Clin Invest Med 2010; 33 (5): E313-E320.
AbstractPurpose: Oxidative damage plays an important role in atherosclerosis development. Statin drugs have anti-oxidant properties, but the clinical value of their antioxidant properties remains unclear. In this study, our aims were: (1) to assess the anti-oxidant effects of statins in patients with coronary artery disease (CAD) using a newly developed valid measure of total oxidant and anti-oxidant capacity; and (2) to identify whether statins influence ceruloplamin levels. Methods: Within a cross-sectional study, 67 dyslipidemic CAD patients on atorvastatin for at least three months were compared with 69 age-and gender-matched CAD patients not using atorvastatin. All patients were either newlydiagnosed with or already had established CAD. Patients and controls were selected from among patients who had undergone coronary angiography for a variety of reasons. Immediately prior to angiography, plasma total oxidant and antioxidant capacity and ceruloplasmin (Cp) levels were measured by means of a relatively new and highly-reliable method. Results: Total oxidant capacity levels were significantly lower and total antioxidant capacity significantly higher in those on atorvastatin; serum seruloplasmin levels also were significanly increased in the atorvastatin groups (all p < 0.05). On multivariate analysis, atorvastatin use was a significant determinant of Cp increase, independent of any antioxidant effect. Conclusions: This study clearly demonstrates increased anti-oxidant capacity and decreased oxidative stress with statin use. Atorvastatin use may also increase Cp levels although this effect appears to be independent of its antioxidant effects.Free radicals and oxidants are produced in metabolic and physiological processes, and their effects are controlled by exogenous and endogenous antioxidants. If the quantity of free radicals exceeds the capacity of anti-oxidant defense mechanisms, oxidative stress occurs. 1,2 Oxidative stress alters normal endothelial functions, inducing proinflammatory, prothrombotic, proliferative and vasoconstrictor mechanisms that support atherogenic processes. 2,3 A number of reports in the literature implicate oxidative stress and/or inadequate antioxidant defences in the pathogenesis of, or as a risk factor for, cardiovascular disease. 4,5 Ischemic heart disease is an ideal example of a clinical situation in which there is an increased production of oxygen free radicals. 6 Oxi-ORIGINAL RESEARCH