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The Cholesteryl ester transfer protein (CEPT) TaqIB polymorphism in the Cholesterol and Recurrent Events study: No interaction with the response to pravastatin therapy and no effects on cardiovascular outcome a prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy
On the basis of quantitative coronary angiography data, the cholesteryl ester transfer protein (CETP) TaqIB gene polymorphism has been postulated to predict the progression of coronary atherosclerosis and response to cholesterol-lowering therapy. Cholesteryl ester transfer protein mediates the excha...
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Published in: | Journal of the American College of Cardiology 2004-03, Vol.43 (5), p.854-857 |
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creator | DE GROOTH, Greetje J ZERBA, Kim E JUKEMA, J. Wouter SACKS, Frank M KASTELEIN, John J. P KUIVENHOVEN, Jan Albert HUANG, Shu-Pang TSUCHIHASHI, Zenta KIRCHGESSNER, Todd BELDER, René VISHNUPAD, Priya BEIHONG HU KLERKX, Anke H. E. M ZWINDERMAN, Aeilko H |
description | On the basis of quantitative coronary angiography data, the cholesteryl ester transfer protein (CETP) TaqIB gene polymorphism has been postulated to predict the progression of coronary atherosclerosis and response to cholesterol-lowering therapy.
Cholesteryl ester transfer protein mediates the exchange of lipids between anti-atherogenic high-density lipoprotein (HDL) and atherogenic apolipoprotein B containing lipoproteins and therefore plays a key role in human lipid metabolism. Hence, CETP gene polymorphisms may alter susceptibility to atherosclerosis.
To investigate the significance of the CETP TaqIB gene polymorphism with respect to clinical end points, we used the Cholesterol And Recurrent Events (CARE) cohort. The CARE study was designed to investigate the effect of five years of pravastatin therapy on coronary events.
We found that the odds ratios for the primary end point were not significantly different from unity for the three genetic subgroups after five years of placebo treatment. Furthermore, pravastatin induced similar changes in total cholesterol, low-density lipoprotein cholesterol, and HDL cholesterol among TaqIB genotypes, and both nonfatal myocardial infarction and deaths from coronary heart disease were reduced to the same extent in all three genotypes.
In the CARE cohort, the CETP TaqIB polymorphism does not predict cardiovascular events or discriminate between those who will or will not benefit from pravastatin treatment. |
doi_str_mv | 10.1016/j.jacc.2003.08.056 |
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Cholesteryl ester transfer protein mediates the exchange of lipids between anti-atherogenic high-density lipoprotein (HDL) and atherogenic apolipoprotein B containing lipoproteins and therefore plays a key role in human lipid metabolism. Hence, CETP gene polymorphisms may alter susceptibility to atherosclerosis.
To investigate the significance of the CETP TaqIB gene polymorphism with respect to clinical end points, we used the Cholesterol And Recurrent Events (CARE) cohort. The CARE study was designed to investigate the effect of five years of pravastatin therapy on coronary events.
We found that the odds ratios for the primary end point were not significantly different from unity for the three genetic subgroups after five years of placebo treatment. Furthermore, pravastatin induced similar changes in total cholesterol, low-density lipoprotein cholesterol, and HDL cholesterol among TaqIB genotypes, and both nonfatal myocardial infarction and deaths from coronary heart disease were reduced to the same extent in all three genotypes.
In the CARE cohort, the CETP TaqIB polymorphism does not predict cardiovascular events or discriminate between those who will or will not benefit from pravastatin treatment.</description><identifier>ISSN: 0735-1097</identifier><identifier>EISSN: 1558-3597</identifier><identifier>DOI: 10.1016/j.jacc.2003.08.056</identifier><identifier>PMID: 14998629</identifier><identifier>CODEN: JACCDI</identifier><language>eng</language><publisher>New York, NY: Elsevier Science</publisher><subject>Adult ; Aged ; Angiography ; Anticholesteremic Agents - therapeutic use ; Apolipoprotein B ; Arteriosclerosis ; Atherosclerosis ; Biological and medical sciences ; Cardiology ; Cardiology. Vascular system ; Cardiovascular disease ; Cardiovascular diseases ; Carrier Proteins - genetics ; CETP gene ; Cholesterol ; Cholesterol Ester Transfer Proteins ; Cholesteryl ester transfer protein ; Coronary artery disease ; Coronary Artery Disease - blood ; Coronary Artery Disease - drug therapy ; Coronary Artery Disease - genetics ; Data transfer (computers) ; Density ; Female ; Gene polymorphism ; Genotypes ; Glycoproteins ; Heart attacks ; Heart diseases ; High density lipoprotein ; Humans ; Lipid metabolism ; Lipids ; Lipoproteins ; Male ; Medical sciences ; Metabolism ; Middle Aged ; Myocardial infarction ; Polymorphism ; Polymorphism, Genetic ; Pravastatin ; Pravastatin - therapeutic use ; Prospective Studies ; Proteins ; Recurrence ; Site-Specific DNA-Methyltransferase (Adenine-Specific) - genetics ; Subgroups ; Therapy ; Time Factors ; Treatment Outcome</subject><ispartof>Journal of the American College of Cardiology, 2004-03, Vol.43 (5), p.854-857</ispartof><rights>2004 INIST-CNRS</rights><rights>Copyright Elsevier Limited Mar 3, 2004</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></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=15524217$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14998629$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>DE GROOTH, Greetje J</creatorcontrib><creatorcontrib>ZERBA, Kim E</creatorcontrib><creatorcontrib>JUKEMA, J. Wouter</creatorcontrib><creatorcontrib>SACKS, Frank M</creatorcontrib><creatorcontrib>KASTELEIN, John J. P</creatorcontrib><creatorcontrib>KUIVENHOVEN, Jan Albert</creatorcontrib><creatorcontrib>HUANG, Shu-Pang</creatorcontrib><creatorcontrib>TSUCHIHASHI, Zenta</creatorcontrib><creatorcontrib>KIRCHGESSNER, Todd</creatorcontrib><creatorcontrib>BELDER, René</creatorcontrib><creatorcontrib>VISHNUPAD, Priya</creatorcontrib><creatorcontrib>BEIHONG HU</creatorcontrib><creatorcontrib>KLERKX, Anke H. E. M</creatorcontrib><creatorcontrib>ZWINDERMAN, Aeilko H</creatorcontrib><title>The Cholesteryl ester transfer protein (CEPT) TaqIB polymorphism in the Cholesterol and Recurrent Events study: No interaction with the response to pravastatin therapy and no effects on cardiovascular outcome a prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy</title><title>Journal of the American College of Cardiology</title><addtitle>J Am Coll Cardiol</addtitle><description>On the basis of quantitative coronary angiography data, the cholesteryl ester transfer protein (CETP) TaqIB gene polymorphism has been postulated to predict the progression of coronary atherosclerosis and response to cholesterol-lowering therapy.
Cholesteryl ester transfer protein mediates the exchange of lipids between anti-atherogenic high-density lipoprotein (HDL) and atherogenic apolipoprotein B containing lipoproteins and therefore plays a key role in human lipid metabolism. Hence, CETP gene polymorphisms may alter susceptibility to atherosclerosis.
To investigate the significance of the CETP TaqIB gene polymorphism with respect to clinical end points, we used the Cholesterol And Recurrent Events (CARE) cohort. The CARE study was designed to investigate the effect of five years of pravastatin therapy on coronary events.
We found that the odds ratios for the primary end point were not significantly different from unity for the three genetic subgroups after five years of placebo treatment. Furthermore, pravastatin induced similar changes in total cholesterol, low-density lipoprotein cholesterol, and HDL cholesterol among TaqIB genotypes, and both nonfatal myocardial infarction and deaths from coronary heart disease were reduced to the same extent in all three genotypes.
In the CARE cohort, the CETP TaqIB polymorphism does not predict cardiovascular events or discriminate between those who will or will not benefit from pravastatin treatment.</description><subject>Adult</subject><subject>Aged</subject><subject>Angiography</subject><subject>Anticholesteremic Agents - therapeutic use</subject><subject>Apolipoprotein B</subject><subject>Arteriosclerosis</subject><subject>Atherosclerosis</subject><subject>Biological and medical sciences</subject><subject>Cardiology</subject><subject>Cardiology. Vascular system</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Carrier Proteins - genetics</subject><subject>CETP gene</subject><subject>Cholesterol</subject><subject>Cholesterol Ester Transfer Proteins</subject><subject>Cholesteryl ester transfer protein</subject><subject>Coronary artery disease</subject><subject>Coronary Artery Disease - blood</subject><subject>Coronary Artery Disease - drug therapy</subject><subject>Coronary Artery Disease - genetics</subject><subject>Data transfer (computers)</subject><subject>Density</subject><subject>Female</subject><subject>Gene polymorphism</subject><subject>Genotypes</subject><subject>Glycoproteins</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>High density lipoprotein</subject><subject>Humans</subject><subject>Lipid metabolism</subject><subject>Lipids</subject><subject>Lipoproteins</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Myocardial infarction</subject><subject>Polymorphism</subject><subject>Polymorphism, Genetic</subject><subject>Pravastatin</subject><subject>Pravastatin - therapeutic use</subject><subject>Prospective Studies</subject><subject>Proteins</subject><subject>Recurrence</subject><subject>Site-Specific DNA-Methyltransferase (Adenine-Specific) - genetics</subject><subject>Subgroups</subject><subject>Therapy</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><issn>0735-1097</issn><issn>1558-3597</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><recordid>eNp9ksFu1DAQhgMC0aXwAhyQpQoEhwQ7iRObG6wWqFRBVYXzauo4rFdOnNrOVnl7ht2tigBx8djyN__8M5okecFoxiir3m2zLSiV5ZQWGRUZ5dXDZME4F2nBZf0oWdC64Cmjsj5JnoawpZRWgsknyQkrpRRVLhcPrpqNJsuNszpE7WdL9pFED0Po8DJ6F7UZyJvl6rJ5Sxq4Of9IRmfn3vlxY0JP8DP-ruEsgaElV1pN3ushktUOz0BCnNr5PfnqMAMxUNG4gdyauNnnex1GNwRNosOisIMQIR60PYzzXnNwRHedVqiGqQp8axyCarLgiZuicr0m8MtzGJEyO3wNYOdgMKE72Fw1l__q4j96WPgvx-q-29S6W-3N8OPO6rPkcQc26OfHeJp8_7Rqll_Si2-fz5cfLtJNQVlMednqHLRUJQjFmW4ZaMWl4qWCqspr0fLrrqaszUte1l0hBChBBQdVsUoyWZwmrw-62O_NhG7WvQlKWwuDdlNY14hJXgkEz_4At27yOJiwZpxWrKxzxpB6eaSm616369GbHvy8vtsVBF4dARwR2A5XRJlwz3Gelzmri5-ET9id</recordid><startdate>20040303</startdate><enddate>20040303</enddate><creator>DE GROOTH, Greetje J</creator><creator>ZERBA, Kim E</creator><creator>JUKEMA, J. Wouter</creator><creator>SACKS, Frank M</creator><creator>KASTELEIN, John J. P</creator><creator>KUIVENHOVEN, Jan Albert</creator><creator>HUANG, Shu-Pang</creator><creator>TSUCHIHASHI, Zenta</creator><creator>KIRCHGESSNER, Todd</creator><creator>BELDER, René</creator><creator>VISHNUPAD, Priya</creator><creator>BEIHONG HU</creator><creator>KLERKX, Anke H. E. 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P ; KUIVENHOVEN, Jan Albert ; HUANG, Shu-Pang ; TSUCHIHASHI, Zenta ; KIRCHGESSNER, Todd ; BELDER, René ; VISHNUPAD, Priya ; BEIHONG HU ; KLERKX, Anke H. E. M ; ZWINDERMAN, Aeilko H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h301t-54de2ae9c4a8c51ed1aec59c54ca66278d5bf701d24547f388ac8085ac6169193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Angiography</topic><topic>Anticholesteremic Agents - therapeutic use</topic><topic>Apolipoprotein B</topic><topic>Arteriosclerosis</topic><topic>Atherosclerosis</topic><topic>Biological and medical sciences</topic><topic>Cardiology</topic><topic>Cardiology. Vascular system</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Carrier Proteins - genetics</topic><topic>CETP gene</topic><topic>Cholesterol</topic><topic>Cholesterol Ester Transfer Proteins</topic><topic>Cholesteryl ester transfer protein</topic><topic>Coronary artery disease</topic><topic>Coronary Artery Disease - blood</topic><topic>Coronary Artery Disease - drug therapy</topic><topic>Coronary Artery Disease - genetics</topic><topic>Data transfer (computers)</topic><topic>Density</topic><topic>Female</topic><topic>Gene polymorphism</topic><topic>Genotypes</topic><topic>Glycoproteins</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>High density lipoprotein</topic><topic>Humans</topic><topic>Lipid metabolism</topic><topic>Lipids</topic><topic>Lipoproteins</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Myocardial infarction</topic><topic>Polymorphism</topic><topic>Polymorphism, Genetic</topic><topic>Pravastatin</topic><topic>Pravastatin - therapeutic use</topic><topic>Prospective Studies</topic><topic>Proteins</topic><topic>Recurrence</topic><topic>Site-Specific DNA-Methyltransferase (Adenine-Specific) - genetics</topic><topic>Subgroups</topic><topic>Therapy</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>DE GROOTH, Greetje J</creatorcontrib><creatorcontrib>ZERBA, Kim E</creatorcontrib><creatorcontrib>JUKEMA, J. 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P</au><au>KUIVENHOVEN, Jan Albert</au><au>HUANG, Shu-Pang</au><au>TSUCHIHASHI, Zenta</au><au>KIRCHGESSNER, Todd</au><au>BELDER, René</au><au>VISHNUPAD, Priya</au><au>BEIHONG HU</au><au>KLERKX, Anke H. E. M</au><au>ZWINDERMAN, Aeilko H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The Cholesteryl ester transfer protein (CEPT) TaqIB polymorphism in the Cholesterol and Recurrent Events study: No interaction with the response to pravastatin therapy and no effects on cardiovascular outcome a prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy</atitle><jtitle>Journal of the American College of Cardiology</jtitle><addtitle>J Am Coll Cardiol</addtitle><date>2004-03-03</date><risdate>2004</risdate><volume>43</volume><issue>5</issue><spage>854</spage><epage>857</epage><pages>854-857</pages><issn>0735-1097</issn><eissn>1558-3597</eissn><coden>JACCDI</coden><abstract>On the basis of quantitative coronary angiography data, the cholesteryl ester transfer protein (CETP) TaqIB gene polymorphism has been postulated to predict the progression of coronary atherosclerosis and response to cholesterol-lowering therapy.
Cholesteryl ester transfer protein mediates the exchange of lipids between anti-atherogenic high-density lipoprotein (HDL) and atherogenic apolipoprotein B containing lipoproteins and therefore plays a key role in human lipid metabolism. Hence, CETP gene polymorphisms may alter susceptibility to atherosclerosis.
To investigate the significance of the CETP TaqIB gene polymorphism with respect to clinical end points, we used the Cholesterol And Recurrent Events (CARE) cohort. The CARE study was designed to investigate the effect of five years of pravastatin therapy on coronary events.
We found that the odds ratios for the primary end point were not significantly different from unity for the three genetic subgroups after five years of placebo treatment. Furthermore, pravastatin induced similar changes in total cholesterol, low-density lipoprotein cholesterol, and HDL cholesterol among TaqIB genotypes, and both nonfatal myocardial infarction and deaths from coronary heart disease were reduced to the same extent in all three genotypes.
In the CARE cohort, the CETP TaqIB polymorphism does not predict cardiovascular events or discriminate between those who will or will not benefit from pravastatin treatment.</abstract><cop>New York, NY</cop><pub>Elsevier Science</pub><pmid>14998629</pmid><doi>10.1016/j.jacc.2003.08.056</doi><tpages>4</tpages></addata></record> |
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subjects | Adult Aged Angiography Anticholesteremic Agents - therapeutic use Apolipoprotein B Arteriosclerosis Atherosclerosis Biological and medical sciences Cardiology Cardiology. Vascular system Cardiovascular disease Cardiovascular diseases Carrier Proteins - genetics CETP gene Cholesterol Cholesterol Ester Transfer Proteins Cholesteryl ester transfer protein Coronary artery disease Coronary Artery Disease - blood Coronary Artery Disease - drug therapy Coronary Artery Disease - genetics Data transfer (computers) Density Female Gene polymorphism Genotypes Glycoproteins Heart attacks Heart diseases High density lipoprotein Humans Lipid metabolism Lipids Lipoproteins Male Medical sciences Metabolism Middle Aged Myocardial infarction Polymorphism Polymorphism, Genetic Pravastatin Pravastatin - therapeutic use Prospective Studies Proteins Recurrence Site-Specific DNA-Methyltransferase (Adenine-Specific) - genetics Subgroups Therapy Time Factors Treatment Outcome |
title | The Cholesteryl ester transfer protein (CEPT) TaqIB polymorphism in the Cholesterol and Recurrent Events study: No interaction with the response to pravastatin therapy and no effects on cardiovascular outcome a prospective analysis of the CETP TaqIB polymorphism on cardiovascular outcome and interaction with cholesterol-lowering therapy |
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