Abstract

Statin treatment is considered as one of the most effective therapies for the stabilization of vulnerable atherosclerotic plaques, and have been shown to reduce overall morbidity and mortality when used for either primary [1,2] or secondary prevention [3,4] of cardiovascular disease (CVD). The mechanism by which statins provide cardiovascular benefit in these clinical settings, however, is not fully elucidated. Statins are known to have a wide range of biological effects, including decrease in pro-atherogenic plasma lipoproteins, as well as a modest increase of high-density lipoprotein-cholesterol (HDLC) levels [5]. However, the favorable outcomes of these drugs have been assigned thus far to changes in LDL-C and HDL-C only. Indeed, statins have important non-lipid effects that include antiinflammatory, antioxidant and, antithrombotic actions as well as mobilization of endothelial progenitor cells [6] and modification of plaque cholesterol crystallization [7]. These combined effects lead to atherosclerotic plaque stabilization in both quantitative (slowing

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