Raising HDL-C can be achieved by both lifestyle changes and pharmacological means. Introduction

Lowering low-density lipoprotein-cholesterol (LDL-C) levels using statins can significantly reduce cardiovascular (CV) risk in patients with dyslipidemia. However, the risk of major vascular events in those attaining the maximum levels of LDL-C-reduction is only reduced by around one third, which leaves a substantial residual risk. The Emerging Risk Factors Collaboration has shown that low levels of high-density lipoprotein-C (HDL-C) are independent risk factors for CV disease. It is therefore important that treatment strategies for dyslipidemia should target HDL-C in addition to LDL-C. Raising HDL-C can be achieved by both lifestyle changes and pharmacological means. Therapeutic strategies include niacin, fibrates, thiazolidinediones, apolipoprotein A1 mimetics, cholesteryl ester transfer protein inhibitors, statins and combinations thereof. In general, statins produce inconsistent increases in HDL-C. However, pitavastatin, a new member of the statin family that was launched in 2003, and rosuvastatin consistently elicit marked increases in HDL-C that are sustained over time. This supplement will discuss the contribution of HDL-C as a possible predictor and modifiable risk factor for CV disease and will examine the potential role for pitavastatin in reducing residual CV risk.