Abstract
‘Atherogenic dyslipidaemia’ and the ‘lipid triad’ are collective terms for the low HDL-cholesterol, elevated triglycerides, and small, dense LDL that is often found in insulin-resistant patients with abdominal obesity, the metabolic syndrome, or type 2 diabetes. This dyslipidaemia phenotype is believed to underlie a substantial burden of excess cardiovascular risk. Although statins provide effective control of LDL-cholesterol, their effects on the lipid triad are relatively modest and combination therapies will be required to normalize the lipid profiles of these patients. Increasing HDL-cholesterol, in particular, exerts a range of anti-atherogenic effects within the evolving atherosclerotic plaque. Fibrates and nicotinic acid (niacin) each increase HDL-cholesterol, with nicotinic acid being the more effective of the two. Studies with Niaspan®, a prolonged-release formulation of nicotinic acid with equivalent efficacy but superior tolerability compared with immediate-release nicotinic acid, shows that this agent preferentially increases levels of larger, more atheroprotective, ApoAI-containing HDLs. Combinations of nicotinic acid with a statin appears to provide effective control of LDL-cholesterol while maximizing the anti-atherogenic potential of HDL-cholesterol.
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