Abstract
Low levels of circulating HDL cholesterol (HDL-C) is an independent cardiovascular risk factor. However, whether increases in HDL-C levels protect against cardiovascular disease remains unclear. This review proposes that HMG-CoA reductase inhibitors (statins) increase HDL-C levels through the production of small and lipid-poor nascent HDL/apoA-I. Statins seem to upregulate apoA-I synthesis, leading to an increase in HDL particle number and inhibition of CETP, which results in increased HDL particle size. Pitavastatin causes a greater rise in blood HDL-C levels with more efficacious production of apoA-I compared with other statins such as atorvastatin, pravastatin, simvastatin and rosuvastatin, and has relatively low inhibitory action on CETP. This article reviews the potential role of pitavastatin in HDL therapy.