Distribution of ApoA-I–Containing HDL Subpopulations in Patients With Coronary Heart Disease
Abstract—High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater...
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| Veröffentlicht in: | Arteriosclerosis, thrombosis, and vascular biology thrombosis, and vascular biology, 2000-12, Vol.20 (12), p.2670-2676 |
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| container_title | Arteriosclerosis, thrombosis, and vascular biology |
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| creator | Asztalos, Bela F Roheim, Paul S Milani, Richard L Lefevre, Michael McNamara, Judith R Horvath, Katalin V Schaefer, Ernst J |
| description | Abstract—High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I–containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (−14%, P |
| doi_str_mv | 10.1161/01.ATV.20.12.2670 |
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HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I–containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (−14%, P<0.001), whereas total cholesterol and the low density lipoprotein cholesterol/HDL-C ratio were higher (9% [P <0.05] and 21% [P <0.01], respectively) compared with control levels. No significant differences were found for low density lipoprotein cholesterol, triglyceride, and apoA-I levels. In CHD subjects, there were significantly (P <0.001) lower concentrations of the large lipoprotein (Lp)A-I α1 (−35%), pre-α1 (−50%), pre-α2 (−33%), and pre-α3 (−31%) subpopulations, whereas the concentrations of the small LpA-I/A-II α3 particles were significantly (P <0.001) higher (20%). Because α1 was decreased more than HDL-C and plasma apoA-I concentrations in CHD subjects, the ratios of HDL-C to α1 and of apoA-I to α1 were significantly (P <0.001) higher by 36% and 57%, respectively, compared with control values. Subjects with low HDL-C levels (≤35 mg/dL) have different distributions of apoA-I–containing HDL subpopulations than do subjects with normal HDL-C levels (>35 mg/dL). Therefore, we stratified participants according to HDL-C concentrations into low and normal groups. The differences in lipid levels between controls and HDL-C–matched cases substantially decreased; however, the significant differences in HDL subspecies remained. Our research findings support the concept that compared with control subjects, CHD patients not only have HDL deficiency but also have a major rearrangement in the HDL subpopulations with significantly lower α1 and pre-α1–3 (LpA-I) and significantly higher α3 (LpA-I/A-II) particles.]]></description><identifier>ISSN: 1079-5642</identifier><identifier>EISSN: 1524-4636</identifier><identifier>DOI: 10.1161/01.ATV.20.12.2670</identifier><identifier>PMID: 11116070</identifier><identifier>CODEN: ATVBFA</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Adult ; Aged ; Aged, 80 and over ; Analysis of Variance ; Apolipoprotein A-I - chemistry ; Apolipoprotein A-I - metabolism ; Biological and medical sciences ; Cardiology. Vascular system ; Cholesterol - blood ; Cholesterol, HDL - blood ; Cholesterol, LDL - blood ; Coronary Disease - blood ; Coronary Disease - metabolism ; Coronary heart disease ; Electrophoresis, Gel, Two-Dimensional ; Heart ; Humans ; Lipoproteins, HDL - chemistry ; Lipoproteins, HDL - metabolism ; Male ; Medical sciences ; Middle Aged ; Risk Factors</subject><ispartof>Arteriosclerosis, thrombosis, and vascular biology, 2000-12, Vol.20 (12), p.2670-2676</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Dec 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5234-7378db261cc18dcc62c7dd7fcb2187f5a9c23a09d367e980ccc2752dce21677e3</citedby><cites>FETCH-LOGICAL-c5234-7378db261cc18dcc62c7dd7fcb2187f5a9c23a09d367e980ccc2752dce21677e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=833216$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11116070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Asztalos, Bela F</creatorcontrib><creatorcontrib>Roheim, Paul S</creatorcontrib><creatorcontrib>Milani, Richard L</creatorcontrib><creatorcontrib>Lefevre, Michael</creatorcontrib><creatorcontrib>McNamara, Judith R</creatorcontrib><creatorcontrib>Horvath, Katalin V</creatorcontrib><creatorcontrib>Schaefer, Ernst J</creatorcontrib><title>Distribution of ApoA-I–Containing HDL Subpopulations in Patients With Coronary Heart Disease</title><title>Arteriosclerosis, thrombosis, and vascular biology</title><addtitle>Arterioscler Thromb Vasc Biol</addtitle><description><![CDATA[Abstract—High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I–containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (−14%, P<0.001), whereas total cholesterol and the low density lipoprotein cholesterol/HDL-C ratio were higher (9% [P <0.05] and 21% [P <0.01], respectively) compared with control levels. No significant differences were found for low density lipoprotein cholesterol, triglyceride, and apoA-I levels. In CHD subjects, there were significantly (P <0.001) lower concentrations of the large lipoprotein (Lp)A-I α1 (−35%), pre-α1 (−50%), pre-α2 (−33%), and pre-α3 (−31%) subpopulations, whereas the concentrations of the small LpA-I/A-II α3 particles were significantly (P <0.001) higher (20%). Because α1 was decreased more than HDL-C and plasma apoA-I concentrations in CHD subjects, the ratios of HDL-C to α1 and of apoA-I to α1 were significantly (P <0.001) higher by 36% and 57%, respectively, compared with control values. Subjects with low HDL-C levels (≤35 mg/dL) have different distributions of apoA-I–containing HDL subpopulations than do subjects with normal HDL-C levels (>35 mg/dL). Therefore, we stratified participants according to HDL-C concentrations into low and normal groups. The differences in lipid levels between controls and HDL-C–matched cases substantially decreased; however, the significant differences in HDL subspecies remained. Our research findings support the concept that compared with control subjects, CHD patients not only have HDL deficiency but also have a major rearrangement in the HDL subpopulations with significantly lower α1 and pre-α1–3 (LpA-I) and significantly higher α3 (LpA-I/A-II) particles.]]></description><subject>Adult</subject><subject>Aged</subject><subject>Aged, 80 and over</subject><subject>Analysis of Variance</subject><subject>Apolipoprotein A-I - chemistry</subject><subject>Apolipoprotein A-I - metabolism</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Cholesterol - blood</subject><subject>Cholesterol, HDL - blood</subject><subject>Cholesterol, LDL - blood</subject><subject>Coronary Disease - blood</subject><subject>Coronary Disease - metabolism</subject><subject>Coronary heart disease</subject><subject>Electrophoresis, Gel, Two-Dimensional</subject><subject>Heart</subject><subject>Humans</subject><subject>Lipoproteins, HDL - chemistry</subject><subject>Lipoproteins, HDL - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Risk Factors</subject><issn>1079-5642</issn><issn>1524-4636</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkd-K1DAUxoMo7h99AG8kKOxdx-SkTdrLYVadhQEFV70zpGnqZO0kNWlZvPMdfEOfxFNmUDCQnC_wOx85Xwh5xtmKc8lfMb5a335aAV5hBVKxB-ScV1AWpRTyIWqmmqKSJZyRi5zvGGMlAHtMzjguyRQ7J1-ufZ6Sb-fJx0BjT9djXBc3v3_-2sQwGR98-Eq31zv6YW7HOM6DWcBMfaDvUbowZfrZT3u6iSkGk37QrTNpomjrTHZPyKPeDNk9PdVL8vHN69vNtti9e3uzWe8KW4EoCyVU3bUgubW87qyVYFXXqd62wGvVV6axIAxrOiGVa2pmrQVVQWcdcKmUE5fk6ug7pvh9dnnSB5-tGwYTXJyzVlAiLxoEX_wH3sU5BXybBkynkaypEeJHyKaYc3K9HpM_4HCaM70krxnXmDy2aA56SR57np-M5_bgun8dp6gReHkCTLZm6JMJ1ue_XC0EzoJUeaTu4zC5lL8N871Leu_MMO318oNCsqoAVHw5CtyiFH8AQEeawQ</recordid><startdate>200012</startdate><enddate>200012</enddate><creator>Asztalos, Bela F</creator><creator>Roheim, Paul S</creator><creator>Milani, Richard L</creator><creator>Lefevre, Michael</creator><creator>McNamara, Judith R</creator><creator>Horvath, Katalin V</creator><creator>Schaefer, Ernst J</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>200012</creationdate><title>Distribution of ApoA-I–Containing HDL Subpopulations in Patients With Coronary Heart Disease</title><author>Asztalos, Bela F ; Roheim, Paul S ; Milani, Richard L ; Lefevre, Michael ; McNamara, Judith R ; Horvath, Katalin V ; Schaefer, Ernst J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5234-7378db261cc18dcc62c7dd7fcb2187f5a9c23a09d367e980ccc2752dce21677e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Aged, 80 and over</topic><topic>Analysis of Variance</topic><topic>Apolipoprotein A-I - chemistry</topic><topic>Apolipoprotein A-I - metabolism</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Cholesterol - blood</topic><topic>Cholesterol, HDL - blood</topic><topic>Cholesterol, LDL - blood</topic><topic>Coronary Disease - blood</topic><topic>Coronary Disease - metabolism</topic><topic>Coronary heart disease</topic><topic>Electrophoresis, Gel, Two-Dimensional</topic><topic>Heart</topic><topic>Humans</topic><topic>Lipoproteins, HDL - chemistry</topic><topic>Lipoproteins, HDL - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Risk Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Asztalos, Bela F</creatorcontrib><creatorcontrib>Roheim, Paul S</creatorcontrib><creatorcontrib>Milani, Richard L</creatorcontrib><creatorcontrib>Lefevre, Michael</creatorcontrib><creatorcontrib>McNamara, Judith R</creatorcontrib><creatorcontrib>Horvath, Katalin V</creatorcontrib><creatorcontrib>Schaefer, Ernst J</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 & 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>Asztalos, Bela F</au><au>Roheim, Paul S</au><au>Milani, Richard L</au><au>Lefevre, Michael</au><au>McNamara, Judith R</au><au>Horvath, Katalin V</au><au>Schaefer, Ernst J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Distribution of ApoA-I–Containing HDL Subpopulations in Patients With Coronary Heart Disease</atitle><jtitle>Arteriosclerosis, thrombosis, and vascular biology</jtitle><addtitle>Arterioscler Thromb Vasc Biol</addtitle><date>2000-12</date><risdate>2000</risdate><volume>20</volume><issue>12</issue><spage>2670</spage><epage>2676</epage><pages>2670-2676</pages><issn>1079-5642</issn><eissn>1524-4636</eissn><coden>ATVBFA</coden><abstract><![CDATA[Abstract—High density lipoproteins (HDLs) and their subspecies play a role in the development of coronary heart disease (CHD). HDL subpopulations were measured by 2-dimensional nondenaturing gel electrophoresis in 79 male control subjects and 76 male CHD patients to test the hypothesis that greater differences in apolipoprotein (apo)A-I–containing HDL subpopulations would exist between these 2 groups than for traditional lipid levels. In CHD subjects, HDL cholesterol (HDL-C) was lower (−14%, P<0.001), whereas total cholesterol and the low density lipoprotein cholesterol/HDL-C ratio were higher (9% [P <0.05] and 21% [P <0.01], respectively) compared with control levels. No significant differences were found for low density lipoprotein cholesterol, triglyceride, and apoA-I levels. In CHD subjects, there were significantly (P <0.001) lower concentrations of the large lipoprotein (Lp)A-I α1 (−35%), pre-α1 (−50%), pre-α2 (−33%), and pre-α3 (−31%) subpopulations, whereas the concentrations of the small LpA-I/A-II α3 particles were significantly (P <0.001) higher (20%). Because α1 was decreased more than HDL-C and plasma apoA-I concentrations in CHD subjects, the ratios of HDL-C to α1 and of apoA-I to α1 were significantly (P <0.001) higher by 36% and 57%, respectively, compared with control values. Subjects with low HDL-C levels (≤35 mg/dL) have different distributions of apoA-I–containing HDL subpopulations than do subjects with normal HDL-C levels (>35 mg/dL). Therefore, we stratified participants according to HDL-C concentrations into low and normal groups. The differences in lipid levels between controls and HDL-C–matched cases substantially decreased; however, the significant differences in HDL subspecies remained. Our research findings support the concept that compared with control subjects, CHD patients not only have HDL deficiency but also have a major rearrangement in the HDL subpopulations with significantly lower α1 and pre-α1–3 (LpA-I) and significantly higher α3 (LpA-I/A-II) particles.]]></abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>11116070</pmid><doi>10.1161/01.ATV.20.12.2670</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1079-5642 |
| ispartof | Arteriosclerosis, thrombosis, and vascular biology, 2000-12, Vol.20 (12), p.2670-2676 |
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| subjects | Adult Aged Aged, 80 and over Analysis of Variance Apolipoprotein A-I - chemistry Apolipoprotein A-I - metabolism Biological and medical sciences Cardiology. Vascular system Cholesterol - blood Cholesterol, HDL - blood Cholesterol, LDL - blood Coronary Disease - blood Coronary Disease - metabolism Coronary heart disease Electrophoresis, Gel, Two-Dimensional Heart Humans Lipoproteins, HDL - chemistry Lipoproteins, HDL - metabolism Male Medical sciences Middle Aged Risk Factors |
| title | Distribution of ApoA-I–Containing HDL Subpopulations in Patients With Coronary Heart Disease |
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