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Current lipid management guidelines are focused on decreasing low-density lipoprotein (LDL-C) levels as the primary target for reducing coronary heart disease (CHD) risk. Yet, many recent studies suggest that low levels of high-density lipoprotein (HDL-C) are a major independent risk factor for cardiovascular diseases. According to several clinical trials, a 1% increase in HDL-C is associated with a 0.7%-3% decrease in CHD events. The direct link between high levels of triglycerides (TG) and CHD, on the other hand, is less well defined. A large reduction in TG is needed to show a difference in CHD events, especially in men. Evidence for a shift in lipid management toward targeting both LDL-C and HDL-C as primary targets for therapy is presented. Currently, the 3-hydroxy-3-methylgutaryl coenzyme A reductase inhibitors (HMG-CoA reductase inhibitors) have proven to significantly decrease LDL-C levels, reduce CHD morbidity/mortality and improve overall survival. However, improvement of survival with statins may be due to other pleiotropic effects beyond LDL-C lowering. Fibric acid derivatives and niacin are primarily used to increase HDL-C levels, although with side effects. Future therapies targeting HDL-C may have profound results on reducing CHD morbidity and mortality. This article highlights existing and future targets in lipid management and is based on available clinical data. There is an urgent need for new treatments using a combination of drugs targeting both LDL-C and HDL-C. Such treatments are expected to have a superior outcome for dyslipidemia therapy, along with TG management.

Cardiovascular (CV) risk remains in some patients who are treated with statins. Evidence supports a role for triglycerides (TGs) in CV disease. TG-lowering agent outcomes studies have been inconsistent, but eicosapentaenoic acid signifi cantly reduced coronary events in hypercholesterolemic patients who were treated with statins. Ongoing outcomes studies will clarify the role of TG-lowering treatments in CV risk reduction. [ABSTRACT FROM AUTHOR]

Abstract: Objectives: Atherogenic dyslipidemia is emerging as a target of lipid-modifying therapy. However, an optimal pharmacologic approach has not yet been established. The aim of this study is to compare the efficacy and tolerability of the typical doses of fenofibrate and niacin. Methods: After an eight-week dietary run-in, 201 patients who had triglyceride (TG) levels of 150–499mg/dL, high-density lipoprotein-cholesterol (HDL-C) levels of <45mg/dL and low-density lipoprotein-cholesterol (LDL-C) levels of <130mg/dL were randomly assigned to one of two treatment groups for 16 weeks: fenofibrate 160mg or niacin extended release 1500mg (starting at 500mg and up-titrated at the fifth and ninth weeks). Results: One hundred forty patients completed the study. The percent reductions in apoB/A1 were not different between the two groups (−20% and −22% in the fenofibrate and niacin groups, respectively, p =0.47). The effects of the two regimens on HDL-C were similar (24% and 20%, respectively, p =0.22), while fenofibrate reduced TG more than did niacin (−53% and −48%, respectively, p =0.045). Niacin was more effective at lowering LDL-C, Lp (a), and hs-CRP. However, niacin worsened the parameters of glycemic control, whereas fenofibrate improved them. Niacin showed more frequent adverse events including pruritus and skin flushing. Conclusions: These two regimens have largely comparable lipid-modifying effects. However, their effects on glucose metabolism and inflammation, and their adverse events need to be considered additionally. Our results underscore more individualized pharmacologic approaches to patients with atherogenic dyslipidemia. [Copyright &y& Elsevier]