ABSTRACT
The critical importance of high-density lipoprotein cholesterol (HDL‐C) as an independent and predictive factor for coronary heart disease (CHD) has been increasingly recognised in treatment guidelines for prevention and treatment of cardiovascular disease. The association of low HDL‐C with an increased incidence of CHD implies a critical role for raising HDL‐C in protection against atherosclerotic disease. HDL‐C appears to exert this effect via a number of mechanisms. HDL‐C is involved in reverse cholesterol transport, prevents endothelial dysfunction and has anti-inflammatory, anti-oxidant and anti-thrombotic properties. Therapeutic interventions that increase HDL‐C include statins, fibrates and nicotinic acid. Of these, nicotinic acid raises HDL‐C more effectively than either statin or fibrate therapy and has been proven to reduce cardiovascular events in monotherapy studies. Preliminary clinical studies have shown that addition of nicotinic acid to primary statin therapy is safe, has proven beneficial effects on atherosclerosis and may also reduce the incidence of major coronary events. The available clinical evidence suggests that addition of nicotinic acid to primary lipid-lowering therapy has an important atheroprotective role in patients with or at risk of developing CHD.