New research helps explain why drugs designed to raise high-density lipoprotein (HDL) cholesterol levels have failed to significantly improve cardiovascular health by showing that in atherosclerosis-laden arteries, a large proportion of apolipoprotein A1 (apoA1)—the primary protein present in HDL cholesterol—becomes oxidized by the enzyme myeloperoxidase. This causes HDL to lose its cardioprotective properties and instead contribute to the development of coronary artery disease.
Hampton T. Dysfunctional HDL May Increase Heart Disease Risk. JAMA. 2014;311(9):894. doi:10.1001/jama.2014.1872