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This editorial refers to ‘HPS2-THRIVE randomized placebo-controlled in 25 673 high-risk patients of ER niacin/laropiprant: trial design, pre-specified muscle and liver outcomes, and reasons for stopping study treatment’[†][1], by The HPS2-THRIVE Collaborative Group, on page 1279 Current studies evaluating the efficacy and safety of lipid-targeted therapies to reduce cardiovascular events are being performed on the background of statin therapy, given the overwhelming evidence from numerous randomized clinical studies indicating a reduction of occlusive vascular events by statin therapy.1Already in 1955 Dr Altschul and colleagues described that high doses of the vitamin B3 (niacin) reduced serum cholesterol levels ( Figure 1 ).2 Later, the Coronary Drug Project (CDP) sponsored by the National Heart and Lung Institute (published in 1975) tested the efficacy and safety of long-term therapy with a high dose of niacin (3 g/day) in men after myocardial infarction.3 In the CDP there was no significant effect of niacin therapy on the primary endpoint, i.e. all-cause mortality, but a significant reduction in the rate of recurrent non-fatal myocardial infarction by 27% was observed.3 The authors concluded that the ‘Coronary Drug Project data yield no evidence that niacin influences mortality of survivors of myocardial infarction; this medication may be slightly beneficial in protecting persons to some degree against recurrent nonfatal myocardial infarction’, that is to say the authors were not overly enthusiastic with respect to the efficacy of the compound to prevent major cardiovascular events. Already in this early study it became apparent that the adherence to niacin therapy was significantly reduced as compared with placebo, probably due to the well-known skin and gastrointestinal side effects of the compound.3 Figure 1 Niacin (vitamin B3)—a lipid-modifying agent with a long history.The mechanisms underlying the effects of niacin on lipids are still not completely understood, but … [1]: #fn-2

The difficult search for a ‘partner’ of statins in lipid-targeted prevention of vascular events: the re-emergence and fall of niacin