Strategies for modifying high-density lipoprotein cholesterol: a role for nicotinic acid.

Statin-mediated lowering of low-density lipoprotein cholesterol (LDL-C) is regarded as the foundation of lipid-modifying therapy. However, the residual cardiovascular risk for statin-treated patients remains high, indicating the need for therapeutic intervention against other lipid targets as well as non-lipid risk factors. Low levels of high-density lipoprotein cholesterol (HDL-C) are established as a strong independent risk factor for cardiovascular disease. Intervention studies have also demonstrated clinical benefits associated with HDL-C raising. Although lifestyle modification does play an important role in raising HDL-C, most patients with a low HDL-C and at high risk of coronary events also require pharmacological treatment to achieve the target. Of the available treatment options, nicotinic acid is the most potent agent for raising HDL-C (by 26% at clinically recommended doses), while substantially lowering triglycerides and LDL-C. The addition of nicotinic acid to primary statin therapy is a logical approach to dyslipidaemia management, given their complementary mechanism of action, and is supported by recent clinical trials such as the Arterial Biology for the Investigation of the Treatment Effects of Reducing cholesterol (ARBITER) 2 study. Raising HDL-C will increasingly become an important secondary focus of dyslipidaemia management.