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. Less is known about the relevance of HDL after CABG,162 although data from the prestatin era suggested that a rela- tionship exists between lower HDL levels and higher risk of atherosclerosis progression and adverse events after sur- Through reverse cholesterol transport, HDL prevents the development of foam cells in a vessel wall.142,144 Moreover, independently of its involvement in cholesterol metabolism, HDL has properties that reduce vascular inflammation and thrombosis, improve endothelial function, and promote endothelial repair.142 Ultimately, higher levels of HDL particles may help slow the process of saphenous vein graft disease and decrease the risk of adverse outcome Previous observational studies have dem- onstrated associations between lower HDL and both worse long-term survival and higher risk of cardiovascular events In the only HDL clinical trial involving CABG patients, the Lopid Coronary Angiography Trial (LOCAT) enrolled 395 men with HDL levels <42.5 mg/dL who had undergone CABG on average 2 years earlier. From an era before the rou- tine use of statins after CABG, patients were randomized to receive either slow-release gemfibrozil 1200 mg/d or match- ing placebo. 