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Ex vivo measures of LDL oxidative susceptibility predict carotid artery disease

Authors :
Hendrickson, Audrey
McKinstry, Laura A.
Lewis, Julieann K.
Lum, Jeremy
Louie, Andy
Schellenberg, Gerard D.
Hatsukami, Thomas S.
Chait, Alan
Jarvik, Gail P.
Source :
Atherosclerosis (00219150). Mar2005, Vol. 179 Issue 1, p147-153. 7p.
Publication Year :
2005

Abstract

Abstract: Aim:: The purpose of the study was to assess whether ex vivo measures of low-density lipoprotein (LDL) oxidation improved prediction of carotid artery disease (CAAD) case-control status compared to standard lipid and smoking measures. Methods:: One hundred and forty cases with a high degree of carotid artery stenosis aged 40–83 years and an equal number of controls without stenosis or other vascular disease were matched by censored age within 2 years. Matched logistic regression evaluated the significance of copper-induced oxidative measures with and without covariates. The relationship of LDL oxidation measures with statin use and current smoking was also evaluated. Results:: Logistic regression demonstrated a significant effect of the three correlated measures of oxidative susceptibility (lag time, oxidation rate and maximal rate of oxidation) separately on disease prediction (all p <0.05). These oxidative measures remained significant predictors of case-control status when other cardiovascular disease predictors (age; LDL-C, HDL-C and ApoAI levels; current smoking, ever smoking and pack-years smoked) were jointly considered. This relationship was not attributable to the effects of statin use on LDL oxidation. Conclusions:: Ex vivo measures of oxidation improved the prediction of carotid artery disease status, suggesting that this is an important determinant of atherosclerotic risk in this older population. [Copyright &y& Elsevier]

Details

Language :
English
ISSN :
00219150
Volume :
179
Issue :
1
Database :
Academic Search Index
Journal :
Atherosclerosis (00219150)
Publication Type :
Academic Journal
Accession number :
17411824
Full Text :
https://doi.org/10.1016/j.atherosclerosis.2004.09.015