Despite current best therapy, many patients remain at high risk of cardiovascular disease. Reducing LDL cholesterol (LDL-C) with statins is a cornerstone of such management,1 and recent evidence supports the addition of ezetimibe to lower LDL-C further2 (and proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are showing promise to lower LDL-C yet more).3 Other components of the lipid profile are also associated with cardiovascular risk and their modification has been explored to reduce this residual risk. For example, it has been recognised for several decades that HDL cholesterol (HDL-C) is inversely associated with cardiovascular risk in the general population4 and among patients already receiving intensive statin therapy5 although trials of cholesterol ester transfer protein inhibitors that raise HDL-C substantially have not been successful to date.6 Lipoprotein (a) is positively associated with risk, and genetic data suggest this association is causal,7 and triglycerides may also be positively associated with risk, although observational and genetic data differ.8 ,9 A treatment that raises HDL-C and reduces Lp(a) and triglycerides is therefore very attractive. Niacin has been available for 60 years and is currently the most potent treatment that can effect all these changes in the lipid profile.10

Niacin is widely used, especially in North America.11 Despite niacin's promising lipid effects, two contemporary trials found no evidence that it reduces …