LDL Oxidation and Extent of Coronary Atherosclerosis

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 su...

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Veröffentlicht in:Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 1998-02, Vol.18 (2), p.193-199
Hauptverfasser: van de Vijver, Lucy P.L, Kardinaal, Alwine F.M, Kruijssen, Dick A.C.M, Grobbee, Diederick E, van Poppel, Geert, Princen, Hans M.G
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container_end_page 199
container_issue 2
container_start_page 193
container_title Arteriosclerosis, thrombosis, and vascular biology
container_volume 18
creator van de Vijver, Lucy P.L
Kardinaal, Alwine F.M
Kruijssen, Dick A.C.M
Grobbee, Diederick E
van Poppel, Geert
Princen, Hans M.G
description 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 (>or= to 85% stenosis in one and >or= to 50% stenosis in a second major coronary vessel) were classified as case subjects (n = 91). Hospital control subjects with no or minor stenosis (
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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 (&gt;or= to 85% stenosis in one and &gt;or= to 50% stenosis in a second major coronary vessel) were classified as case subjects (n = 91). Hospital control subjects with no or minor stenosis (&lt;or= equal to 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 &lt; .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. 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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 (&gt;or= to 85% stenosis in one and &gt;or= to 50% stenosis in a second major coronary vessel) were classified as case subjects (n = 91). Hospital control subjects with no or minor stenosis (&lt;or= equal to 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 &lt; .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. (Arterioscler Thromb Vasc Biol. 1998;18:193-199.)</description><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Angiography</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - diagnostic imaging</subject><subject>Coronary Artery Disease - etiology</subject><subject>Female</subject><subject>Humans</subject><subject>Lipoproteins - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Odds Ratio</subject><subject>Oxidation-Reduction</subject><subject>Predictive Value of Tests</subject><subject>Risk Factors</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkU1rGzEQhkVpcJ20554KSym57VoafR-Nm6QBgy9ur2K8q8WbrleutEvSfx8ZmxxyGM2IeWbQ-4qQr4xWjCm2oKxabv9UzFRQMcs_kDmTIEqhuPqYa6ptKZWAT-Q6pSdKqQCgMzKzwghr-JyI9c91sXnpGhy7MBQ4NMXdy-iHsQhtsQoxDBj_F8tx72NIdX86u_SZXLXYJ__lkm_I7_u77epXud48PK6W67IWSusSGm7QWGF32DLP0GrUyqtWNNxz1YIUFhtpcad9LXcUEAxIS2vOoEXOBb8ht-e9xxj-TT6N7tCl2vc9Dj5MyWmrqQYwGfz-DnwKUxzy2xxkyVYJfoIWZ6jOIlL0rTvG7pDlOUbdyUxHmctmOmYcuGxmnvh2WTvtDr554y_u5f6PSx9TjX0bcai79IYBE4ZLmTFxxp5DP_qY_vbTs49u77Ef9-70KVxRWTJrDYV8LXNQzV8BPECJjA</recordid><startdate>199802</startdate><enddate>199802</enddate><creator>van de Vijver, Lucy P.L</creator><creator>Kardinaal, Alwine F.M</creator><creator>Kruijssen, Dick A.C.M</creator><creator>Grobbee, Diederick E</creator><creator>van Poppel, Geert</creator><creator>Princen, Hans M.G</creator><general>American Heart Association, Inc</general><general>Lippincott</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>7X8</scope></search><sort><creationdate>199802</creationdate><title>LDL Oxidation and Extent of Coronary Atherosclerosis</title><author>van de Vijver, Lucy P.L ; Kardinaal, Alwine F.M ; Kruijssen, Dick A.C.M ; Grobbee, Diederick E ; van Poppel, Geert ; Princen, Hans M.G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4677-2d38a8949baf1e1a97a76e6f4d3e36f2549ad59ab7ec5b02a282590c312fa3343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Angiography</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - diagnostic imaging</topic><topic>Coronary Artery Disease - etiology</topic><topic>Female</topic><topic>Humans</topic><topic>Lipoproteins - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Odds Ratio</topic><topic>Oxidation-Reduction</topic><topic>Predictive Value of Tests</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>van de Vijver, Lucy P.L</creatorcontrib><creatorcontrib>Kardinaal, Alwine F.M</creatorcontrib><creatorcontrib>Kruijssen, Dick A.C.M</creatorcontrib><creatorcontrib>Grobbee, Diederick E</creatorcontrib><creatorcontrib>van Poppel, Geert</creatorcontrib><creatorcontrib>Princen, Hans M.G</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>MEDLINE - Academic</collection><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>van de Vijver, Lucy P.L</au><au>Kardinaal, Alwine F.M</au><au>Kruijssen, Dick A.C.M</au><au>Grobbee, Diederick E</au><au>van Poppel, Geert</au><au>Princen, Hans M.G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LDL Oxidation and Extent of Coronary Atherosclerosis</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>1998-02</date><risdate>1998</risdate><volume>18</volume><issue>2</issue><spage>193</spage><epage>199</epage><pages>193-199</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><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 (&gt;or= to 85% stenosis in one and &gt;or= to 50% stenosis in a second major coronary vessel) were classified as case subjects (n = 91). Hospital control subjects with no or minor stenosis (&lt;or= equal to 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 &lt; .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. (Arterioscler Thromb Vasc Biol. 1998;18:193-199.)</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9484983</pmid><doi>10.1161/01.ATV.18.2.193</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Aged
Aged, 80 and over
Atherosclerosis (general aspects, experimental research)
Biological and medical sciences
Blood and lymphatic vessels
Cardiology. Vascular system
Coronary Angiography
Coronary Artery Disease - blood
Coronary Artery Disease - diagnostic imaging
Coronary Artery Disease - etiology
Female
Humans
Lipoproteins - metabolism
Male
Medical sciences
Middle Aged
Odds Ratio
Oxidation-Reduction
Predictive Value of Tests
Risk Factors
title LDL Oxidation and Extent of Coronary Atherosclerosis
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