D. Halevy et al., INCREASED OXIDATION OF LDL IN PATIENTS WITH CORONARY-ARTERY DISEASE IS INDEPENDENT FROM DIETARY VITAMIN-E AND VITAMIN-C, Arteriosclerosis, thrombosis, and vascular biology, 17(7), 1997, pp. 1432-1437
There is increasing experimental evidence that oxidation of LDL plays
a major role in the pathogenesis of coronary artery disease (CAD). How
ever, results from clinical studies on LDL oxidation and CAD are not c
onsistent. 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 thos
e without CAD (n=70). We determined the susceptibility of LDL to in vi
tro oxidation (lag phase), potential prooxidative and antioxidative pl
asma 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 thio
barbituric acid-reactive substances), plasma lipids and lipoproteins,
smoking habits, and other coronary risk factors in both groups. The la
g phase was significantly shorter in patients with CAD than in patient
s without CAD (101 +/- 38.6 versus 119 +/- 40.6 minutes, P<.01). There
was no correlation between the lag phase and the other oxidation para
meters or the coronary risk factors. In multivariate regression analys
es the lag phase remained significant in all tested models. Our data s
uggest that a short lag phase of LDL oxidation might be an independent
risk factor of CAD.