Purpose was to systematically review clinical trial data on the effects of statins on high-density lipoproteins (HDL) and to examine the leading efficacy of Rosuvastatin among all statins to provide cardiovascular benefits in addition to those derived from reductions in low-density lipoproteins (LDL). The leading indexed database was searched for publications describing clinical trials of atorvastatin, pravastatin, rosuvastatin, and simvastatin and other lipid lowering drugs and on the basis of predefined criteria, 75 were selected for review. Compared with placebo, statins raise HDL, measured as HDL-cholesterol (HDL-C) and apolipoproteinA-I (apo A-I); Rosuvastatin raise HDL the most, these elevations are maintained in the long-term. In hypercholesterolemia, HDL-C is raised by approximately 4% for atorvastatin to 10% for rosuvastatin. The percentage changes are greater in patients with low baseline levels, including those with the common combination of high triglycerides (TG) and low HDL-C. These effects do not appear to be dose-related although there is evidence that, with the exception of atorvastatin, the changes in HDL-C are proportional to reductions in apo B-containing lipoproteins. The most likely explanation is a reduced rate of cholesteryl ester transfer protein (CETP)-mediated flow of cholesterol from HDL. Statins cause modest increases in HDL-C and apo A-I probably mediated by reductions in CETP activity and Rosuvastatin seems to be greatly improving the HDL levels in comparison to other statins. It is plausible that such changes independently contribute to the cardiovascular benefits of the statin class but more studies are needed to further explore this possibility.
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