Arthritis care & research · 2026
Rheumatoid Arthritis and Coronary Artery Calcium Progression: A Case Cohort Analysis From ELSA-Brasil.
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Fonseca Estrada Patrícia, Rafael N Cavalcante Marcos, de Souza Santos Itamar, S Bittencourt Márcio, Meneghini Vandrize, A Lotufo Paulo, C Goulart Alessandra, M Bensenor Isabela
Аннотация
OBJECTIVE: To investigate the association between rheumatoid arthritis (RA) and coronary artery calcium (CAC) prevalence, incidence, and progression over four years in adults without prior cardiovascular disease.
METHODS: A case-cohort study within the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil) included 585 participants (86 patients with RA, 499 controls). Longitudinal analyses were restricted to those with CAC reassessed at four years (58 patients with RA, 352 controls). CAC was quantified by computed tomography (Agatston method). Incidence was defined as new CAC among those with baseline zero CAC; progression used Berry criteria. Multivariable regression models were hierarchically adjusted. Nonparametric bootstrap estimated 95% confidence intervals (CIs) for progression.
RESULTS: Mean ± SD age was 51.5 ± 8.9 years; 55.5% were female. RA was not associated with CAC prevalence (odds ratio [OR] 1.34; 95% CI 0.69-2.55) or incidence (OR 0.83; 95% CI 0.05-3.08) after adjustment. Conversely, RA was associated with CAC progression after multivariable adjustment (Model 1 OR 3.11; 95% bootstrap CI 1.52-8.41; Model 2 OR 4.29; 95% bootstrap CI 1.98-14.65).
CONCLUSION: In this cohort, RA was associated with CAC progression despite no association with prevalence or incidence. These findings suggest chronic inflammation may drive calcification progression through nontraditional pathways, supporting longitudinal cardiovascular monitoring in RA.
METHODS: A case-cohort study within the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil) included 585 participants (86 patients with RA, 499 controls). Longitudinal analyses were restricted to those with CAC reassessed at four years (58 patients with RA, 352 controls). CAC was quantified by computed tomography (Agatston method). Incidence was defined as new CAC among those with baseline zero CAC; progression used Berry criteria. Multivariable regression models were hierarchically adjusted. Nonparametric bootstrap estimated 95% confidence intervals (CIs) for progression.
RESULTS: Mean ± SD age was 51.5 ± 8.9 years; 55.5% were female. RA was not associated with CAC prevalence (odds ratio [OR] 1.34; 95% CI 0.69-2.55) or incidence (OR 0.83; 95% CI 0.05-3.08) after adjustment. Conversely, RA was associated with CAC progression after multivariable adjustment (Model 1 OR 3.11; 95% bootstrap CI 1.52-8.41; Model 2 OR 4.29; 95% bootstrap CI 1.98-14.65).
CONCLUSION: In this cohort, RA was associated with CAC progression despite no association with prevalence or incidence. These findings suggest chronic inflammation may drive calcification progression through nontraditional pathways, supporting longitudinal cardiovascular monitoring in RA.