Several studies over the last years have demonstrated that statins exhibit actions beyond that of lipid-lowering (pleiotropic effects) ranging from improving endothelial function, modulating the inflammatory response, maintaining plaque stability and preventing thrombus formation. Since the interplay among platelets, cells and other components of atherosclerotic lesions as well as the coagulation system play an important role in the progression of atherosclerosis and in the development of acute coronary syndromes, these non-lipid properties of statins may help to explain the early and significant reduction of cardiovascular events reported in several clinical trials of statin therapy. This review focuses on the experimental and clinical results regarding the antiplatelet/antithrombotic effects of statins.
Keywords: Atherosclerosis, coronary artery disease, platelets, statins, thrombosis, HMG-CoA, lipoprotein (LDL) receptors, pleiotropic effects, prothrombotic, fibrinolytic mechanisms, atherothrombosis, atherosclerotic lesions, acute coronary syndromes, angioplasty, subendothelial collagen, Willebrand factor, 21, GPVI, GPIb-IX, hypercholesterolaemia, normocholesterolaemic, cytosolic calcium, thromboxane A2 (TxA2), dehydro-TxB2 (a major metabolite of TxA2), protein 8, LDL oxLDL, simvastatin, atorvastatin, flu-vastatin, pravastatin, mitogen activated protein kinases (MAP, especially Erk2, nuclear factor kappa B (NF-B), Akt modulation, Atherosclerotic tissues, oxide (NO) syn-thase (NOS) activity, oxLDL, CD36, fibrinopeptide, aspirin, thrombin cleavage peptides, lovastatin therapy, GREACE, HERS, Clopidogrel, cytochrome, P450 (CYP450) isoenzymes, sim-vastatin, lovastatin
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