Enhanced susceptibility of low-density lipoproteins to oxidation in coronary bypass patients with progression of atherosclerosis
article
Oxidation of low-density lipoprotein (LDL) may play a causal role in atherosclerosis. In this study we analyzed whether the severity of progression of coronary atherosclerosis is related to the susceptibility of LDL to oxidative modification. On the basis of repeated coronary angiography, 28 coronary bypass patients were divided into two groups: group A, 12 patients with, and group B, 16 patients without progression of coronary atherosclerosis. The lag time, reflecting the resistance of LDL to oxidative modification, was significantly smaller in group A as compared with group B (81 ± 10 and 93 ± 15 min, respectively). Besides differences in cholesterol and apolipoprotein B concentrations, the difference in susceptibility of LDL to oxidation significantly contributes to the differences between the progression and the nonprogression group (P = 0.02). In the combined groups of patients, the lag phase of LDL for oxidation was positively correlated with LDL cholesterol ester to protein ratio (r = 0.53, P = 0.01). It is concluded that LDL samples obtained from coronary bypass patients differ with respect to their oxidizability depending on progression of atherosclerosis following coronary bypass surgery. Chemicals/CAS: Apolipoproteins; Ascorbic Acid, 50-81-7; Lipoproteins, LDL; Triglycerides; Vitamin E, 1406-18-4
Topics
apolipoprotein Bcoronary artery bypass surgerycoronary atherosclerosislipid peroxidationlow-density lipoproteinapolipoprotein aapolipoprotein bcholesterolhigh density lipoproteinlow density lipoproteinretinoltriacylglyceroladultagedangiographyarticleatherosclerosisblood analysisclinical articlecontrolled studycoronary artery bypass grafthumanhuman tissuelipid analysislipid oxidationmalepriority journalApolipoproteinsArteriosclerosisAscorbic AcidCentrifugation, Density GradientCoronary Artery BypassDisease ProgressionFollow-Up StudiesHumansLipoproteins, LDLMaleMiddle AgedOxidation-ReductionTriglyceridesVitamin E
TNO Identifier
233105
ISSN
00098981
Source
Clinica Chimica Acta, 243(2), pp. 137-149.
Pages
137-149
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