Apolipoprotein A1 (CSL112) Increases Lecithin-Cholesterol Acyltransferase Levels in HDL Particles and Promotes Reverse Cholesterol Transport.

Although high-density lipoprotein (HDL) cholesterol is inversely correlated with cardiovascular risk, an emerging paradigm is focused on increasing reverse cholesterol transport (RCT) and HDL function via apolipoprotein A1 (ApoA1). The objective of this study was to investigate the effect of ApoA1 (CSL112) infusion on HDL protein composition, cholesterol esterification rate (CER), and cholesterol efflux capacity (CEC) in patients treated after acute myocardial infarction. CSL112 reduced levels of apolipoproteins A2, B, C, and E and serum amyloids A1 and A4, whereas ApoA1, ApoM, and lecithin-cholesterol acyltransferase were significantly elevated. Increased CEC, plasma HDL cholesterol levels, CER, and CEC also were observed in CSL112-treated patients.