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Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18:193-199

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*Coronary Artery Disease
(Arteriosclerosis, Thrombosis, and Vascular Biology. 1998;18:193-199.)
© 1998 American Heart Association, Inc.


Original Contributions

LDL Oxidation and Extent of Coronary Atherosclerosis

Lucy P. L. van de Vijver; Alwine F. M. Kardinaal; Wim van Duyvenvoorde; Dick A. C. M. Kruijssen; Diederick E. Grobbee; Geert van Poppel; ; Hans M. G. Princen

From the Department of Consumer Research and Epidemiology, Dutch Organization for Applied Scientific Research Nutrition and Food Research Institute, Zeist (L.P.L.v.d.V., A.F.M.K., G.v.P.); Department of Epidemiology and Biostatistics, Erasmus University, Rotterdam (L.P.L.v.d.V., D.E.G.); Gaubius Laboratory, Dutch Organization for Applied Scientific Research Prevention and Health, Leiden (W.v.D., H.M.P.G.); Thorax Centre, Academic Hospital Dijkzigt, Rotterdam (D.A.C.M.K.); and Julius Centre for Patient Oriented Research, Utrecht University, Utrecht (D.E.G.), the Netherlands.

Correspondence to Dr Hans M.G. Princen, Gaubius Laboratory, TNO-PG, Zernikedreef 9, PO Box 2215, 2301 CE Leiden, the Netherlands. E-mail jmg.princen{at}pg.tno.nl

Abstract—Accumulated evidence indicates that oxidative modification of LDL plays an important role in the atherogenic process. Therefore, we investigated the relation between coronary atherosclerosis and susceptibility of LDL to oxidation in a case-control study in men between 45 and 80 years of age. Case subjects and hospital control subjects were selected from subjects undergoing a first coronary angiography. Subjects with severe coronary stenosis (>=85% stenosis in one and >=50% stenosis in a second major coronary vessel) were classified as case subjects (n=91). Hospital control subjects with no or minor stenosis (<=50% stenosis in no more than two of the three major coronary vessels, n=94) and population control subjects free of plaques in the carotid artery (n=85) were pooled for the statistical analysis into one control category. Enrollment procedures allowed for similar distributions in age and smoking habits. Case subjects had higher levels of total and LDL cholesterol and triglycerides and lower levels of HDL cholesterol. Resistance time, maximum rate of oxidation, and maximum diene production were measured ex vivo using copper-induced LDL oxidation. A borderline significant inverse trend was observed for coronary atherosclerosis risk at increasing resistance time. Odds ratios (95% confidence interval) for the successive quartiles were 1.0 (reference), 0.77 (0.39 to 1.53), 0.67 (0.33 to 1.34), and 0.55 (0.27 to 1.15) (ptrend=0.07). No relation with maximum rate of oxidation was found, and higher maximum diene levels were found in control subjects (P<.01). The main determinant of oxidation was the fatty acid composition of LDL. No effect of smoking or use of medication was observed. We conclude that although LDL resistance to oxidation may be a factor in atherogenesis, the ex vivo measure is not a strong predictor of severity of coronary atherosclerosis.


Key Words: LDL oxidation • atherosclerosis • resistance time • propagation rate • LDL composition




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