Association of Genetic Variants Related to CETP Inhibitors and Statins With Lipoprotein Levels and Cardiovascular Risk.
Identifieur interne : 000520 ( PubMed/Corpus ); précédent : 000519; suivant : 000521Association of Genetic Variants Related to CETP Inhibitors and Statins With Lipoprotein Levels and Cardiovascular Risk.
Auteurs : Brian A. Ference ; John J P. Kastelein ; Henry N. Ginsberg ; M John Chapman ; Stephen J. Nicholls ; Kausik K. Ray ; Chris J. Packard ; Ulrich Laufs ; Robert D. Brook ; Clare Oliver-Williams ; Adam S. Butterworth ; John Danesh ; George Davey Smith ; Alberico L. Catapano ; Marc S. SabatineSource :
- JAMA [ 1538-3598 ] ; 2017.
English descriptors
- KwdEn :
- Anticholesteremic Agents (therapeutic use), Apolipoproteins B (blood), Cardiovascular Diseases (genetics), Cardiovascular Diseases (prevention & control), Cholesterol Ester Transfer Proteins (antagonists & inhibitors), Cholesterol Ester Transfer Proteins (genetics), Cholesterol, HDL (blood), Cholesterol, LDL (blood), Female, Genetic Variation, Humans, Hydroxymethylglutaryl CoA Reductases (genetics), Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use), Hypercholesterolemia (blood), Hypercholesterolemia (drug therapy), Hypercholesterolemia (genetics), Male, Mendelian Randomization Analysis, Middle Aged, Risk Factors.
- MESH :
- chemical , antagonists & inhibitors : Cholesterol Ester Transfer Proteins.
- chemical , blood : Apolipoproteins B, Cholesterol, HDL, Cholesterol, LDL.
- chemical , genetics : Cholesterol Ester Transfer Proteins, Hydroxymethylglutaryl CoA Reductases.
- chemical , therapeutic use : Anticholesteremic Agents, Hydroxymethylglutaryl-CoA Reductase Inhibitors.
- blood : Hypercholesterolemia.
- drug therapy : Hypercholesterolemia.
- genetics : Cardiovascular Diseases, Hypercholesterolemia.
- prevention & control : Cardiovascular Diseases.
- Female, Genetic Variation, Humans, Male, Mendelian Randomization Analysis, Middle Aged, Risk Factors.
Abstract
Some cholesteryl ester transfer protein (CETP) inhibitors lower low-density lipoprotein cholesterol (LDL-C) levels without reducing cardiovascular events, suggesting that the clinical benefit of lowering LDL-C may depend on how LDL-C is lowered.
DOI: 10.1001/jama.2017.11467
PubMed: 28846118
Links to Exploration step
pubmed:28846118Le document en format XML
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Catapano</name><affiliation><nlm:affiliation>Department of Pharmacological and Biomolecular Sciences, University of Milan and Multimedica IRCCS, Milano, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Sabatine, Marc S" sort="Sabatine, Marc S" uniqKey="Sabatine M" first="Marc S" last="Sabatine">Marc S. Sabatine</name><affiliation><nlm:affiliation>Thrombolysis in Myocardial Infarction (TIMI) Study Group, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.</nlm:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2017">2017</date><idno type="RBID">pubmed:28846118</idno><idno type="pmid">28846118</idno><idno type="doi">10.1001/jama.2017.11467</idno><idno type="wicri:Area/PubMed/Corpus">000520</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000520</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Association of Genetic Variants Related to CETP Inhibitors and Statins With Lipoprotein Levels and Cardiovascular Risk.</title><author><name sortKey="Ference, Brian A" sort="Ference, Brian A" uniqKey="Ference B" first="Brian A" last="Ference">Brian A. Ference</name><affiliation><nlm:affiliation>Division of Cardiovascular Medicine, Wayne State University School of Medicine, Detroit, Michigan.</nlm:affiliation></affiliation></author><author><name sortKey="Kastelein, John J P" sort="Kastelein, John J P" uniqKey="Kastelein J" first="John J P" last="Kastelein">John J P. Kastelein</name><affiliation><nlm:affiliation>Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.</nlm:affiliation></affiliation></author><author><name sortKey="Ginsberg, Henry N" sort="Ginsberg, Henry N" uniqKey="Ginsberg H" first="Henry N" last="Ginsberg">Henry N. Ginsberg</name><affiliation><nlm:affiliation>Irving Institute for Clinical and Translational Research, Columbia University College of Physicians and Surgeons, New York, New York.</nlm:affiliation></affiliation></author><author><name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M John" last="Chapman">M John Chapman</name><affiliation><nlm:affiliation>National Institute for Health and Medical Research (INSERM), Pitie-Salpetriere University Hospital, Paris, France.</nlm:affiliation></affiliation></author><author><name sortKey="Nicholls, Stephen J" sort="Nicholls, Stephen J" uniqKey="Nicholls S" first="Stephen J" last="Nicholls">Stephen J. Nicholls</name><affiliation><nlm:affiliation>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.</nlm:affiliation></affiliation></author><author><name sortKey="Ray, Kausik K" sort="Ray, Kausik K" uniqKey="Ray K" first="Kausik K" last="Ray">Kausik K. Ray</name><affiliation><nlm:affiliation>Imperial Centre for Cardiovascular Disease Prevention, Department of Primary Care and Public Health, School of Public Health, Imperial College London, London, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Packard, Chris J" sort="Packard, Chris J" uniqKey="Packard C" first="Chris J" last="Packard">Chris J. Packard</name><affiliation><nlm:affiliation>Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Laufs, Ulrich" sort="Laufs, Ulrich" uniqKey="Laufs U" first="Ulrich" last="Laufs">Ulrich Laufs</name><affiliation><nlm:affiliation>Department of Cardiology, University of Leipzig, Leipzig, Germany.</nlm:affiliation></affiliation></author><author><name sortKey="Brook, Robert D" sort="Brook, Robert D" uniqKey="Brook R" first="Robert D" last="Brook">Robert D. Brook</name><affiliation><nlm:affiliation>Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor.</nlm:affiliation></affiliation></author><author><name sortKey="Oliver Williams, Clare" sort="Oliver Williams, Clare" uniqKey="Oliver Williams C" first="Clare" last="Oliver-Williams">Clare Oliver-Williams</name><affiliation><nlm:affiliation>MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Butterworth, Adam S" sort="Butterworth, Adam S" uniqKey="Butterworth A" first="Adam S" last="Butterworth">Adam S. Butterworth</name><affiliation><nlm:affiliation>MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Danesh, John" sort="Danesh, John" uniqKey="Danesh J" first="John" last="Danesh">John Danesh</name><affiliation><nlm:affiliation>MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Smith, George Davey" sort="Smith, George Davey" uniqKey="Smith G" first="George Davey" last="Smith">George Davey Smith</name><affiliation><nlm:affiliation>MRC Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom.</nlm:affiliation></affiliation></author><author><name sortKey="Catapano, Alberico L" sort="Catapano, Alberico L" uniqKey="Catapano A" first="Alberico L" last="Catapano">Alberico L. Catapano</name><affiliation><nlm:affiliation>Department of Pharmacological and Biomolecular Sciences, University of Milan and Multimedica IRCCS, Milano, Italy.</nlm:affiliation></affiliation></author><author><name sortKey="Sabatine, Marc S" sort="Sabatine, Marc S" uniqKey="Sabatine M" first="Marc S" last="Sabatine">Marc S. Sabatine</name><affiliation><nlm:affiliation>Thrombolysis in Myocardial Infarction (TIMI) Study Group, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.</nlm:affiliation></affiliation></author></analytic><series><title level="j">JAMA</title><idno type="eISSN">1538-3598</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Anticholesteremic Agents (therapeutic use)</term><term>Apolipoproteins B (blood)</term><term>Cardiovascular Diseases (genetics)</term><term>Cardiovascular Diseases (prevention & control)</term><term>Cholesterol Ester Transfer Proteins (antagonists & inhibitors)</term><term>Cholesterol Ester Transfer Proteins (genetics)</term><term>Cholesterol, HDL (blood)</term><term>Cholesterol, LDL (blood)</term><term>Female</term><term>Genetic Variation</term><term>Humans</term><term>Hydroxymethylglutaryl CoA Reductases (genetics)</term><term>Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use)</term><term>Hypercholesterolemia (blood)</term><term>Hypercholesterolemia (drug therapy)</term><term>Hypercholesterolemia (genetics)</term><term>Male</term><term>Mendelian Randomization Analysis</term><term>Middle Aged</term><term>Risk Factors</term></keywords><keywords scheme="MESH" type="chemical" qualifier="antagonists & inhibitors" xml:lang="en"><term>Cholesterol Ester Transfer Proteins</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Apolipoproteins B</term><term>Cholesterol, HDL</term><term>Cholesterol, LDL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cholesterol Ester Transfer Proteins</term><term>Hydroxymethylglutaryl CoA Reductases</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Anticholesteremic Agents</term><term>Hydroxymethylglutaryl-CoA Reductase Inhibitors</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Hypercholesterolemia</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Hypercholesterolemia</term></keywords><keywords scheme="MESH" qualifier="genetics" xml:lang="en"><term>Cardiovascular Diseases</term><term>Hypercholesterolemia</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Cardiovascular Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Female</term><term>Genetic Variation</term><term>Humans</term><term>Male</term><term>Mendelian Randomization Analysis</term><term>Middle Aged</term><term>Risk Factors</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Some cholesteryl ester transfer protein (CETP) inhibitors lower low-density lipoprotein cholesterol (LDL-C) levels without reducing cardiovascular events, suggesting that the clinical benefit of lowering LDL-C may depend on how LDL-C is lowered.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28846118</PMID><DateCreated><Year>2017</Year><Month>08</Month><Day>28</Day></DateCreated><DateCompleted><Year>2017</Year><Month>09</Month><Day>20</Day></DateCompleted><DateRevised><Year>2017</Year><Month>09</Month><Day>22</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1538-3598</ISSN><JournalIssue CitedMedium="Internet"><Volume>318</Volume><Issue>10</Issue><PubDate><Year>2017</Year><Month>09</Month><Day>12</Day></PubDate></JournalIssue><Title>JAMA</Title><ISOAbbreviation>JAMA</ISOAbbreviation></Journal><ArticleTitle>Association of Genetic Variants Related to CETP Inhibitors and Statins With Lipoprotein Levels and Cardiovascular Risk.</ArticleTitle><Pagination><MedlinePgn>947-956</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1001/jama.2017.11467</ELocationID><Abstract><AbstractText Label="Importance">Some cholesteryl ester transfer protein (CETP) inhibitors lower low-density lipoprotein cholesterol (LDL-C) levels without reducing cardiovascular events, suggesting that the clinical benefit of lowering LDL-C may depend on how LDL-C is lowered.</AbstractText><AbstractText Label="Objective">To estimate the association between changes in levels of LDL-C (and other lipoproteins) and the risk of cardiovascular events related to variants in the CETP gene, both alone and in combination with variants in the 3-hydroxy-3-methylglutaryl-CoA reductase (HMGCR) gene.</AbstractText><AbstractText Label="Design, Setting, and Participants">Mendelian randomization analyses evaluating the association between CETP and HMGCR scores, changes in lipid and lipoprotein levels, and the risk of cardiovascular events involving 102 837 participants from 14 cohort or case-control studies conducted in North America or the United Kingdom between 1948 and 2012. The associations with cardiovascular events were externally validated in 189 539 participants from 48 studies conducted between 2011 and 2015.</AbstractText><AbstractText Label="Exposures">Differences in mean high-density lipoprotein cholesterol (HDL-C), LDL-C, and apolipoprotein B (apoB) levels in participants with CETP scores at or above vs below the median.</AbstractText><AbstractText Label="Main Outcomes and Measures">Odds ratio (OR) for major cardiovascular events.</AbstractText><AbstractText Label="Results">The primary analysis included 102 837 participants (mean age, 59.9 years; 58% women) who experienced 13 821 major cardiovascular events. The validation analyses included 189 539 participants (mean age, 58.5 years; 39% women) with 62 240 cases of coronary heart disease (CHD). Considered alone, the CETP score was associated with higher levels of HDL-C, lower LDL-C, concordantly lower apoB, and a corresponding lower risk of major vascular events (OR, 0.946 [95% CI, 0.921-0.972]) that was similar in magnitude to the association between the HMGCR score and risk of major cardiovascular events per unit change in levels of LDL-C (and apoB). When combined with the HMGCR score, the CETP score was associated with the same reduction in LDL-C levels but an attenuated reduction in apoB levels and a corresponding attenuated nonsignificant risk of major cardiovascular events (OR, 0.985 [95% CI, 0.955-1.015]). In external validation analyses, a genetic score consisting of variants with naturally occurring discordance between levels of LDL-C and apoB was associated with a similar risk of CHD per unit change in apoB level (OR, 0.782 [95% CI, 0.720-0.845] vs 0.793 [95% CI, 0.774-0.812]; P = .79 for difference), but a significantly attenuated risk of CHD per unit change in LDL-C level (OR, 0.916 [95% CI, 0.890-0.943] vs 0.831 [95% CI, 0.816-0.847]; P < .001) compared with a genetic score associated with concordant changes in levels of LDL-C and apoB.</AbstractText><AbstractText Label="Conclusions and Relevance">Combined exposure to variants in the genes that encode the targets of CETP inhibitors and statins was associated with discordant reductions in LDL-C and apoB levels and a corresponding risk of cardiovascular events that was proportional to the attenuated reduction in apoB but significantly less than expected per unit change in LDL-C. The clinical benefit of lowering LDL-C levels may therefore depend on the corresponding reduction in apoB-containing lipoprotein particles.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ference</LastName><ForeName>Brian A</ForeName><Initials>BA</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, Wayne State University School of Medicine, Detroit, Michigan.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Institute for Advanced Studies, University of Bristol, Bristol, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kastelein</LastName><ForeName>John J P</ForeName><Initials>JJP</Initials><AffiliationInfo><Affiliation>Department of Vascular Medicine, Academic Medical Center, University of Amsterdam, Amsterdam, the Netherlands.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ginsberg</LastName><ForeName>Henry N</ForeName><Initials>HN</Initials><AffiliationInfo><Affiliation>Irving Institute for Clinical and Translational Research, Columbia University College of Physicians and Surgeons, New York, New York.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chapman</LastName><ForeName>M John</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>National Institute for Health and Medical Research (INSERM), Pitie-Salpetriere University Hospital, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nicholls</LastName><ForeName>Stephen J</ForeName><Initials>SJ</Initials><AffiliationInfo><Affiliation>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ray</LastName><ForeName>Kausik K</ForeName><Initials>KK</Initials><AffiliationInfo><Affiliation>Imperial Centre for Cardiovascular Disease Prevention, Department of Primary Care and Public Health, School of Public Health, Imperial College London, London, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Packard</LastName><ForeName>Chris J</ForeName><Initials>CJ</Initials><AffiliationInfo><Affiliation>Institute of Cardiovascular and Medical Sciences, University of Glasgow, Glasgow, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Laufs</LastName><ForeName>Ulrich</ForeName><Initials>U</Initials><AffiliationInfo><Affiliation>Department of Cardiology, University of Leipzig, Leipzig, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Brook</LastName><ForeName>Robert D</ForeName><Initials>RD</Initials><AffiliationInfo><Affiliation>Division of Cardiovascular Medicine, University of Michigan Medical School, Ann Arbor.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Oliver-Williams</LastName><ForeName>Clare</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Butterworth</LastName><ForeName>Adam S</ForeName><Initials>AS</Initials><AffiliationInfo><Affiliation>MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Danesh</LastName><ForeName>John</ForeName><Initials>J</Initials><AffiliationInfo><Affiliation>MRC/BHF Cardiovascular Epidemiology Unit, Department of Public Health and Primary Care, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>National Institute for Health Research Blood and Transplant Research Unit in Donor Health and Genomics, University of Cambridge, Cambridge, United Kingdom.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Wellcome Trust Sanger Institute, Hinxton, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Smith</LastName><ForeName>George Davey</ForeName><Initials>GD</Initials><AffiliationInfo><Affiliation>MRC Integrative Epidemiology Unit, University of Bristol, Bristol, United Kingdom.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Catapano</LastName><ForeName>Alberico L</ForeName><Initials>AL</Initials><AffiliationInfo><Affiliation>Department of Pharmacological and Biomolecular Sciences, University of Milan and Multimedica IRCCS, Milano, Italy.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sabatine</LastName><ForeName>Marc S</ForeName><Initials>MS</Initials><AffiliationInfo><Affiliation>Thrombolysis in Myocardial Infarction (TIMI) Study Group, Division of Cardiovascular Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>JAMA</MedlineTA><NlmUniqueID>7501160</NlmUniqueID><ISSNLinking>0098-7484</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000924">Anticholesteremic 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