Niacin increased HDL levels by 20% but failed to reduce the rate of cardiovascular events over the 5-year trial duration (5.8% versus 5.6%, niacin versus placebo; P=NS). The trial was halted prematurely because of the absence of clinical benefit, and a small increase in ischemic stroke was noted in the niacin group.143 Presented in 2013, the Treatment of HDL to Reduce the Incidence of Vascular Events (HPS2-THRIVE) trial yielded similarly disappoint- ing results for niacin. In this trial, 25 673 patients with Kulik et al Secondary Prevention After CABG 935 well-controlled LDL levels were randomized to extended- release niacin plus an antiflushing agent (laropiprant) or placebo. Niacin increased HDL by 14% but failed to reduce the primary clinical end point (fatal or nonfatal MI, stroke, or coronary revascularization; 14.5% versus 15.0%, niacin versus placebo; P=NS). Moreover, niacin increased the risk of myopathy in this trial.155 Although it increases HDL lev- els, adding niacin to statin therapy does not improve choles- terol efflux or the antioxidant functions of HDL, which may explain the lack of clinical effect in clinical trials.161 Casting doubt on the HDL theory, no therapy to date has been shown to increase HDL levels and to improve outcomes in a clinical trial enrolling CAD patients already treated with Therapies to increase HDL appear to be ineffective in terms of reducing adverse cardiovascular events, and no evidence exists to support the premise that raising HDL cholesterol leads to clinical benefit in CAD (and specifi- cally non-CABG) patient populations. 