Niacin does, however, favorably alter atherosclerotic plaque architecture.

Update on Niacin

• 1.Low serum levels of HDL-C and high levels of non-HDL-C are frequent phenotypic features of patients with acute coronary syndromes and contribute significantly to residual risk after LDL-C lowering with statin therapy.
• 2.Adjuvant therapy with niacin in patients with stable ischemic heart disease and well-controlled atherogenic lipoprotein burden was shown not to be efficacious in both the AIM-HIGH and HPS-2 THRIVE trials. Niacin does, however, favorably alter atherosclerotic plaque architecture.
• 3.Low HDL-C is a reliable predictor of risk for recurrent events in patients who have sustained an acute coronary syndrome. Raising HDL-C with niacin does not appear to contribute to risk reduction. HDL-C is not currently a target of therapy and niacin should not be used to raise low HDL-C levels.
• 4.There is renewed interest in the atherogenicity of triglyceride enriched remnant lipoproteins. Non-HDL-C encompasses triglyceride-enriched lipoproteins such as VLDL-C remnants and IDL-C.
• 5.Recent meta-analyses and one post hoc analysis suggest that niacin therapy contributes to risk reduction in patients with mixed dyslipidemia characterized by elevated levels of triglyceride-enriched lipoproteins.
• 6.Consistent with guidelines from around the world (including those of the NLA) that emphasize risk stratified non-HDL-C goal attainment, niacin therapy can be considered in patients with established coronary disease on statin therapy but whose non-HDL-C still exceeds 100 mg/dL.