C-reactive protein, but not low-density lipoprotein cholesterol levels, associate with coronary atheroma regression and cardiovascular events after maximally intensive statin therapy.
Identifieur interne : 001466 ( Ncbi/Merge ); précédent : 001465; suivant : 001467C-reactive protein, but not low-density lipoprotein cholesterol levels, associate with coronary atheroma regression and cardiovascular events after maximally intensive statin therapy.
Auteurs : Rishi Puri ; Steven E. Nissen ; Peter Libby ; Mingyuan Shao ; Christie M. Ballantyne ; Phillip J. Barter ; M John Chapman ; Raimund Erbel ; Joel S. Raichlen ; Kiyoko Uno ; Yu Kataoka ; Stephen J. NichollsSource :
- Circulation [ 1524-4539 ] ; 2013.
Descripteurs français
- KwdFr :
- Acides heptanoïques (administration et posologie), Adulte d'âge moyen, Analyse multivariée, Atorvastatine de calcium, Cholestérol LDL (métabolisme), Estimation de Kaplan-Meier, Femelle, Fluorobenzènes (administration et posologie), Humains, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (administration et posologie), Lipoprotéines LDL (métabolisme), Maladie des artères coronaires (mortalité), Maladie des artères coronaires (métabolisme), Maladie des artères coronaires (traitement médicamenteux), Modèles de hasards proportionnels, Mâle, Protéine C-réactive (métabolisme), Pyrimidines (administration et posologie), Pyrroles (administration et posologie), Rosuvastatine de calcium, Sujet âgé, Sulfonamides (administration et posologie), Études de suivi.
- MESH :
- administration et posologie : Acides heptanoïques, Fluorobenzènes, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase, Pyrimidines, Pyrroles, Sulfonamides.
- mortalité : Maladie des artères coronaires.
- métabolisme : Cholestérol LDL, Lipoprotéines LDL, Maladie des artères coronaires, Protéine C-réactive.
- traitement médicamenteux : Maladie des artères coronaires.
- Adulte d'âge moyen, Analyse multivariée, Atorvastatine de calcium, Estimation de Kaplan-Meier, Femelle, Humains, Modèles de hasards proportionnels, Mâle, Rosuvastatine de calcium, Sujet âgé, Études de suivi.
English descriptors
- KwdEn :
- Aged, Atorvastatin Calcium, C-Reactive Protein (metabolism), Cholesterol, LDL (metabolism), Coronary Artery Disease (drug therapy), Coronary Artery Disease (metabolism), Coronary Artery Disease (mortality), Female, Fluorobenzenes (administration & dosage), Follow-Up Studies, Heptanoic Acids (administration & dosage), Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors (administration & dosage), Kaplan-Meier Estimate, Lipoproteins, LDL (metabolism), Male, Middle Aged, Multivariate Analysis, Proportional Hazards Models, Pyrimidines (administration & dosage), Pyrroles (administration & dosage), Rosuvastatin Calcium, Sulfonamides (administration & dosage).
- MESH :
- chemical , administration & dosage : Fluorobenzenes, Heptanoic Acids, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Pyrimidines, Pyrroles, Sulfonamides.
- chemical , metabolism : C-Reactive Protein, Cholesterol, LDL, Lipoproteins, LDL.
- chemical : Atorvastatin Calcium, Rosuvastatin Calcium.
- drug therapy : Coronary Artery Disease.
- metabolism : Coronary Artery Disease.
- mortality : Coronary Artery Disease.
- Aged, Female, Follow-Up Studies, Humans, Kaplan-Meier Estimate, Male, Middle Aged, Multivariate Analysis, Proportional Hazards Models.
Abstract
Baseline C-reactive protein (CRP) levels predict major adverse cardiovascular events (MACE: death, myocardial infarction, stroke, coronary revascularization, and hospitalization for unstable angina). The association between changes in CRP levels with plaque progression and MACE in the setting of maximally intensive statin therapy is unknown.
DOI: 10.1161/CIRCULATIONAHA.113.004243
PubMed: 24043299
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 003B04
- to stream PubMed, to step Curation: 003974
- to stream PubMed, to step Checkpoint: 003974
Links to Exploration step
pubmed:24043299Le document en format XML
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<term>Atorvastatin Calcium</term>
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<term>Cholesterol, LDL (metabolism)</term>
<term>Coronary Artery Disease (drug therapy)</term>
<term>Coronary Artery Disease (metabolism)</term>
<term>Coronary Artery Disease (mortality)</term>
<term>Female</term>
<term>Fluorobenzenes (administration & dosage)</term>
<term>Follow-Up Studies</term>
<term>Heptanoic Acids (administration & dosage)</term>
<term>Humans</term>
<term>Hydroxymethylglutaryl-CoA Reductase Inhibitors (administration & dosage)</term>
<term>Kaplan-Meier Estimate</term>
<term>Lipoproteins, LDL (metabolism)</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Multivariate Analysis</term>
<term>Proportional Hazards Models</term>
<term>Pyrimidines (administration & dosage)</term>
<term>Pyrroles (administration & dosage)</term>
<term>Rosuvastatin Calcium</term>
<term>Sulfonamides (administration & dosage)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>Acides heptanoïques (administration et posologie)</term>
<term>Adulte d'âge moyen</term>
<term>Analyse multivariée</term>
<term>Atorvastatine de calcium</term>
<term>Cholestérol LDL (métabolisme)</term>
<term>Estimation de Kaplan-Meier</term>
<term>Femelle</term>
<term>Fluorobenzènes (administration et posologie)</term>
<term>Humains</term>
<term>Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (administration et posologie)</term>
<term>Lipoprotéines LDL (métabolisme)</term>
<term>Maladie des artères coronaires (mortalité)</term>
<term>Maladie des artères coronaires (métabolisme)</term>
<term>Maladie des artères coronaires (traitement médicamenteux)</term>
<term>Modèles de hasards proportionnels</term>
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<term>Protéine C-réactive (métabolisme)</term>
<term>Pyrimidines (administration et posologie)</term>
<term>Pyrroles (administration et posologie)</term>
<term>Rosuvastatine de calcium</term>
<term>Sujet âgé</term>
<term>Sulfonamides (administration et posologie)</term>
<term>Études de suivi</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Fluorobenzenes</term>
<term>Heptanoic Acids</term>
<term>Hydroxymethylglutaryl-CoA Reductase Inhibitors</term>
<term>Pyrimidines</term>
<term>Pyrroles</term>
<term>Sulfonamides</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>C-Reactive Protein</term>
<term>Cholesterol, LDL</term>
<term>Lipoproteins, LDL</term>
</keywords>
<keywords scheme="MESH" type="chemical" xml:lang="en"><term>Atorvastatin Calcium</term>
<term>Rosuvastatin Calcium</term>
</keywords>
<keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Acides heptanoïques</term>
<term>Fluorobenzènes</term>
<term>Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase</term>
<term>Pyrimidines</term>
<term>Pyrroles</term>
<term>Sulfonamides</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronary Artery Disease</term>
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<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Coronary Artery Disease</term>
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<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Cholestérol LDL</term>
<term>Lipoprotéines LDL</term>
<term>Maladie des artères coronaires</term>
<term>Protéine C-réactive</term>
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<term>Female</term>
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<term>Kaplan-Meier Estimate</term>
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<term>Atorvastatine de calcium</term>
<term>Estimation de Kaplan-Meier</term>
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<term>Modèles de hasards proportionnels</term>
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<front><div type="abstract" xml:lang="en">Baseline C-reactive protein (CRP) levels predict major adverse cardiovascular events (MACE: death, myocardial infarction, stroke, coronary revascularization, and hospitalization for unstable angina). The association between changes in CRP levels with plaque progression and MACE in the setting of maximally intensive statin therapy is unknown.</div>
</front>
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<DateCreated><Year>2013</Year>
<Month>11</Month>
<Day>26</Day>
</DateCreated>
<DateCompleted><Year>2014</Year>
<Month>01</Month>
<Day>28</Day>
</DateCompleted>
<DateRevised><Year>2016</Year>
<Month>07</Month>
<Day>01</Day>
</DateRevised>
<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1524-4539</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>128</Volume>
<Issue>22</Issue>
<PubDate><Year>2013</Year>
<Month>Nov</Month>
<Day>26</Day>
</PubDate>
</JournalIssue>
<Title>Circulation</Title>
<ISOAbbreviation>Circulation</ISOAbbreviation>
</Journal>
<ArticleTitle>C-reactive protein, but not low-density lipoprotein cholesterol levels, associate with coronary atheroma regression and cardiovascular events after maximally intensive statin therapy.</ArticleTitle>
<Pagination><MedlinePgn>2395-403</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1161/CIRCULATIONAHA.113.004243</ELocationID>
<Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Baseline C-reactive protein (CRP) levels predict major adverse cardiovascular events (MACE: death, myocardial infarction, stroke, coronary revascularization, and hospitalization for unstable angina). The association between changes in CRP levels with plaque progression and MACE in the setting of maximally intensive statin therapy is unknown.</AbstractText>
<AbstractText Label="METHODS AND RESULTS" NlmCategory="RESULTS">The Study of Coronary Atheroma by Intravascular Ultrasound: Effect of Rosuvastatin Versus Atorvastatin (SATURN) used serial intravascular ultrasound measures of coronary atheroma volume in patients treated with rosuvastatin 40 mg or atorvastatin 80 mg for 24 months. The treatment groups did not differ significantly in the change from baseline of percent atheroma volume on intravascular ultrasound, CRP-modulating effects, or MACE rates, thus allowing for a (prespecified) post hoc analysis to test associations between the changes in CRP levels with coronary disease progression and MACE. Patients with nonincreasing CRP levels (n=621) had higher baseline (2.3 [1.1-4.7] versus 1.1 [0.5-1.8] mg/L; P<0.001) and lower follow-up CRP levels (0.8 [0.5-1.7] versus 1.6 [0.7-4.1] mg/L; P<0.001) versus those with increasing CRP levels (n=364). Multivariable analysis revealed a nonincreasing CRP level to independently associate with greater percent atheroma volume regression (P=0.01). Although the (log) change in CRP did not associate with MACE (hazard ratio, 1.18; 95% confidence interval, 0.93-1.50; P=0.17), the (log) on-treatment CRP associated significantly with MACE (hazard ratio, 1.28; 95% confidence interval, 1.04-1.56; P=0.02). On-treatment low-density lipoprotein cholesterol levels did not correlate with MACE (hazard ratio, 1.09; 95% confidence interval, 0.88-1.35; P=0.45).</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Following 24 months of potent statin therapy, on-treatment CRP levels associated with MACE. Inflammation may be an important driver of residual cardiovascular risk in patients with coronary artery disease despite aggressive statin therapy.</AbstractText>
<AbstractText Label="CLINICAL TRIAL REGISTRATION URL" NlmCategory="BACKGROUND">http://clinicaltrials.gov. Unique identifier: NCT000620542.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Puri</LastName>
<ForeName>Rishi</ForeName>
<Initials>R</Initials>
<AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH (R.P., S.E.N., K.U., Y.K., S.J.N.); Cardiovascular Division, Brigham and Women's Hospital, Boston, MA (P.L.); C5Research, Cleveland Clinic, Cleveland, OH (M.S.); Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston, TX (C.M.B.); Centre for Vascular Research, University of New South Wales, Sydney, Australia (P.J.B.); INSERM Dyslipidaemia and Atherosclerosis Research Unit, Hôpital de la Pitié, Paris, France (M.J.C.); West German Heart Center, Essen, Germany (R.E.); AstraZeneca, Wilmington, DE (J.S.R.); and South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia (S.J.N.).</Affiliation>
</AffiliationInfo>
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<ForeName>Steven E</ForeName>
<Initials>SE</Initials>
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<Author ValidYN="Y"><LastName>Libby</LastName>
<ForeName>Peter</ForeName>
<Initials>P</Initials>
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<ForeName>Mingyuan</ForeName>
<Initials>M</Initials>
</Author>
<Author ValidYN="Y"><LastName>Ballantyne</LastName>
<ForeName>Christie M</ForeName>
<Initials>CM</Initials>
</Author>
<Author ValidYN="Y"><LastName>Barter</LastName>
<ForeName>Phillip J</ForeName>
<Initials>PJ</Initials>
</Author>
<Author ValidYN="Y"><LastName>Chapman</LastName>
<ForeName>M John</ForeName>
<Initials>MJ</Initials>
</Author>
<Author ValidYN="Y"><LastName>Erbel</LastName>
<ForeName>Raimund</ForeName>
<Initials>R</Initials>
</Author>
<Author ValidYN="Y"><LastName>Raichlen</LastName>
<ForeName>Joel S</ForeName>
<Initials>JS</Initials>
</Author>
<Author ValidYN="Y"><LastName>Uno</LastName>
<ForeName>Kiyoko</ForeName>
<Initials>K</Initials>
</Author>
<Author ValidYN="Y"><LastName>Kataoka</LastName>
<ForeName>Yu</ForeName>
<Initials>Y</Initials>
</Author>
<Author ValidYN="Y"><LastName>Nicholls</LastName>
<ForeName>Stephen J</ForeName>
<Initials>SJ</Initials>
</Author>
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<AccessionNumberList><AccessionNumber>NCT00620542</AccessionNumber>
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<Month>09</Month>
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<MeshHeading><DescriptorName UI="D002097" MajorTopicYN="N">C-Reactive Protein</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008078" MajorTopicYN="N">Cholesterol, LDL</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D003324" MajorTopicYN="Y">Coronary Artery Disease</DescriptorName>
<QualifierName UI="Q000188" MajorTopicYN="N">drug therapy</QualifierName>
<QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName>
<QualifierName UI="Q000401" MajorTopicYN="N">mortality</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName>
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<MeshHeading><DescriptorName UI="D006538" MajorTopicYN="N">Heptanoic Acids</DescriptorName>
<QualifierName UI="Q000008" MajorTopicYN="Y">administration & dosage</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D019161" MajorTopicYN="N">Hydroxymethylglutaryl-CoA Reductase Inhibitors</DescriptorName>
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<MeshHeading><DescriptorName UI="D053208" MajorTopicYN="N">Kaplan-Meier Estimate</DescriptorName>
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<MeshHeading><DescriptorName UI="D008077" MajorTopicYN="N">Lipoproteins, LDL</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName>
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<MeshHeading><DescriptorName UI="D015999" MajorTopicYN="N">Multivariate Analysis</DescriptorName>
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<MeshHeading><DescriptorName UI="D011743" MajorTopicYN="N">Pyrimidines</DescriptorName>
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<KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">C-reactive protein</Keyword>
<Keyword MajorTopicYN="N">atherosclerosis</Keyword>
<Keyword MajorTopicYN="N">atorvastatin</Keyword>
<Keyword MajorTopicYN="N">cholesterol, LDL</Keyword>
<Keyword MajorTopicYN="N">inflammation</Keyword>
<Keyword MajorTopicYN="N">rosuvastatin</Keyword>
<Keyword MajorTopicYN="N">ultrasonography</Keyword>
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</MedlineCitation>
<PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2013</Year>
<Month>9</Month>
<Day>18</Day>
<Hour>6</Hour>
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<PubMedPubDate PubStatus="pubmed"><Year>2013</Year>
<Month>9</Month>
<Day>18</Day>
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<PubMedPubDate PubStatus="medline"><Year>2014</Year>
<Month>1</Month>
<Day>29</Day>
<Hour>6</Hour>
<Minute>0</Minute>
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<ArticleIdList><ArticleId IdType="pubmed">24043299</ArticleId>
<ArticleId IdType="pii">CIRCULATIONAHA.113.004243</ArticleId>
<ArticleId IdType="doi">10.1161/CIRCULATIONAHA.113.004243</ArticleId>
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<affiliations><list></list>
<tree><noCountry><name sortKey="Ballantyne, Christie M" sort="Ballantyne, Christie M" uniqKey="Ballantyne C" first="Christie M" last="Ballantyne">Christie M. Ballantyne</name>
<name sortKey="Barter, Phillip J" sort="Barter, Phillip J" uniqKey="Barter P" first="Phillip J" last="Barter">Phillip J. Barter</name>
<name sortKey="Chapman, M John" sort="Chapman, M John" uniqKey="Chapman M" first="M John" last="Chapman">M John Chapman</name>
<name sortKey="Erbel, Raimund" sort="Erbel, Raimund" uniqKey="Erbel R" first="Raimund" last="Erbel">Raimund Erbel</name>
<name sortKey="Kataoka, Yu" sort="Kataoka, Yu" uniqKey="Kataoka Y" first="Yu" last="Kataoka">Yu Kataoka</name>
<name sortKey="Libby, Peter" sort="Libby, Peter" uniqKey="Libby P" first="Peter" last="Libby">Peter Libby</name>
<name sortKey="Nicholls, Stephen J" sort="Nicholls, Stephen J" uniqKey="Nicholls S" first="Stephen J" last="Nicholls">Stephen J. Nicholls</name>
<name sortKey="Nissen, Steven E" sort="Nissen, Steven E" uniqKey="Nissen S" first="Steven E" last="Nissen">Steven E. Nissen</name>
<name sortKey="Puri, Rishi" sort="Puri, Rishi" uniqKey="Puri R" first="Rishi" last="Puri">Rishi Puri</name>
<name sortKey="Raichlen, Joel S" sort="Raichlen, Joel S" uniqKey="Raichlen J" first="Joel S" last="Raichlen">Joel S. Raichlen</name>
<name sortKey="Shao, Mingyuan" sort="Shao, Mingyuan" uniqKey="Shao M" first="Mingyuan" last="Shao">Mingyuan Shao</name>
<name sortKey="Uno, Kiyoko" sort="Uno, Kiyoko" uniqKey="Uno K" first="Kiyoko" last="Uno">Kiyoko Uno</name>
</noCountry>
</tree>
</affiliations>
</record>
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