In Reply Dr Whayne suggests that “there is ample support to use nicotinic acid” when low-density lipoprotein cholesterol and high-density lipoprotein cholesterol targets have not been reached by citing the Coronary Drug Project, the Cholesterol Lowering Atherosclerosis Study, and a recent meta-analysis.1-3 As cited by Dr Whayne, some of the strongest evidence for niacin comes from the secondary prevention Coronary Drug Project trial. However, it is perhaps not as strong as some may recall. It is often forgotten that niacin actually failed to demonstrate a significant reduction in the trial’s primary end point of total mortality at 5 years compared with placebo in the post–myocardial infarction population studied, although it significantly reduced the secondary end point of nonfatal MI and cardiac death.4 A significant reduction in mortality only appeared after 15 years of follow-up with a greater time off niacin therapy than receiving it (6.2 years taking niacin and 8.8 years after stopping niacin therapy).1 In the most recent of many niacin meta-analyses cited by Dr Whayne, because many heterogenous niacin trials were pooled and niacin was primarily combined with other lipid-lowering agents, it fails to isolate and confirm a benefit of niacin itself.3 Furthermore, without the inclusion of HPS-2-THRIVE (Heart Protection Study 2–Treatment of HDL to Reduce the Incidence of Vascular Events), this latest meta-analysis remains an incomplete reflection of the totality of niacin evidence to date.3,5
Jackevicius CA, Krumholz HM. Role of Nicotinic Acid in Atherosclerosis Prevention—Reply. JAMA Intern Med. 2014;174(4):649. doi:10.1001/jamainternmed.2013.12811
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