Predictors of cardiovascular damage in patients with systemic lupus erythematosus: data from LUMINA (LXVIII), a multiethnic US cohort
Identifieur interne : 001782 ( Main/Exploration ); précédent : 001781; suivant : 001783Predictors of cardiovascular damage in patients with systemic lupus erythematosus: data from LUMINA (LXVIII), a multiethnic US cohort
Auteurs : Guillermo J. Pons-Estel [États-Unis] ; Luis A. González [États-Unis] ; Jie Zhang [États-Unis] ; Paula I. Burgos [États-Unis] ; John D. Reveille [États-Unis] ; Luis M. Vilá [États-Unis] ; Graciela S. Alarc N [États-Unis]Source :
- Rheumatology [ 1462-0324 ] ; 2009.
Abstract
Objective. To determine the features predictive of atherosclerotic cardiovascular damage in patients with SLE. Methods. SLE LUMINA (LUpus in MInorities: NAture vs nurture) patients (n = 637), aged ⩾16 years, disease duration ⩽5 years at baseline (T0), of African–American, Hispanic and Caucasian ethnicity were studied. Atherosclerotic cardiovascular damage was defined by the following items of the SLICC Damage Index (SDI) cardiovascular domain: angina or coronary artery by pass surgery, myocardial infarction and/or congestive heart failure; factors associated with its occurrence were examined by univariable and multivariable regression analyses. Results. Forty-three (6.8%) of 637 patients developed cardiovascular damage over a mean ± s.d. total disease duration of 6.6 ± 3.6 years. Nearly 90% of the patients were women with a mean ± s.d. age of 36.5 (12.6) years; all ethnic groups were represented. By multivariable analyses, after adjusting for the cardiovascular manifestations present, age [odds ratio (OR) = 1.06; 95% CI 1.03, 1.09], male gender (OR = 3.57; 95% CI 1.35, 9.09) SDI at baseline (OR = 1.28; 95% CI 1.09, 1.50) and CRP levels [highest tertile (OR = 2.63; 95% CI 1.17, 5.91)] were associated with the occurrence of cardiovascular damage, whereas the number of years of education was negatively associated with such outcome (OR = 0.85; 95% CI 0.74, 0.94). Conclusions. Our data suggest that atherosclerotic cardiovascular damage in SLE is multifactorial; traditional (age, gender) and disease-related factors (CRP levels, SDI at baseline) appear to be important contributors to such an occurrence. Tight control of the inflammatory process must be achieved to prevent it.
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DOI: 10.1093/rheumatology/kep102
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Reveille</name></author><author><name sortKey="Vila, Luis M" sort="Vila, Luis M" uniqKey="Vila L" first="Luis M." last="Vilá">Luis M. Vilá</name></author><author><name sortKey="Alarc N, Graciela S" sort="Alarc N, Graciela S" uniqKey="Alarc N G" first="Graciela S." last="Alarc N">Graciela S. 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Pons-Estel</name><affiliation wicri:level="2"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Medicine, Division of Clinical Immunology and Rheumatology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL,Department of Medicine, Division of Rheumatology, The University of Texas Health Science Center at Houston, Houston, TX, USA,Department of Medicine, Division of Rheumatology, The University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, Spain and Department of Epidemiology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Gonzalez, Luis A" sort="Gonzalez, Luis A" uniqKey="Gonzalez L" first="Luis A." last="González">Luis A. González</name><affiliation wicri:level="2"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Medicine, Division of Clinical Immunology and Rheumatology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL,Department of Medicine, Division of Rheumatology, The University of Texas Health Science Center at Houston, Houston, TX, USA,Department of Medicine, Division of Rheumatology, The University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, Spain and Department of Epidemiology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Zhang, Jie" sort="Zhang, Jie" uniqKey="Zhang J" first="Jie" last="Zhang">Jie Zhang</name><affiliation wicri:level="2"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Medicine, Division of Clinical Immunology and Rheumatology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL,Department of Medicine, Division of Rheumatology, The University of Texas Health Science Center at Houston, Houston, TX, USA,Department of Medicine, Division of Rheumatology, The University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, Spain and Department of Epidemiology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Burgos, Paula I" sort="Burgos, Paula I" uniqKey="Burgos P" first="Paula I." last="Burgos">Paula I. Burgos</name><affiliation wicri:level="2"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Medicine, Division of Clinical Immunology and Rheumatology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL,Department of Medicine, Division of Rheumatology, The University of Texas Health Science Center at Houston, Houston, TX, USA,Department of Medicine, Division of Rheumatology, The University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, Spain and Department of Epidemiology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Reveille, John D" sort="Reveille, John D" uniqKey="Reveille J" first="John D." last="Reveille">John D. 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Vilá</name><affiliation wicri:level="2"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Medicine, Division of Clinical Immunology and Rheumatology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL,Department of Medicine, Division of Rheumatology, The University of Texas Health Science Center at Houston, Houston, TX, USA,Department of Medicine, Division of Rheumatology, The University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, Spain and Department of Epidemiology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation></author><author><name sortKey="Alarc N, Graciela S" sort="Alarc N, Graciela S" uniqKey="Alarc N G" first="Graciela S." last="Alarc N">Graciela S. Alarc N</name><affiliation wicri:level="2"><country xml:lang="fr" wicri:curation="lc">États-Unis</country><wicri:regionArea>Department of Medicine, Division of Clinical Immunology and Rheumatology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL,Department of Medicine, Division of Rheumatology, The University of Texas Health Science Center at Houston, Houston, TX, USA,Department of Medicine, Division of Rheumatology, The University of Puerto Rico Medical Sciences Campus, San Juan, Puerto Rico, Spain and Department of Epidemiology, Schools of Medicine and Public Health, The University of Alabama at Birmingham, Birmingham, AL</wicri:regionArea><placeName><region type="state">Alabama</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Rheumatology</title><idno type="ISSN">1462-0324</idno><idno type="eISSN">1462-0332</idno><imprint><publisher>Oxford University Press</publisher><date when="2009-07">2009</date><date type="e-published" when="2009-05-19">2009</date><biblScope unit="vol">48</biblScope><biblScope unit="issue">7</biblScope><biblScope unit="page" from="817">817</biblScope><biblScope unit="page" to="822">822</biblScope></imprint><idno type="ISSN">1462-0324</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">1462-0324</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract">Objective. To determine the features predictive of atherosclerotic cardiovascular damage in patients with SLE. Methods. SLE LUMINA (LUpus in MInorities: NAture vs nurture) patients (n = 637), aged ⩾16 years, disease duration ⩽5 years at baseline (T0), of African–American, Hispanic and Caucasian ethnicity were studied. Atherosclerotic cardiovascular damage was defined by the following items of the SLICC Damage Index (SDI) cardiovascular domain: angina or coronary artery by pass surgery, myocardial infarction and/or congestive heart failure; factors associated with its occurrence were examined by univariable and multivariable regression analyses. Results. Forty-three (6.8%) of 637 patients developed cardiovascular damage over a mean ± s.d. total disease duration of 6.6 ± 3.6 years. Nearly 90% of the patients were women with a mean ± s.d. age of 36.5 (12.6) years; all ethnic groups were represented. By multivariable analyses, after adjusting for the cardiovascular manifestations present, age [odds ratio (OR) = 1.06; 95% CI 1.03, 1.09], male gender (OR = 3.57; 95% CI 1.35, 9.09) SDI at baseline (OR = 1.28; 95% CI 1.09, 1.50) and CRP levels [highest tertile (OR = 2.63; 95% CI 1.17, 5.91)] were associated with the occurrence of cardiovascular damage, whereas the number of years of education was negatively associated with such outcome (OR = 0.85; 95% CI 0.74, 0.94). Conclusions. Our data suggest that atherosclerotic cardiovascular damage in SLE is multifactorial; traditional (age, gender) and disease-related factors (CRP levels, SDI at baseline) appear to be important contributors to such an occurrence. Tight control of the inflammatory process must be achieved to prevent it.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Alabama</li></region></list><tree><country name="États-Unis"><region name="Alabama"><name sortKey="Pons Estel, Guillermo J" sort="Pons Estel, Guillermo J" uniqKey="Pons Estel G" first="Guillermo J." last="Pons-Estel">Guillermo J. Pons-Estel</name></region><name sortKey="Alarc N, Graciela S" sort="Alarc N, Graciela S" uniqKey="Alarc N G" first="Graciela S." last="Alarc N">Graciela S. Alarc N</name><name sortKey="Alarc N, Graciela S" sort="Alarc N, Graciela S" uniqKey="Alarc N G" first="Graciela S." last="Alarc N">Graciela S. Alarc N</name><name sortKey="Burgos, Paula I" sort="Burgos, Paula I" uniqKey="Burgos P" first="Paula I." last="Burgos">Paula I. Burgos</name><name sortKey="Gonzalez, Luis A" sort="Gonzalez, Luis A" uniqKey="Gonzalez L" first="Luis A." last="González">Luis A. González</name><name sortKey="Reveille, John D" sort="Reveille, John D" uniqKey="Reveille J" first="John D." last="Reveille">John D. Reveille</name><name sortKey="Vila, Luis M" sort="Vila, Luis M" uniqKey="Vila L" first="Luis M." last="Vilá">Luis M. Vilá</name><name sortKey="Zhang, Jie" sort="Zhang, Jie" uniqKey="Zhang J" first="Jie" last="Zhang">Jie Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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