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dc.contributor.authorRojas-Giménez, Marta
dc.contributor.authorLópez Medina, Eloísa Clementina
dc.contributor.authorLadehesa-Pineda, Lourdes
dc.contributor.authorPuche-Larrubia, María Ángeles
dc.contributor.authorGómez-García, Ignacio
dc.contributor.authorCalvo Gutiérrez, Jerusalém
dc.contributor.authorSeguí-Azpilcueta, Pedro
dc.contributor.authorÁbalos-Aguilera, María del Carmen
dc.contributor.authorRuiz-Vilchez, Desirée
dc.contributor.authorEscudero Contreras, Alejandro
dc.contributor.authorCollantes Estévez, Eduardo
dc.date.accessioned2022-01-27T12:27:03Z
dc.date.available2022-01-27T12:27:03Z
dc.date.issued2022
dc.identifier.urihttp://hdl.handle.net/10396/22394
dc.description.abstractObjective: To compare the effect of inflammation on subclinical atherosclerosis using carotid ultrasound in patients with rheumatoid arthritis (RA) and spondyloarthritis (SpA). Methods: Cross-sectional study including 347 participants (148 RA, 159 SpA, and 40 controls). We measured the carotid intima media thickness (cIMT) and detection of atheromatous plaques using carotid ultrasound. We recorded disease activity (DAS28-CRP/ASDAS-CRP) and traditional cardiovascular risk factors. We performed descriptive, bivariate, and linear multivariate analyses (dependent variable: cIMT) to evaluate the influence of diagnosis on cIMT in all patients. Two additional multivariate analyses were performed by stratifying patients according to their inflammatory activity. Results: cIMT correlated with the mean CRP during the previous 5 years in RA, but not with CRP at the cut-off date. We did not find such differences in patients with SpA. The first multivariate model revealed that increased cIMT was more common in patients with RA than in those with SpA (β coefficient, 0.045; 95% confidence interval (95% CI), 0.0002–0.09; p = 0.048) after adjusting for age, sex, disease course, and differential cardiovascular risk factors (arterial hypertension, smoking, statins, and corticosteroids). The second model revealed no differences in cIMT between the 2 groups of patients classified as remission–low activity (β coefficient, 0.020; 95% CI, −0.03 to 0.080; p = 0.500). However, when only patients with moderate–high disease activity were analysed, the cIMT was 0.112 mm greater in those with RA (95% CI, 0.013–0.212; p = 0.026) than in those with SpA after adjusting for the same variables. Conclusions: Subclinical atherosclerosis measured by carotid ultrasound in patients with RA and SpA is comparable when the disease is well controlled. However, when patients have moderate–high disease activity, cIMT is greater in patients with RA than in those with SpA after adjusting for age, sex, disease course, and cardiovascular risk factors. Our results point to greater involvement of disease activity in subclinical atherosclerosis in patients with RA than in those with SpA.es_ES
dc.format.mimetypeapplication/pdfes_ES
dc.language.isoenges_ES
dc.publisherMDPIes_ES
dc.rightshttps://creativecommons.org/licenses/by/4.0/es_ES
dc.sourceJournal of Clinical Medicine 11(3), 662 (2022)es_ES
dc.subjectRheumatoid arthritises_ES
dc.subjectSpondyloarthritises_ES
dc.subjectSubclinical atherosclerosises_ES
dc.subjectCardiovascular riskes_ES
dc.subjectInflammatory activityes_ES
dc.titleSubclinical Atherosclerosis Measure by Carotid Ultrasound and Inflammatory Activity in Patients with Rheumatoid Arthritis and Spondylarthritises_ES
dc.typeinfo:eu-repo/semantics/articlees_ES
dc.relation.publisherversionhttps://doi.org/10.3390/jcm11030662es_ES
dc.rights.accessRightsinfo:eu-repo/semantics/openAccesses_ES


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