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(Arteriosclerosis, Thrombosis, and Vascular Biology. 1997;17:1432-1437.)
© 1997 American Heart Association, Inc.

Articles

Increased Oxidation of LDL in Patients With Coronary Artery Disease Is Independent From Dietary Vitamins E and C

Daniel Halevy; Joachim Thiery; Dorothea Nagel; Sebastian Arnold; Erland Erdmann; Berthold Höfling; Peter Cremer; ; Dietrich Seidel

From the Institute of Clinical Chemistry, University Hospital Großhadern, Munich, Germany (D.H., J.T., D.N., S.A., P.C., D.S.); Klinik II für Innere Medizin, University Hospital Köln (Germany) (E.E.); and Medizinische Klinik I, University Hospital Großhadern, Munich, Germany (B.H.).

Correspondence to Joachim Thiery, MD, Institute of Clinical Chemistry, University Hospital Großhadern, Marchioninistr 15, D-81377 Munich, Germany.

Abstract There is increasing experimental evidence that oxidation of LDL plays a major role in the pathogenesis of coronary artery disease (CAD). However, results from clinical studies on LDL oxidation and CAD are not consistent. In most studies only single plasma factors of LDL oxidation have been determined. We studied 207 patients who underwent coronary angiography. They were divided into subjects with CAD (n=137) and those without CAD (n=70). We determined the susceptibility of LDL to in vitro oxidation (lag phase), potential prooxidative and antioxidative plasma factors (plasma vitamin E, LDL vitamin E, ascorbate, iron, copper, ferritin, and ceruloplasmin), and markers of in vivo LDL oxidation (autoantibodies to malondialdehyde-modified LDL, oxidized LDL, and thiobarbituric acid–reactive substances), plasma lipids and lipoproteins, smoking habits, and other coronary risk factors in both groups. The lag phase was significantly shorter in patients with CAD than in patients without CAD (101± 38.6 versus 119± 40.6 minutes, P<.01). There was no correlation between the lag phase and the other oxidation parameters or the coronary risk factors. In multivariate regression analyses the lag phase remained significant in all tested models. Our data suggest that a short lag phase of LDL oxidation might be an independent risk factor of CAD.

Key Words: coronary artery disease • oxidation • lipoproteins • lag phase • antioxidants

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