In recent years, it became evident that reactive oxygen species (ROS) are implicated in the thrombotic process. Statins are lipid-lowering agents able to lower serum cholesterol levels and retard atherosclerotic complications and their clinical sequelae. There is evidence that, among statins, atorvastatin may exert antiplatelet effects by interfering with redox signaling. Recent studies demonstrated that atorvastatin possesses antiplatelet activity via inhibition of platelet formation of NADPH oxidase-derived ROS. This effect results in down-regulation of isoprostanes, which are pro-aggregating molecules, and up-regulation of nitric oxide, which is a platelet inhibitor; such changes occurred immediately after atorvastatin administration and were independent from lipid-lowering property. Experimental and clinical studies documented that statins possess antithrombotic effects, which may account for the reduction of thrombotic-related vascular outcomes. This has been evidenced in different cardiovascular clinical settings such as percutaneous coronary intervention (PCI), myocardial infarction (MI), and venous thrombosis. Future studies should be addressed to analyze if the antiplatelet effect of atorvastatin may preferentially occur at high dosage. Interestingly, the antiplatelet effects of statins could be useful in clinical settings where the clinical efficacy of aspirin and other antiplatelet drugs is still uncertain.
© 2013 Published by Elsevier Inc.