective pharmacologic agent for increasing HDL, as well as lowering TG. Used in combination with a statin, niacin provides an option to help patients attain their low-density lipoprotein cholesterol (LDL-C) goals, non-HDL goals, and HDL goals. Based on the National Health and Nutrition Examination Survey, 1999 to 2000, only 12% of the surveyed adult population were under treatment for diagnosed hypercholesterolemia. Furthermore, only 5.4% of the surveyed population had attained goal total cholesterol levels of < 5.2 mmol/I (< 200 mg/dl). Combination therapy offers a means to get more people to goal. This paper reviews the impact of lipid-modifying combination therapy with niacin plus a statin on lipid profile outcomes.

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    ABSTRACT: INTRODUCTION: Although reduction of LDL-C levels is a priority in the treatment of dyslipidemia, not all coronary events are prevented despite aggressive LDL-C lowering, and risk reduction can be improved by treating additional lipid abnormalities. The Framingham Study was the first to demonstrate the inverse relationship between HDL-C and risk of coronary heart disease (CHD). This relationship was present at all levels of LDL-C, whereas the highest risk was associated with low HDL-C and high LDL-C. THE ANTIATHEROGENIC ACTIONS OF HDL-CHOLESTEROL: The antiatherogenic actions of HDL-C are complex. HDL-C plays a major role in reverse cholesterol transport, mobilizing cholesterol from the periphery to the liver. In addition, cardioprotective effects of HDL-C include endothelial protection, anti-inflammatory activity, as well as antioxidant and antithrombotic effects. TREATMENT OF LOW HDL CHOLESTEROL: In addition to lowering LDL-C, statins increase HDL-C by 5 to 15% by increasing apolipoprotein A-I synthesis. Fibrate therapy results in an increase in HDL-C of 10 to 25 % by activating PPAR- , which stimulates hepatic apolipoprotein A-I gene expression. Niacin is the most effective agent used for increasing HDL-C, causing increase of 15 to 35%. The side effects of niacin therapy, which is largely mediated by prostaglandins, may be minimized by the use of prolonged-release formulation of nicotinic acid. Combination therapy with HDL-raising agents, such as nicotinic acid and statin, markedly increases HDL-C, lowers LDL-C and improves the lipoproteins subclass distribution. CONCLUSION: New therapeutic modalities in the treatment of low HDL-C and lowering LDL-C, either in combination or as a monotherapy, may provide additional benefits in reducing CHD risk.
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