10-YEAR ATHEROSCLEROTIC PLAQUE PROGRESSION AND INCIDENT CARDIOVASCULAR EVENTS IN SYSTEMIC LUPUS ERYTHEMATOSUS: THE IMPACT OF PERSISTENT CARDIOVASCULAR RISK FACTOR TARGET ATTAINMENT AND SUSTAINED DORIS REMISSION

O033 / #701 Topic: AS23 - SLE-Diagnosis, Manifestations, & Outcomes ABSTRACT CONCURRENT SESSION 05: EMERGING INSIGHTS ON THE MANAGEMENT OF LUPUS MANIFESTATIONS AND COMORBIDITIES 23-05-2025 1:40 PM - 2:40 PM Background/Purpose Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in Systemic Lupus Erythematosus (SLE). The role of sustained cardiovascular risk factor (CVRF) control and minimal disease activity on clinical and subclinical atherosclerosis remains underexplored in SLE. We assessed the impact of persistent traditional CVRF target attainment and sustained minimal disease activity on atherosclerotic plaque progression and incident cardiovascular events in patients with SLE over a 10-year follow-up period. Methods We prospectively analyzed 738 carotid ultrasound measurements (413 in SLE patients and 325 in age/sex-matched healthy controls [HC]) to assess new plaque development from baseline to 3-, 7-, and 10-year follow-up assessments. Multivariate mixed-effects Poisson regression models examined potential predictors of plaque progression, including patient demographic characteristics, Systemic Coronary Risk Evaluation (SCORE), SCORE2, traditional cardiovascular risk factor (CVRF) target attainment as per the 2016 European Society of Cardiology guidelines, sustained achievement of Lupus Low Disease Activity State (LLDAS) and Definition of Remission in SLE (DORIS) clinical remission, cumulative glucocorticoid exposure, consistent hydroxychloroquine use, CVD-related medications, and persistent triple antiphospholipid antibody (aPL) positivity during the 10-year follow-up period. We assessed 10-year incident CVD events in SLE vs HC, and univariate Cox regression analysis examined potential associations. We evaluated the efficacy of carotid ultrasound in predicting CVD risk in the SLE cohort, comparing its performance to SCORE and SCORE2 alone. Results Patients with SLE had a 2.3-fold higher 10-year risk of carotid plaque progression than HC (Incidence Rate Ratio [IRR]: 2.26, 95% CI 1.34-3.81, p = 0.002) (Table 1, model A). The expected 10-year evolution of the number of carotid plaques was higher in SLE vs HC (Figure 1A). The risk of plaque progression in SLE patients was reduced by 32% (IRR: 0.68, 95% CI 0.53-0.89, p = 0.004) for each CVRF persistently on target during the 10-year follow-up, including blood pressure, lipids, smoking, body weight, and physical activity (Table 1, model B). DORIS achievement ≥ 75% of the follow-up period was associated with a 43% decrease in atherosclerotic plaque progression risk (IRR: 0.57, 95% CI 0.34-0.95, p = 0.033) (Table 1, Model B). The expected 10-year evolution of the number of carotid plaques was lower in patients with more persistently attained CVRF targets during follow-up (Figure 1B), and in those achieving DORIS remission ≥ 75% of follow-up vs those who did not (Figure 1C). Ten-year risk of incident cardiovascular events was higher in SLE than HC individuals (8 vs 1 event, permutation-based log-rank p = 0.036), and was associated with persistent triple aPL positivity. The incorporation of carotid ultrasound in CVD risk assessment in SLE patients tripled our ability to predict the 10-year risk for CVD events from 12.5% to 37.5%. Table 1. Multivariate mixed effects Poisson regression models of carotid plaque progression in SLF versus healthy controls (model A), and within SLE (model B) Figure 1. Expected 10-year evolution of the number of carotid plaques A) for typical SLE and healthy control (HCs). B) for typical SLE individuals with varying numbers of cardiovascular risk factor (CVRF) targets sustainedly attained, and C) for typical SLE individuals with versus without DORIS remission for ≥75% of follow-up *A) Typical individuals are SLE patients or HCs with baseline characteristic values (included in multivariate model 4A of plaque progression in SLE versus HCs) set at the median for quantitative and at the mode for qualitative variables: no use of antihypertensives, lipid-lowering agents or antiplatelets, SCORE 0.1. eGFR 111 mL/min/1.73 m 2 , no carotid plaques. B) Typical SLE individuals are patients with baseline characteristic values (included in multivariate model 5A of plaque progression in SLE) set at the median for quantitative and at the mode for qualitative variable: 43 years old, no use of antihypertensives, lipid-lowering agents, or antiplatelets, no DORIS remission ≥75% of follow-up. C) Typical SLE individuals are patients with baseline characteristic values (included in multivariate model 5A) set at the median for quantitative and at the mode for qualitative variables: 43 years old, no use of antihypertensives, lipid-lowering agents, or antiplatelets, and two CVRF targets sustainedly attained during the follow-up. Conclusions Patients with SLE experience a 2.3-fold higher 10-year atherosclerosis progression risk than HC, which is significantly mitigated by sustained CVRF control and prolonged clinical remission. Persistent triple aPL positivity is associated with increased incidence of CVD events in SLE. Carotid ultrasound may have an additive role in enhancing CVD risk assessment in patients with SLE.

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