Abstract
Low high-density lipoprotein cholesterol (HDL-C) levels are associated with higher risk of cardiovascular disease, even in patients receiving statin therapy. HDL-C has a number of potential atheroprotective mechanisms, including reverse cholesterol transport. HDL-C also has antioxidant, anti-inflammatory, vasodilatory and antithrombotic effects. A number of targets with the potential to raise HDL-C levels and/or increase reverse cholesterol transport have been identified. Plasma concentrations of HDL-C are the net result of the de novo production, catabolism and recycling of HDL-C particles, as well as the contribution to HDL-C from components of other lipoproteins. HDL-C levels can be modified by increasing the production of apolipoprotein A-I or by delaying the clearance of HDL-C from the plasma. Whether manipulation of these drug targets to raise HDL-C will result in cardiovascular event reduction remains to be determined.