The inflammatory response has also been shown to be modulated by the use of perioperative statin therapy.5,6 Statins were initially employed to lower serum cholesterol concentrations through 3-hydroxy-3-methyl-glutaryl-CoA (HMG-CoA) reductase inhibition. The overwhelming majority of patients presenting for cardiac anesthesia and surgery are on preoperative statin therapy. Although effective in lowering cholesterol, statins have also been shown to decrease inflammation, reduce thrombosis, and minimize ischemia-reperfusion injury. Patients on statins are at risk of increased morbidity if the statins are discontinued perioperatively. Statins inhibit generation of isoprenoids, which bind to Rho and Ras guanosine triphosphatases. Therefore, through the inhibition of Rho, statins have direct anti-inflammatory effects, and lead to a reduction in inflammatory cytokines, an increase in anti-inflammatory cytokines and an up-regulation of endothelial nitric oxide (NO) synthetase.5 Consequently, statins result in less inflammation but increased NO production. Moreover, statins increase thrombomodulin expression and reduce tissue factor expression on endothelial cells resulting in an antithrombotic effect. Since inflammatory and thrombotic effects can contribute to neural, cardiac, and renal injury perioperatively, preoperative statin therapy may reduce all these. Discontinuation of statin therapy results in down-regulation of endothelial nitric oxide synthetase reducing production of vasodilating nitric oxide.