High-intensity statin therapy alters the natural history of diabetic coronary atherosclerosis: insights from SATURN.
Identifieur interne : 003189 ( PubMed/Curation ); précédent : 003188; suivant : 003190High-intensity statin therapy alters the natural history of diabetic coronary atherosclerosis: insights from SATURN.
Auteurs : Brian Stegman [États-Unis] ; Rishi Puri [États-Unis] ; Leslie Cho [États-Unis] ; Mingyuan Shao [États-Unis] ; Christie M. Ballantyne [États-Unis] ; Phillip J. Barter [Australie] ; M John Chapman [France] ; Raimund Erbel [Allemagne] ; Peter Libby [États-Unis] ; Joel S. Raichlen [États-Unis] ; Kiyoko Uno [États-Unis] ; Yu Kataoka [Australie] ; Steven E. Nissen [États-Unis] ; Stephen J. Nicholls [Oman]Source :
- Diabetes care [ 1935-5548 ] ; 2014.
Descripteurs français
- KwdFr :
- Acides heptanoïques (usage thérapeutique), Adulte d'âge moyen, Atorvastatine de calcium, Cholestérol HDL (sang), Cholestérol LDL (sang), Diabète (traitement médicamenteux), Femelle, Fluorobenzènes (usage thérapeutique), Humains, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (usage thérapeutique), Maladie des artères coronaires (traitement médicamenteux), Mâle, Plaque d'athérosclérose (traitement médicamenteux), Plaque d'athérosclérose (étiologie), Pyrimidines (usage thérapeutique), Pyrroles (usage thérapeutique), Rosuvastatine de calcium, Sujet âgé, Sulfonamides (usage thérapeutique), Échographie interventionnelle.
- MESH :
- sang : Cholestérol HDL, Cholestérol LDL.
- traitement médicamenteux : Diabète, Maladie des artères coronaires, Plaque d'athérosclérose.
- usage thérapeutique : Acides heptanoïques, Fluorobenzènes, Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase, Pyrimidines, Pyrroles, Sulfonamides.
- étiologie : Plaque d'athérosclérose.
- Adulte d'âge moyen, Atorvastatine de calcium, Femelle, Humains, Mâle, Rosuvastatine de calcium, Sujet âgé, Échographie interventionnelle.
English descriptors
- KwdEn :
- Aged, Atorvastatin Calcium, Cholesterol, HDL (blood), Cholesterol, LDL (blood), Coronary Artery Disease (drug therapy), Diabetes Mellitus (drug therapy), Female, Fluorobenzenes (therapeutic use), Heptanoic Acids (therapeutic use), Humans, Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use), Male, Middle Aged, Plaque, Atherosclerotic (drug therapy), Plaque, Atherosclerotic (etiology), Pyrimidines (therapeutic use), Pyrroles (therapeutic use), Rosuvastatin Calcium, Sulfonamides (therapeutic use), Ultrasonography, Interventional.
- MESH :
- chemical , blood : Cholesterol, HDL, Cholesterol, LDL.
- chemical , therapeutic use : Fluorobenzenes, Heptanoic Acids, Hydroxymethylglutaryl-CoA Reductase Inhibitors, Pyrimidines, Pyrroles, Sulfonamides.
- chemical : Atorvastatin Calcium, Rosuvastatin Calcium.
- drug therapy : Coronary Artery Disease, Diabetes Mellitus, Plaque, Atherosclerotic.
- etiology : Plaque, Atherosclerotic.
- Aged, Female, Humans, Male, Middle Aged, Ultrasonography, Interventional.
Abstract
Although statins can induce coronary atheroma regression, this benefit has yet to be demonstrated in diabetic individuals. We tested the hypothesis that high-intensity statin therapy may promote coronary atheroma regression in patients with diabetes.
DOI: 10.2337/dc14-1121
PubMed: 25190674
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Ballantyne</name><affiliation wicri:level="2"><nlm:affiliation>Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston, TX.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Texas</region></placeName><wicri:cityArea>Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston</wicri:cityArea></affiliation></author><author><name sortKey="Barter, Phillip J" sort="Barter, Phillip J" uniqKey="Barter P" first="Phillip J" last="Barter">Phillip J. Barter</name><affiliation wicri:level="1"><nlm:affiliation>Centre for Vascular Research, University of New South Wales, Sydney, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>Centre for Vascular Research, University of New South Wales, Sydney</wicri:regionArea></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 wicri:level="1"><nlm:affiliation>INSERM Dyslipidaemia and Atherosclerosis Research Unit, Pitié-Salpètrière University Hospital, Paris, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM Dyslipidaemia and Atherosclerosis Research Unit, Pitié-Salpètrière University Hospital, Paris</wicri:regionArea></affiliation></author><author><name sortKey="Erbel, Raimund" sort="Erbel, Raimund" uniqKey="Erbel R" first="Raimund" last="Erbel">Raimund Erbel</name><affiliation wicri:level="1"><nlm:affiliation>West German Heart Center, Essen, Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>West German Heart Center, Essen</wicri:regionArea></affiliation></author><author><name sortKey="Libby, Peter" sort="Libby, Peter" uniqKey="Libby P" first="Peter" last="Libby">Peter Libby</name><affiliation wicri:level="2"><nlm:affiliation>Cardiovascular Division, Brigham and Women's Hospital, Boston, MA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Massachusetts</region></placeName><wicri:cityArea>Cardiovascular Division, Brigham and Women's Hospital, Boston</wicri:cityArea></affiliation></author><author><name sortKey="Raichlen, Joel S" sort="Raichlen, Joel S" uniqKey="Raichlen J" first="Joel S" last="Raichlen">Joel S. Raichlen</name><affiliation wicri:level="2"><nlm:affiliation>AstraZeneca, Wilmington, DE.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Delaware</region></placeName><wicri:cityArea>AstraZeneca, Wilmington</wicri:cityArea></affiliation></author><author><name sortKey="Uno, Kiyoko" sort="Uno, Kiyoko" uniqKey="Uno K" first="Kiyoko" last="Uno">Kiyoko Uno</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Ohio</region></placeName><wicri:cityArea>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland</wicri:cityArea></affiliation></author><author><name sortKey="Kataoka, Yu" sort="Kataoka, Yu" uniqKey="Kataoka Y" first="Yu" last="Kataoka">Yu Kataoka</name><affiliation wicri:level="1"><nlm:affiliation>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.</nlm:affiliation><country xml:lang="fr">Australie</country><wicri:regionArea>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide</wicri:regionArea></affiliation></author><author><name sortKey="Nissen, Steven E" sort="Nissen, Steven E" uniqKey="Nissen S" first="Steven E" last="Nissen">Steven E. Nissen</name><affiliation wicri:level="2"><nlm:affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</nlm:affiliation><country xml:lang="fr">États-Unis</country><placeName><region type="state">Ohio</region></placeName><wicri:cityArea>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland</wicri:cityArea></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 wicri:level="1"><nlm:affiliation>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia stephen.nicholls@sahmri.com.</nlm:affiliation><country wicri:rule="url">Oman</country><wicri:regionArea>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide</wicri:regionArea></affiliation></author></analytic><series><title level="j">Diabetes care</title><idno type="eISSN">1935-5548</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Atorvastatin Calcium</term><term>Cholesterol, HDL (blood)</term><term>Cholesterol, LDL (blood)</term><term>Coronary Artery Disease (drug therapy)</term><term>Diabetes Mellitus (drug therapy)</term><term>Female</term><term>Fluorobenzenes (therapeutic use)</term><term>Heptanoic Acids (therapeutic use)</term><term>Humans</term><term>Hydroxymethylglutaryl-CoA Reductase Inhibitors (therapeutic use)</term><term>Male</term><term>Middle Aged</term><term>Plaque, Atherosclerotic (drug therapy)</term><term>Plaque, Atherosclerotic (etiology)</term><term>Pyrimidines (therapeutic use)</term><term>Pyrroles (therapeutic use)</term><term>Rosuvastatin Calcium</term><term>Sulfonamides (therapeutic use)</term><term>Ultrasonography, Interventional</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acides heptanoïques (usage thérapeutique)</term><term>Adulte d'âge moyen</term><term>Atorvastatine de calcium</term><term>Cholestérol HDL (sang)</term><term>Cholestérol LDL (sang)</term><term>Diabète (traitement médicamenteux)</term><term>Femelle</term><term>Fluorobenzènes (usage thérapeutique)</term><term>Humains</term><term>Inhibiteurs de l'hydroxyméthylglutaryl-CoA réductase (usage thérapeutique)</term><term>Maladie des artères coronaires (traitement médicamenteux)</term><term>Mâle</term><term>Plaque d'athérosclérose (traitement médicamenteux)</term><term>Plaque d'athérosclérose (étiologie)</term><term>Pyrimidines (usage thérapeutique)</term><term>Pyrroles (usage thérapeutique)</term><term>Rosuvastatine de calcium</term><term>Sujet âgé</term><term>Sulfonamides (usage thérapeutique)</term><term>Échographie interventionnelle</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Cholesterol, HDL</term><term>Cholesterol, LDL</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" 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" xml:lang="en"><term>Atorvastatin Calcium</term><term>Rosuvastatin Calcium</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Coronary Artery Disease</term><term>Diabetes Mellitus</term><term>Plaque, Atherosclerotic</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Plaque, Atherosclerotic</term></keywords><keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Cholestérol HDL</term><term>Cholestérol LDL</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Diabète</term><term>Maladie des artères coronaires</term><term>Plaque d'athérosclérose</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" 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></keywords><keywords scheme="MESH" qualifier="étiologie" xml:lang="fr"><term>Plaque d'athérosclérose</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Ultrasonography, Interventional</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Adulte d'âge moyen</term><term>Atorvastatine de calcium</term><term>Femelle</term><term>Humains</term><term>Mâle</term><term>Rosuvastatine de calcium</term><term>Sujet âgé</term><term>Échographie interventionnelle</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Although statins can induce coronary atheroma regression, this benefit has yet to be demonstrated in diabetic individuals. We tested the hypothesis that high-intensity statin therapy may promote coronary atheroma regression in patients with diabetes.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25190674</PMID><DateCreated><Year>2014</Year><Month>10</Month><Day>24</Day></DateCreated><DateCompleted><Year>2015</Year><Month>04</Month><Day>27</Day></DateCompleted><DateRevised><Year>2015</Year><Month>11</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1935-5548</ISSN><JournalIssue CitedMedium="Internet"><Volume>37</Volume><Issue>11</Issue><PubDate><Year>2014</Year><Month>Nov</Month></PubDate></JournalIssue><Title>Diabetes care</Title><ISOAbbreviation>Diabetes Care</ISOAbbreviation></Journal><ArticleTitle>High-intensity statin therapy alters the natural history of diabetic coronary atherosclerosis: insights from SATURN.</ArticleTitle><Pagination><MedlinePgn>3114-20</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.2337/dc14-1121</ELocationID><Abstract><AbstractText Label="OBJECTIVE" NlmCategory="OBJECTIVE">Although statins can induce coronary atheroma regression, this benefit has yet to be demonstrated in diabetic individuals. We tested the hypothesis that high-intensity statin therapy may promote coronary atheroma regression in patients with diabetes.</AbstractText><AbstractText Label="RESEARCH DESIGN AND METHODS" NlmCategory="METHODS">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. This analysis compared changes in biochemistry and coronary percent atheroma volume (PAV) in patients with (n = 159) and without (n = 880) diabetes.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">At baseline, patients with diabetes had lower LDL cholesterol (LDL-C) and HDL cholesterol (HDL-C) levels but higher triglyceride and CRP levels compared with patients without diabetes. At follow-up, diabetic patients had lower levels of LDL-C (61.0 ± 20.5 vs. 66.4 ± 22.9 mg/dL, P = 0.01) and HDL-C (46.3 ± 10.6 vs. 49.9 ± 12.0 mg/dL, P < 0.001) but higher levels of triglycerides (127.6 [98.8, 163.0] vs. 113.0 mg/dL [87.6, 151.9], P = 0.001) and CRP (1.4 [0.7, 3.3] vs. 1.0 [0.5, 2.1] mg/L, P = 0.001). Both patients with and without diabetes demonstrated regression of coronary atheroma as measured by change in PAV (-0.83 ± 0.13 vs. -1.15 ± 0.13%, P = 0.08). PAV regression was less in diabetic compared with nondiabetic patients when on-treatment LDL-C levels were >70 mg/dL (-0.31 ± 0.23 vs. -1.01 ± 0.21%, P = 0.03) but similar when LDL-C levels were ≤70 mg/dL (-1.09 ± 0.16 vs. -1.24 ± 0.16%, P = 0.50).</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">High-intensity statin therapy alters the progressive nature of diabetic coronary atherosclerosis, yielding regression of disease in diabetic and nondiabetic patients.</AbstractText><CopyrightInformation>© 2014 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Stegman</LastName><ForeName>Brian</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Puri</LastName><ForeName>Rishi</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cho</LastName><ForeName>Leslie</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Shao</LastName><ForeName>Mingyuan</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Ballantyne</LastName><ForeName>Christie M</ForeName><Initials>CM</Initials><AffiliationInfo><Affiliation>Section of Cardiovascular Research, Baylor College of Medicine, and the Methodist DeBakey Heart and Vascular Center, Houston, TX.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Barter</LastName><ForeName>Phillip J</ForeName><Initials>PJ</Initials><AffiliationInfo><Affiliation>Centre for Vascular Research, University of New South Wales, Sydney, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Chapman</LastName><ForeName>M John</ForeName><Initials>MJ</Initials><AffiliationInfo><Affiliation>INSERM Dyslipidaemia and Atherosclerosis Research Unit, Pitié-Salpètrière University Hospital, Paris, France.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Erbel</LastName><ForeName>Raimund</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>West German Heart Center, Essen, Germany.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Libby</LastName><ForeName>Peter</ForeName><Initials>P</Initials><AffiliationInfo><Affiliation>Cardiovascular Division, Brigham and Women's Hospital, Boston, MA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Raichlen</LastName><ForeName>Joel S</ForeName><Initials>JS</Initials><AffiliationInfo><Affiliation>AstraZeneca, Wilmington, DE.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uno</LastName><ForeName>Kiyoko</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Kataoka</LastName><ForeName>Yu</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>South Australian Health and Medical Research Institute, University of Adelaide, Adelaide, Australia.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Nissen</LastName><ForeName>Steven E</ForeName><Initials>SE</Initials><AffiliationInfo><Affiliation>Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH C5Research, Department of Cardiovascular Medicine, Cleveland Clinic, Cleveland, OH.</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 stephen.nicholls@sahmri.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D016449">Randomized Controlled Trial</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2014</Year><Month>09</Month><Day>04</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>Diabetes Care</MedlineTA><NlmUniqueID>7805975</NlmUniqueID><ISSNLinking>0149-5992</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008076">Cholesterol, HDL</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D008078">Cholesterol, LDL</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005464">Fluorobenzenes</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D006538">Heptanoic Acids</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D019161">Hydroxymethylglutaryl-CoA Reductase Inhibitors</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011743">Pyrimidines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011758">Pyrroles</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013449">Sulfonamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>48A5M73Z4Q</RegistryNumber><NameOfSubstance UI="D000069059">Atorvastatin Calcium</NameOfSubstance></Chemical><Chemical><RegistryNumber>83MVU38M7Q</RegistryNumber><NameOfSubstance UI="D000068718">Rosuvastatin Calcium</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><CommentsCorrectionsList><CommentsCorrections RefType="CommentIn"><RefSource>Diabetes Care. 2015 Feb;38(2):e28-9</RefSource><PMID Version="1">25614701</PMID></CommentsCorrections><CommentsCorrections RefType="CommentIn"><RefSource>Diabetes Care. 2015 Feb;38(2):e27</RefSource><PMID Version="1">25614700</PMID></CommentsCorrections></CommentsCorrectionsList><MeshHeadingList><MeshHeading><DescriptorName UI="D000368" MajorTopicYN="N">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000069059" MajorTopicYN="N">Atorvastatin Calcium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008076" MajorTopicYN="N">Cholesterol, HDL</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008078" MajorTopicYN="N">Cholesterol, LDL</DescriptorName><QualifierName UI="Q000097" MajorTopicYN="N">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D003324" MajorTopicYN="N">Coronary Artery Disease</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="N">drug 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use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008297" MajorTopicYN="N">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008875" MajorTopicYN="N">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D058226" MajorTopicYN="N">Plaque, Atherosclerotic</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000209" MajorTopicYN="N">etiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011743" MajorTopicYN="N">Pyrimidines</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D011758" MajorTopicYN="N">Pyrroles</DescriptorName><QualifierName UI="Q000627" MajorTopicYN="Y">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000068718" MajorTopicYN="N">Rosuvastatin Calcium</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013449" 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