Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction
Identifieur interne : 002369 ( Istex/Corpus ); précédent : 002368; suivant : 002370Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction
Auteurs : Mariko L. Ishimori ; Megha Agarwal ; Roy Beigel ; Rita K. Ng ; Nazanin Firooz ; Michael H. Weisman ; Robert J. SiegelSource :
- Echocardiography [ 0742-2822 ] ; 2014-05.
Abstract
Objective: Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (SLE). However, most case reports on SLE cardiomyopathy (CM) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (LV) dysfunction in patients with SLE. Methods: The records of 526 SLE patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for SLE were met, (2) testing for erythrocyte sedimentation rate and hs‐CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (LVEF) <50%. Results: We identified 14 patients meeting study criteria. Mean LVEF was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram. Conclusion: The pattern of wall‐motion abnormalities and reversibility demonstrated in the majority of these patients with SLE suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.
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DOI: 10.1111/echo.12425
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Ishimori</name><affiliation><mods:affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Agarwal, Megha" sort="Agarwal, Megha" uniqKey="Agarwal M" first="Megha" last="Agarwal">Megha Agarwal</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Beigel, Roy" sort="Beigel, Roy" uniqKey="Beigel R" first="Roy" last="Beigel">Roy Beigel</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Ng, Rita K" sort="Ng, Rita K" uniqKey="Ng R" first="Rita K." last="Ng">Rita K. Ng</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Firooz, Nazanin" sort="Firooz, Nazanin" uniqKey="Firooz N" first="Nazanin" last="Firooz">Nazanin Firooz</name><affiliation><mods:affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Weisman, Michael H" sort="Weisman, Michael H" uniqKey="Weisman M" first="Michael H." last="Weisman">Michael H. Weisman</name><affiliation><mods:affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Siegel, Robert J" sort="Siegel, Robert J" uniqKey="Siegel R" first="Robert J." last="Siegel">Robert J. Siegel</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: Robert.siegel@cshs.org</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:7B5DC7EA96AA97CA5B9231B1AA07EC2953BAE7A5</idno><date when="2014" year="2014">2014</date><idno type="doi">10.1111/echo.12425</idno><idno type="url">https://api.istex.fr/ark:/67375/WNG-2FZNKRML-9/fulltext.pdf</idno><idno type="wicri:Area/Istex/Corpus">002369</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002369</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main">Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title><author><name sortKey="Ishimori, Mariko L" sort="Ishimori, Mariko L" uniqKey="Ishimori M" first="Mariko L." last="Ishimori">Mariko L. Ishimori</name><affiliation><mods:affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Agarwal, Megha" sort="Agarwal, Megha" uniqKey="Agarwal M" first="Megha" last="Agarwal">Megha Agarwal</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Beigel, Roy" sort="Beigel, Roy" uniqKey="Beigel R" first="Roy" last="Beigel">Roy Beigel</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Ng, Rita K" sort="Ng, Rita K" uniqKey="Ng R" first="Rita K." last="Ng">Rita K. Ng</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Firooz, Nazanin" sort="Firooz, Nazanin" uniqKey="Firooz N" first="Nazanin" last="Firooz">Nazanin Firooz</name><affiliation><mods:affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Weisman, Michael H" sort="Weisman, Michael H" uniqKey="Weisman M" first="Michael H." last="Weisman">Michael H. Weisman</name><affiliation><mods:affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation></author><author><name sortKey="Siegel, Robert J" sort="Siegel, Robert J" uniqKey="Siegel R" first="Robert J." last="Siegel">Robert J. Siegel</name><affiliation><mods:affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: Robert.siegel@cshs.org</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Echocardiography</title><title level="j" type="alt">ECHOCARDIOGRAPHY</title><idno type="ISSN">0742-2822</idno><idno type="eISSN">1540-8175</idno><imprint><biblScope unit="vol">31</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="563">563</biblScope><biblScope unit="page" to="568">568</biblScope><biblScope unit="page-count">6</biblScope><date type="published" when="2014-05">2014-05</date></imprint><idno type="ISSN">0742-2822</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0742-2822</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Objective: Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (SLE). However, most case reports on SLE cardiomyopathy (CM) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (LV) dysfunction in patients with SLE. Methods: The records of 526 SLE patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for SLE were met, (2) testing for erythrocyte sedimentation rate and hs‐CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (LVEF) <50%. Results: We identified 14 patients meeting study criteria. Mean LVEF was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram. Conclusion: The pattern of wall‐motion abnormalities and reversibility demonstrated in the majority of these patients with SLE suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Mariko L. Ishimori M.D.</name><affiliations><json:string>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</json:string></affiliations></json:item><json:item><name>Megha Agarwal M.D.</name><affiliations><json:string>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</json:string></affiliations></json:item><json:item><name>Roy Beigel M.D.</name><affiliations><json:string>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</json:string></affiliations></json:item><json:item><name>Rita K. Ng M.D.</name><affiliations><json:string>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</json:string></affiliations></json:item><json:item><name>Nazanin Firooz M.D.</name><affiliations><json:string>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</json:string></affiliations></json:item><json:item><name>Michael H. Weisman M.D.</name><affiliations><json:string>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</json:string></affiliations></json:item><json:item><name>Robert J. Siegel M.D., F.A.C.C.</name><affiliations><json:string>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</json:string><json:string>E-mail: Robert.siegel@cshs.org</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>cardiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>cardiomyopathy</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>echocardiography</value></json:item></subject><articleId><json:string>ECHO12425</json:string></articleId><arkIstex>ark:/67375/WNG-2FZNKRML-9</arkIstex><language><json:string>eng</json:string></language><originalGenre><json:string>article</json:string></originalGenre><abstract>Objective: Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (SLE). However, most case reports on SLE cardiomyopathy (CM) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (LV) dysfunction in patients with SLE. Methods: The records of 526 SLE patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for SLE were met, (2) testing for erythrocyte sedimentation rate and hs‐CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (LVEF) >50%. Results: We identified 14 patients meeting study criteria. Mean LVEF was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram. Conclusion: The pattern of wall‐motion abnormalities and reversibility demonstrated in the majority of these patients with SLE suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.</abstract><qualityIndicators><score>7.462</score><pdfWordCount>2870</pdfWordCount><pdfCharCount>20033</pdfCharCount><pdfVersion>1.3</pdfVersion><pdfPageCount>6</pdfPageCount><pdfPageSize>593.858 x 782.929 pts</pdfPageSize><pdfWordsPerPage>478</pdfWordsPerPage><pdfText>true</pdfText><refBibsNative>true</refBibsNative><abstractWordCount>216</abstractWordCount><abstractCharCount>1539</abstractCharCount><keywordCount>3</keywordCount></qualityIndicators><title>Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title><genre><json:string>article</json:string></genre><host><title>Echocardiography</title><language><json:string>unknown</json:string></language><doi><json:string>10.1111/(ISSN)1540-8175</json:string></doi><issn><json:string>0742-2822</json:string></issn><eissn><json:string>1540-8175</json:string></eissn><publisherId><json:string>ECHO</json:string></publisherId><volume>31</volume><issue>5</issue><pages><first>563</first><last>568</last><total>6</total></pages><genre><json:string>journal</json:string></genre><subject><json:item><value>Original Investigation</value></json:item><json:item><value>Original Investigations</value></json:item></subject></host><ark><json:string>ark:/67375/WNG-2FZNKRML-9</json:string></ark><categories><wos><json:string>1 - science</json:string><json:string>2 - cardiac & cardiovascular systems</json:string></wos><scienceMetrix><json:string>1 - health sciences</json:string><json:string>2 - clinical medicine</json:string><json:string>3 - cardiovascular system & hematology</json:string></scienceMetrix><scopus><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Cardiology and Cardiovascular Medicine</json:string><json:string>1 - Health Sciences</json:string><json:string>2 - Medicine</json:string><json:string>3 - Radiology Nuclear Medicine and imaging</json:string></scopus><inist><json:string>1 - sciences appliquees, technologies et medecines</json:string><json:string>2 - sciences biologiques et medicales</json:string><json:string>3 - sciences medicales</json:string></inist></categories><publicationDate>2014</publicationDate><copyrightDate>2014</copyrightDate><doi><json:string>10.1111/echo.12425</json:string></doi><id>7B5DC7EA96AA97CA5B9231B1AA07EC2953BAE7A5</id><score>1</score><fulltext><json:item><extension>pdf</extension><original>true</original><mimetype>application/pdf</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-2FZNKRML-9/fulltext.pdf</uri></json:item><json:item><extension>zip</extension><original>false</original><mimetype>application/zip</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-2FZNKRML-9/bundle.zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/ark:/67375/WNG-2FZNKRML-9/fulltext.tei"><teiHeader><fileDesc><titleStmt><title level="a" type="main">Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher ref="https://scientific-publisher.data.istex.fr/ark:/67375/H02-QW5Q88H5-V">Wiley Publishing Ltd</publisher><availability><licence>© 2013, Wiley Periodicals, Inc.</licence></availability><date type="published" when="2014-05"></date></publicationStmt><notesStmt><note type="content-type" subtype="article" source="article" scheme="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</note><note type="publication-type" subtype="journal" scheme="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</note></notesStmt><sourceDesc><biblStruct type="article"><analytic><title level="a" type="main">Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title><author xml:id="author-0000"><persName><forename type="first">Mariko L.</forename><surname>Ishimori</surname><roleName type="degree">M.D.</roleName></persName><affiliation><orgName type="division">Division of Rheumatology</orgName>
<orgName type="institution">Cedars‐Sinai Medical Center</orgName>
<address><settlement>Los Angeles</settlement>
<postCode>California</postCode></address></affiliation></author><author xml:id="author-0001"><persName><forename type="first">Megha</forename><surname>Agarwal</surname><roleName type="degree">M.D.</roleName></persName><affiliation><orgName type="division">The Heart Institute</orgName>
<orgName type="institution">Cedars Sinai Medical Center</orgName>
<address><settlement>Los Angeles</settlement>
<postCode>California</postCode></address></affiliation></author><author xml:id="author-0002"><persName><forename type="first">Roy</forename><surname>Beigel</surname><roleName type="degree">M.D.</roleName></persName><affiliation><orgName type="division">The Heart Institute</orgName>
<orgName type="institution">Cedars Sinai Medical Center</orgName>
<address><settlement>Los Angeles</settlement>
<postCode>California</postCode></address></affiliation></author><author xml:id="author-0003"><persName><forename type="first">Rita K.</forename><surname>Ng</surname><roleName type="degree">M.D.</roleName></persName><affiliation><orgName type="division">The Heart Institute</orgName>
<orgName type="institution">Cedars Sinai Medical Center</orgName>
<address><settlement>Los Angeles</settlement>
<postCode>California</postCode></address></affiliation></author><author xml:id="author-0004"><persName><forename type="first">Nazanin</forename><surname>Firooz</surname><roleName type="degree">M.D.</roleName></persName><affiliation><orgName type="division">Division of Rheumatology</orgName>
<orgName type="institution">Cedars‐Sinai Medical Center</orgName>
<address><settlement>Los Angeles</settlement>
<postCode>California</postCode></address></affiliation></author><author xml:id="author-0005"><persName><forename type="first">Michael H.</forename><surname>Weisman</surname><roleName type="degree">M.D.</roleName></persName><affiliation><orgName type="division">Division of Rheumatology</orgName>
<orgName type="institution">Cedars‐Sinai Medical Center</orgName>
<address><settlement>Los Angeles</settlement>
<postCode>California</postCode></address></affiliation></author><author xml:id="author-0006" role="corresp"><persName><forename type="first">Robert J.</forename><surname>Siegel</surname><roleName type="degree">M.D., F.A.C.C.</roleName></persName><affiliation><orgName type="division">The Heart Institute</orgName>
<orgName type="institution">Cedars Sinai Medical Center</orgName>
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<ref target="http://www.tei-c.org/">We use TEI</ref></desc></application></appInfo></encodingDesc><profileDesc><abstract style="main" xml:id="echo12425-abs-0001"><head>Objective</head><p>Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (<hi rend="fc">SLE</hi>). However, most case reports on <hi rend="fc">SLE</hi> cardiomyopathy (<hi rend="fc">CM</hi>) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (<hi rend="fc">LV</hi>) dysfunction in patients with <hi rend="fc">SLE</hi>.</p><head>Methods</head><p>The records of 526 <hi rend="fc">SLE</hi> patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for <hi rend="fc">SLE</hi> were met, (2) testing for erythrocyte sedimentation rate and hs‐CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (<hi rend="fc">LVEF</hi>) <50%.</p><head>Results</head><p>We identified 14 patients meeting study criteria. Mean <hi rend="fc">LVEF</hi> was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram.</p><head>Conclusion</head><p>The pattern of wall‐motion abnormalities and reversibility demonstrated in the majority of these patients with <hi rend="fc">SLE</hi> suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.</p></abstract><textClass><keywords><term xml:id="echo12425-kwd-0001">cardiology</term><term xml:id="echo12425-kwd-0002">cardiomyopathy</term><term xml:id="echo12425-kwd-0003">echocardiography</term></keywords><keywords rend="articleCategory"><term>Original Investigation</term></keywords><keywords rend="tocHeading1"><term>Original Investigations</term></keywords></textClass><langUsage><language ident="en"></language></langUsage></profileDesc><revisionDesc><change when="2019-12-20" who="#istex" xml:id="pub2tei">formatting</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-2FZNKRML-9/fulltext.txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component type="serialArticle" version="2.0" xml:id="echo12425" xml:lang="en"><header><publicationMeta level="product"><doi origin="wiley" registered="yes">10.1111/(ISSN)1540-8175</doi><issn type="print">0742-2822</issn><issn type="electronic">1540-8175</issn><idGroup><id type="product" value="ECHO"></id></idGroup><titleGroup><title sort="ECHOCARDIOGRAPHY" type="main">Echocardiography</title><title type="short">Echocardiography</title></titleGroup></publicationMeta><publicationMeta level="part" position="50"><doi origin="wiley">10.1111/echo.2014.31.issue-5</doi><copyright ownership="publisher">© 2014, Wiley Periodicals, Inc.</copyright><numberingGroup><numbering type="journalVolume" number="31">31</numbering><numbering type="journalIssue">5</numbering></numberingGroup><coverDate startDate="2014-05">May 2014</coverDate></publicationMeta><publicationMeta level="unit" position="50" status="forIssue" type="article"><doi>10.1111/echo.12425</doi><idGroup><id type="unit" value="ECHO12425"></id></idGroup><countGroup><count number="6" type="pageTotal"></count></countGroup><titleGroup><title type="articleCategory">Original Investigation</title><title type="tocHeading1">Original Investigations</title></titleGroup><copyright ownership="publisher">© 2013, Wiley Periodicals, Inc.</copyright><eventGroup><event date="2013-06-21" type="manuscriptReceived"></event><event date="2013-09-03" type="manuscriptRevised"></event><event date="2013-09-05" type="manuscriptAccepted"></event><event agent="SPS" date="2013-09-20" type="xmlCreated"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.3.0 mode:FullText" date="2014-04-25"></event><event type="publishedOnlineEarlyUnpaginated" date="2013-11-05"></event><event type="firstOnline" date="2013-11-05"></event><event type="publishedOnlineFinalForm" date="2014-04-25"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.6.4 mode:FullText" date="2015-10-07"></event></eventGroup><numberingGroup><numbering type="pageFirst">563</numbering><numbering type="pageLast">568</numbering></numberingGroup><correspondenceTo>Address for correspondence and reprint requests: Robert J. Siegel, MD, FACC, The Heart Institute, Cedars‐Sinai Medical Center, 8700 Beverly Blvd., Los Angeles, California 90048. Fax: 310‐423‐8571; E‐mail: <email>Robert.siegel@cshs.org</email></correspondenceTo><selfCitationGroup><citation type="self" xml:id="echo12425-cit-1001">(<journalTitle>Echocardiography</journalTitle> <pubYear year="2014">2014</pubYear>;<vol>31</vol>:<pageFirst>563</pageFirst>–<pageLast>568</pageLast>)</citation></selfCitationGroup><linkGroup><link type="toTypesetVersion" href="file:ECHO.ECHO12425.pdf"></link></linkGroup></publicationMeta><contentMeta><titleGroup><title type="main">Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title><title type="shortAuthors">Ishimori, et al</title></titleGroup><creators><creator affiliationRef="#echo12425-aff-0001" creatorRole="author" xml:id="echo12425-cr-0001"><personName><givenNames>Mariko L.</givenNames> <familyName>Ishimori</familyName> <degrees>M.D.</degrees></personName></creator><creator affiliationRef="#echo12425-aff-0002" creatorRole="author" xml:id="echo12425-cr-0002"><personName><givenNames>Megha</givenNames> <familyName>Agarwal</familyName> <degrees>M.D.</degrees></personName></creator><creator affiliationRef="#echo12425-aff-0002" creatorRole="author" xml:id="echo12425-cr-0003"><personName><givenNames>Roy</givenNames> <familyName>Beigel</familyName> <degrees>M.D.</degrees></personName></creator><creator affiliationRef="#echo12425-aff-0002" creatorRole="author" xml:id="echo12425-cr-0004"><personName><givenNames>Rita K.</givenNames> <familyName>Ng</familyName> <degrees>M.D.</degrees></personName></creator><creator affiliationRef="#echo12425-aff-0001" creatorRole="author" xml:id="echo12425-cr-0005"><personName><givenNames>Nazanin</givenNames> <familyName>Firooz</familyName> <degrees>M.D.</degrees></personName></creator><creator affiliationRef="#echo12425-aff-0001" creatorRole="author" xml:id="echo12425-cr-0006"><personName><givenNames>Michael H.</givenNames> <familyName>Weisman</familyName> <degrees>M.D.</degrees></personName></creator><creator affiliationRef="#echo12425-aff-0002" corresponding="yes" creatorRole="author" xml:id="echo12425-cr-0007"><personName><givenNames>Robert J.</givenNames> <familyName>Siegel</familyName> <degrees>M.D., F.A.C.C.</degrees></personName></creator></creators><affiliationGroup><affiliation type="organization" xml:id="echo12425-aff-0001"><orgDiv>Division of Rheumatology</orgDiv> <orgName>Cedars‐Sinai Medical Center</orgName> <address><city>Los Angeles</city> <postCode>California</postCode></address></affiliation><affiliation type="organization" xml:id="echo12425-aff-0002"><orgDiv>The Heart Institute</orgDiv> <orgName>Cedars Sinai Medical Center</orgName> <address><city>Los Angeles</city> <postCode>California</postCode></address></affiliation></affiliationGroup><keywordGroup type="author"><keyword xml:id="echo12425-kwd-0001">cardiology</keyword><keyword xml:id="echo12425-kwd-0002">cardiomyopathy</keyword><keyword xml:id="echo12425-kwd-0003">echocardiography</keyword></keywordGroup><abstractGroup><abstract type="main" xml:id="echo12425-abs-0001"><section xml:id="echo12425-sec-0001"><title type="main">Objective</title><p>Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (<fc>SLE</fc>). However, most case reports on <fc>SLE</fc> cardiomyopathy (<fc>CM</fc>) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (<fc>LV</fc>) dysfunction in patients with <fc>SLE</fc>.</p></section><section xml:id="echo12425-sec-0002"><title type="main">Methods</title><p>The records of 526 <fc>SLE</fc> patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for <fc>SLE</fc> were met, (2) testing for erythrocyte sedimentation rate and hs‐CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (<fc>LVEF</fc>) <50%.</p></section><section xml:id="echo12425-sec-0003"><title type="main">Results</title><p>We identified 14 patients meeting study criteria. Mean <fc>LVEF</fc> was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram.</p></section><section xml:id="echo12425-sec-0004"><title type="main">Conclusion</title><p>The pattern of wall‐motion abnormalities and reversibility demonstrated in the majority of these patients with <fc>SLE</fc> suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.</p></section></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction</title></titleInfo><name type="personal"><namePart type="given">Mariko L.</namePart><namePart type="family">Ishimori</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Megha</namePart><namePart type="family">Agarwal</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Roy</namePart><namePart type="family">Beigel</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rita K.</namePart><namePart type="family">Ng</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Nazanin</namePart><namePart type="family">Firooz</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Michael H.</namePart><namePart type="family">Weisman</namePart><namePart type="termsOfAddress">M.D.</namePart><affiliation>Division of Rheumatology, Cedars‐Sinai Medical Center, California, Los Angeles</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Robert J.</namePart><namePart type="family">Siegel</namePart><namePart type="termsOfAddress">M.D., F.A.C.C.</namePart><affiliation>The Heart Institute, Cedars Sinai Medical Center, California, Los Angeles</affiliation><affiliation>E-mail: Robert.siegel@cshs.org</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="article" displayLabel="article" authority="ISTEX" authorityURI="https://content-type.data.istex.fr" valueURI="https://content-type.data.istex.fr/ark:/67375/XTP-6N5SZHKN-D">article</genre><originInfo><publisher>Blackwell Publishing Ltd</publisher><dateIssued encoding="w3cdtf">2014-05</dateIssued><dateCreated encoding="w3cdtf">2013-09-20</dateCreated><dateCaptured encoding="w3cdtf">2013-06-21</dateCaptured><dateValid encoding="w3cdtf">2013-09-05</dateValid><edition>(Echocardiography 2014;31:563–568)</edition><copyrightDate encoding="w3cdtf">2014</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><abstract>Objective: Myocarditis is reported to be a common postmortem finding of systemic lupus erythematosus (SLE). However, most case reports on SLE cardiomyopathy (CM) have not found evidence of myocarditis upon biopsy. Our aim was to characterize the nature, course, and reversibility of left ventricular (LV) dysfunction in patients with SLE. Methods: The records of 526 SLE patients were reviewed. Patients were included if: (1) at least 4 of 11 American College of Rheumatology criteria for SLE were met, (2) testing for erythrocyte sedimentation rate and hs‐CRP were performed during hospitalization, and (3) echocardiogram demonstrated left ventricular ejection function (LVEF) <50%. Results: We identified 14 patients meeting study criteria. Mean LVEF was 33.1 ± 9% upon presentation. The main echocardiographic pattern observed was generalized hypokinesis. Twelve patients demonstrated reversal of cardiomyopathy within 1 week, showing a mean improvement in LVEF of 21.0 ± 7%. Of these, 2 patients underwent coronary angiography demonstrating no evidence of obstructive coronary disease, and 1 underwent cardiac biopsy with no evidence of myocarditis. Four patients (29%) demonstrated improvement within 3 days. Two of the 14 patients died due to their underlying medical illness and did not have a repeat echocardiogram. Conclusion: The pattern of wall‐motion abnormalities and reversibility demonstrated in the majority of these patients with SLE suggests an etiology more consistent with stress cardiomyopathy rather than myocarditis.</abstract><subject><genre>keywords</genre><topic>cardiology</topic><topic>cardiomyopathy</topic><topic>echocardiography</topic></subject><relatedItem type="host"><titleInfo><title>Echocardiography</title></titleInfo><titleInfo type="abbreviated"><title>Echocardiography</title></titleInfo><genre type="journal" authority="ISTEX" authorityURI="https://publication-type.data.istex.fr" valueURI="https://publication-type.data.istex.fr/ark:/67375/JMC-0GLKJH51-B">journal</genre><subject><genre>article-category</genre><topic>Original Investigation</topic><topic>Original Investigations</topic></subject><identifier type="ISSN">0742-2822</identifier><identifier type="eISSN">1540-8175</identifier><identifier type="DOI">10.1111/(ISSN)1540-8175</identifier><identifier type="PublisherID">ECHO</identifier><part><date>2014</date><detail type="volume"><caption>vol.</caption><number>31</number></detail><detail type="issue"><caption>no.</caption><number>5</number></detail><extent unit="pages"><start>563</start><end>568</end><total>6</total></extent></part></relatedItem><relatedItem type="references" displayLabel="echo12425-cit-0001"><titleInfo><title>The heart in systemic lupus erythematosus</title></titleInfo><name type="personal"><namePart type="given">W</namePart><namePart type="family">Brigden</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">EG</namePart><namePart type="family">Bywaters</namePart><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">MH</namePart><namePart type="family">Lessof</namePart><role><roleTerm type="text">author</roleTerm></role></name><genre>journal-article</genre><note type="citation/reference">Brigden W, Bywaters EG, Lessof MH, et al: The heart in systemic lupus erythematosus. 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Chest 1996;109:282–284.</note><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>109</number></detail><extent unit="pages"><start>282</start><end>284</end></extent></part><relatedItem type="host"><titleInfo><title>Chest</title></titleInfo><part><date>1996</date><detail type="volume"><caption>vol.</caption><number>109</number></detail><extent unit="pages"><start>282</start><end>284</end></extent></part></relatedItem></relatedItem><identifier type="istex">7B5DC7EA96AA97CA5B9231B1AA07EC2953BAE7A5</identifier><identifier type="ark">ark:/67375/WNG-2FZNKRML-9</identifier><identifier type="DOI">10.1111/echo.12425</identifier><identifier type="ArticleID">ECHO12425</identifier><accessCondition type="use and reproduction" contentType="copyright">© 2014, Wiley Periodicals, Inc.© 2013, Wiley Periodicals, Inc.</accessCondition><recordInfo><recordContentSource authority="ISTEX" authorityURI="https://loaded-corpus.data.istex.fr" valueURI="https://loaded-corpus.data.istex.fr/ark:/67375/XBH-L0C46X92-X">wiley</recordContentSource><recordOrigin>Converted from (version ) to MODS version 3.6.</recordOrigin><recordCreationDate encoding="w3cdtf">2019-11-14</recordCreationDate></recordInfo></mods><json:item><extension>json</extension><original>false</original><mimetype>application/json</mimetype><uri>https://api.istex.fr/ark:/67375/WNG-2FZNKRML-9/record.json</uri></json:item></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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