Oxidative stress and homocysteine in coronary artery disease

Background: Oxidative stress is present in cardiovascular diseases (CVDs), and hyperhomocysteinemia, an independent risk factor for these diseases, ma y play a role by inducing production of oxygen free radicals. Methods: To evaluate the possible role of homocysteine (Hcy) in inducing ox idative stress in coronary artery disease (CAD), plasma Hey was measured in 68 consecutive cardiovascular patients, and plasma malondialdehyde (MDA), both free and total (free + bound), was measured in 40 patients with CAD (1 8 with chronic stable angina and 22 with unstable angina). As controls, we tested 70 healthy volunteers. Hey was measured by an immunoenzymatic method and MBA, an index of lipid peroxidation, by gas chromatography-mass spectr ometry. Results: Plasma Hey concentrations were significantly higher in cardiovascu lar patients than in controls (10.2 vs 8.9 mu mol/L; P <0.0002), with no si gnificant difference between values in the stable and unstable angina subgr oups. Similarly, total MBA was significantly higher in the CAD group than i n the controls (2.6 vs 1.3 mu mol/L; P <0.00001), again with no significant difference between stable and unstable angina patients. By contrast, free MDA, which was significantly higher in the CAD patients than the controls ( 0.4 vs 0.2 mu mol/L; P <0.00001), was also significantly higher in the unst able than in the stable angina group (0.5 vs 0.3 mu mol/L; P <0.03). Howeve r, no correlation was observed among Hey and free and total MDA. Conclusions: Our findings show that a moderate increase of Hcy is associate d with CVD but that Hey at the detected values cannot be considered complet ely responsible for oxidative damage. That lipid peroxidation is involved i n CAD is shown by our observation of significantly increased plasma free an d total MDA concentrations compared with controls. Moreover, free MDA value s discriminated between unstable and chronic stable angina, and could thus represent a new diagnostic tool. (C) 2001 American Association for Clinical Chemistry.