 Background HMG-CoA reductase inhibitors statins are effective lipid-lowering agents and are known to reduce cardiovascular events. It was initially assumed that cholesterol reduction by statins was the only mechanism responsible for their beneficial effect. However, beneficial effects of statins seem to occur very early in the course of their therapy 1 and subgroup analysis of large trials indicates that subjects in statin-treated arms have less cardiovascular events than subjects in placebo-controlled arm with comparable serum cholesterol levels 2. Therefore, it was suggested that statins may have antiatherogenic effects, such as anti-inflammatory and antioxidative actions, beyond their cholesterol lowering effect. Many studies have demonstrated a rapid improvement in vascular function with atorvastatine which cannot solely be accounted for by achieved lipid reduction 3-5. In the Pravastatin or Atorvastatin evaluation and infection therapy-thrombolysis in myocardial infarction 22 trial PROVE-IT-TIMI 22 trial, with a follow-up period of 2-years and intensive statin therapy, 80 mg atorvastatin showed a stronger reduction of cardiovascular events when compared with 40 mg pravastatin, with an apparent benefit observed early 6. A rapid and a strong oxidative stress lowering effect of atorvastatin has been proposed as the probable mechanism of this action 7. Other statins have been shown to have anti-oxidant effects as well 8,9. However, whether atorvastatine has stronger antioxidant effect and whether atorvastatin lowers oxidative stress early in the course of therapy than other statins has not been demonstrated up to now. 