Newer therapeutic strategies to alter high-density lipoprotein level and function

Measurements of low levels of high-density lipoprotein (HDL) cholesterol have been identified as a risk factor for premature coronary artery disease, however, to date, current pharmacologic approaches for raising HDL have provided little benefit, if at all, in reducing cardiovascular outcomes. It has been shown that HDL can modify many aspects of plaque pathogenesis. Its most established role is in reverse cholesterol transportation, but HDL can also affect oxidation, inflammation, cellular adhesion, and vasodilatation. Considering these potential benefits of HDL, newer treatments have been developed to modify HDL activity, which include the use of oral cholesteryl ester transfer protein inhibitors, apolipoprotein (apo)A-I infusions, apoA-I mimetics, drugs to increase apoA-I synthesis, and agonists of the liver X receptor. These new therapies are reviewed in this article.