Evidence to support aggressive management of HDL-cholesterol: implications of recent trials

Low HDL-cholesterol is an independent risk factor for coronary disease and its prevalence is high and increasing. Lifestyle interventions are recommended for all patients at risk of cardiovascular disease, but exercise has limited effects on HDL-cholesterol. Nicotinic acid is currently the most effective pharmacological agent available for increasing levels of HDL-cholesterol. The HDL Atherosclerosis Treatment study (HATS) showed that combining nicotinic acid with a statin improved HDL-cholesterol and LDL-cholesterol, inhibited the progression of atherosclerosis, and reduced cardiovascular event rates in a high-risk population with established coronary heart disease. A prolonged-release formulation of nicotinic acid (Niaspan(R)) has been developed that is as effective as the immediate-release version, but is better tolerated. The double-blind, randomized Arterial. Biology for the Investigation of the Treatment Effects of Reducing Cholesterol (ARBITER 2) study, and its open-label follow-up study, ARBITER 3, showed that Niaspan shares the anti-atherogenic benefits of immediate-release nicotinic acid. The Atherothrombosis Intervention in Metabolic Syndrome with Low HDL-C/High Triglyceride and Impact on Global Health Outcomes (AIM-HIGH) study will define the potential of correcting low HDL-cholesterol to improve clinical outcomes in patients with well-controlled LDL-cholesterol. In summary, the current evidence base clearly shows that aggressive intervention to correct tow HDL-cholesterol as well as high LDL-cholesterol is a proven strategy for preventing atherosclerotic cardiovascular disease.