Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction
Identifieur interne : 001049 ( Main/Exploration ); précédent : 001048; suivant : 001050Systemic Lupus Erythematosus Cardiomyopathy—A Case Series Demonstrating a Reversible Form of Left Ventricular Dysfunction
Auteurs : Mariko L. Ishimori [États-Unis] ; Megha Agarwal [États-Unis] ; Roy Beigel [États-Unis] ; Rita K. Ng [États-Unis] ; Nazanin Firooz [États-Unis] ; Michael H. Weisman [États-Unis] ; Robert J. Siegel [États-Unis]Source :
- 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.
Url:
DOI: 10.1111/echo.12425
Affiliations:
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Ng</name></author><author><name sortKey="Firooz, Nazanin" sort="Firooz, Nazanin" uniqKey="Firooz N" first="Nazanin" last="Firooz">Nazanin Firooz</name></author><author><name sortKey="Weisman, Michael H" sort="Weisman, Michael H" uniqKey="Weisman M" first="Michael H." last="Weisman">Michael H. Weisman</name></author><author><name sortKey="Siegel, Robert J" sort="Siegel, Robert J" uniqKey="Siegel R" first="Robert J." last="Siegel">Robert J. 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Ishimori</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>Division of Rheumatology, Cedars‐Sinai Medical Center, California</wicri:orgArea></affiliation></author><author><name sortKey="Agarwal, Megha" sort="Agarwal, Megha" uniqKey="Agarwal M" first="Megha" last="Agarwal">Megha Agarwal</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>The Heart Institute, Cedars Sinai Medical Center, California</wicri:orgArea></affiliation></author><author><name sortKey="Beigel, Roy" sort="Beigel, Roy" uniqKey="Beigel R" first="Roy" last="Beigel">Roy Beigel</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>The Heart Institute, Cedars Sinai Medical Center, California</wicri:orgArea></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 wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>The Heart Institute, Cedars Sinai Medical Center, California</wicri:orgArea></affiliation></author><author><name sortKey="Firooz, Nazanin" sort="Firooz, Nazanin" uniqKey="Firooz N" first="Nazanin" last="Firooz">Nazanin Firooz</name><affiliation wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>Division of Rheumatology, Cedars‐Sinai Medical Center, California</wicri:orgArea></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 wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>Division of Rheumatology, Cedars‐Sinai Medical Center, California</wicri:orgArea></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 wicri:level="3"><country>États-Unis</country><placeName><settlement type="city">Los Angeles</settlement><region type="state">Californie</region></placeName><wicri:orgArea>The Heart Institute, Cedars Sinai Medical Center, California</wicri:orgArea></affiliation><affiliation><wicri:noCountry code="no comma">E-mail: Robert.siegel@cshs.org</wicri:noCountry></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><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li></region><settlement><li>Los Angeles</li></settlement></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Ishimori, Mariko L" sort="Ishimori, Mariko L" uniqKey="Ishimori M" first="Mariko L." last="Ishimori">Mariko L. 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