Data from epidemiological and intervention studies have conclusively shown that a low level of high-density lipoprotein cholesterol (HDL-C) is an important risk factor for cardiovascular disease. Increasing low HDL-C levels produces risk reduction comparable with that observed with decreasing low-density lipoprotein cholesterol (LDL-C) in the major statin trials. The latter have shown that, even with effective statin therapy, there is still an unacceptably high residual risk of major coronary events. A substantial proportion of patients with coronary heart disease (CHD) with acceptable levels of LDL-C will have low levels of HDL-C and increased serum triglycerides. Of the available lipid-modifying treatments, nicotinic acid is the most potent agent for increasing HDL-C (by about 30% from baseline). In addition, it effectively decreases triglycerides and has a relatively modest effect in decreasing LDL-C. Modified-release nicotinic acid has been developed to overcome the poor tolerability associated with earlier formulations while maintaining the efficacy of immediate-release nicotinic acid. Modified-release nicotinic acid is effective and safe for the treatment of dyslipidaemia, including the atherogenic dyslipidaemia associated with type 2 diabetes and the metabolic syndrome. Combination therapy with modified-release nicotinic acid and a statin offers complementary therapeutic benefits, as well as reducing the progression of, or even regressing, atherosclerosis. This strategy can represent an important advance for clinical management of at-risk patients with dyslipidaemia.
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