THU0336 Predictors of subclinical carotid atheromatosis in patients with systemic lupus erythematosus: relevance of activity, damage and severity indexes. (12th June 2018)

• Record Type: Journal Article
• Authors: Quevedo, J.C.; Sánchez, H.; Rua-Figueroa, I.; Tejera, B.; de Vera, A.; González-Delgado, A.; Rodríguez-Lozano, C.; Ferraz-Amaro, I.
• Is Part Of: Annals of the rheumatic diseases. Volume 77(2018)Supplement 2
• Page Start: 386
• Page End: 387
• Publication Date: 2018-06-12
• Subjects: Rheumatism -- Periodicals; 616.723005
• DOI: 10.1136/annrheumdis-2018-eular.5749
• Languages: English
• ISSNs: 0003-4967

Abstract

Abstract : Background: The prevalence of subclinical atheromatosis in patients with systemic lupus erythematosus (SLE) is double that the observed in the general population. The mechanisms of this accelerated atherosclerosis are unknown, but they may include factors related to the disease, as well as the interaction of these with classic cardiovascular risk factors (CVRF). Objectives: We analyse wich predictors of subclinical carotid atheromatosis exist in a large series of patients with SLE, with special emphasis on the role of the activity, damage and severity indexes. Methods: Cross-sectional study that included 276 patients with SLE. Lipid serum levels, autoimmunity profile and the activity (SLEDAI), severity (Katz) and damage (SLICC) indexes were determined. The thickness of the carotid intima-media (cIMT) and the presence of plaques were determined by radiofrequency US. The cardiovascular risk was estimated through SCORE. Multivariate regression analysis was performed to assess the relationship of the indexes with CVRF, cIMT and carotid plaque. Predictive capacity for the presence of plaque by comparing the AUC of the different models was performed through the DeLong method Results: 106 (38%), 85 (31%), 47 (17%) and 21 (8%) patients showed respectively SLEDAI null, low, moderate and high, 197 (71%) had a SLICC >1 and 104 (38%) a Katz>3. In 36% (99) of the patients carotid plaques were detected, with an average cIMT of 0.631±0.108 mm. SLEDAI showed a positive relationship with hypertension; the Katz with hypertension and dyslipidemia; and the SLICC with these and also with age, body mass index and abdominal waist. The relationship of the latter with the CVRF was maintained after subtracting its items related to cardiovascular risk. SLICC was univariatelly related to plaque (OR 1.29 [95% CI 1.13–1.48], p=0.000) and a SLICC >1 showed a tendency to be associated with a higher cIMT (beta coefficient 0.03 [95% CI 0.00–0.06 ], p=0.053). No univariate relationships were found between Katz or SLEDAI with subclinical atheromatosis. The relationship of SLICC with plaque was maintained after adjusting for age, sex and CVRF (OR 1.19 [95% CI 1.00–1.42], p=0.047). Similarly, SLICC (even without its vascular damage items) (beta coefficient 0.26 [95% CI 0.12–0.41], p=0.000), but not Katz and SLEDAI, correlated significantly with SCORE. The predictive capacity of SCORE for the presence of plaque was AUC 0.788 (95% CI 0.735–0.842). Analogously SLICC showed an AUC 0.659 (95% CI 0.594–0.724) for plaque; the AUC of Katz and SLEDAI did not reach statistical significance. The AUC of the SCORE +SLICC versus SCORE did not show statistically significant differences (p=0.31). The statistical significance of the reclassification indexes were net reclasification index p=0.61, and integrated discrimination improvement p=0.01. Conclusions: SLICC is independently related to the presence of plaque. SLE activity, severity and damage indexes are related to CVRF but they have little impact on the predictive capacity of SCORE for the presence of carotid plaque. Disclosure of Interest: None declared