Individualized lipid-lowering therapy to further reduce residual cardiovascular risk.

Hypercholesterolemia is a major risk factor for cardiovascular diseases. Serum cholesterol concentrations are regulated by enteral absorption, biliary secretion, and hepatic synthesis. Statins inhibit the rate-limiting enzyme of cholesterol synthesis, HMG-CoA-reductase, and reduce serum cholesterol concentrations as well as cardiovascular morbidity and mortality. Some studies indicate that patients with high baseline cholesterol absorption may show only a small response to statin treatment in terms of cholesterol lowering. Data from genetic association studies and from the IMPROVE-IT trial show that reducing intestinal cholesterol absorption via NCP1L1 further reduces cardiovascular risk. However, some patients do not attain LDL-cholesterol targets on combination therapy. For these patients PCSK9-antibody treatment and lipid-apheresis are options to be considered. This article reviews the current literature on this issue and suggests 'individualized lipid-lowering therapy' as an approach to optimize and personalize lipid-lowering treatment of patients with hypercholesterolemia to further reduce residual cardiovascular risk.