With statin co-administration, drugs designed to increase HDL have no impact on cardiovascular outcomes.

Context Decreasing low-density lipoprotein (LDL) cholesterol with statin treatment reduces cardiovascular disease (CVD) incidence. The National Institute for Health and Care Excellence (NICE) has recently recommended that firstline statin treatment in primary prevention should be atorvastatin 20 mg daily and in secondary prevention atorvastatin 80 mg daily, doses which typically decrease LDL cholesterol by 43% and 55%, respectively. In many patients this will leave little scope to reduce residual CVD risk by additional LDL lowering. Attention is therefore drawn to the epidemiological inverse association between HDL cholesterol and CVD risk. This is widely exploited in the prediction of CVD risk, but is HDL cholesterol also ‘good cholesterol’ in the sense that raising its level therapeutically can prove beneficial? Three lipid-modifying drug classes are known to raise HDL: niacin (nicotinic acid), fibrates and cholesteryl ester transfer protein inhibitors (CETPi’s).