Subclinical coronary artery calcium incidence and progression in rheumatoid arthritis: a 12-year longitudinal cohort study
P F E Estrada, M R N C Cavalcante, M S B Bittencourt, I S S Santos, V M Meneghini, A C G Goulart, P A L Lotufo, I J M B BensenorAbstract
Background
Rheumatoid arthritis (RA) is associated with increased cardiovascular risk, potentially mediated by chronic systemic inflammation. However, longitudinal data evaluating coronary artery calcium (CAC) progression in individuals without clinical cardiovascular disease remain limited, particularly in Latin American populations.
Purpose
To evaluate the association between RA and both incidence and progression of CAC over 12 years in a multicentre longitudinal cohort without prior cardiovascular disease.
Methods
Participants from the Brazilian Longitudinal Study of Adult Health (ELSA-Brasil), a multicentre cohort of civil servants from public teaching and research institutions, underwent computed tomography for CAC assessment at baseline and follow-up. RA was identified using validated clinical criteria based on physician diagnosis, use of disease-modifying antirheumatic medication or positive serological biomarkers. CAC incidence was assessed among participants with baseline scores of 0 who developed detectable CAC at follow-up. CAC progression was defined according to Berry criteria among those with baseline CAC > 0. Multivariable logistic regression, adjusted for sociodemographic characteristics and traditional cardiovascular risk factors, was used to estimate odds ratios (OR) and 95% confidence intervals (CI).
Results
Of the 491 participants (69 RA; 422 controls), mean age was 52.0 years in the RA group and 50.1 years in controls, and women comprised 81.2% and 54.3%, respectively. CAC incidence occurred in 32.5% of the RA group and 37.1% of controls, showing no association after multivariable adjustment (OR 0.96; 95% CI 0.42–2.21; p=0.930). Among participants with pre-existing calcification, progression occurred more frequently in RA compared with controls (76.5% vs 67.5%). RA remained independently associated with CAC progression after full adjustment (OR 5.29; 95% CI 1.04–26.79; p=0.044).
Conclusions
Over a 12-year follow-up, RA was independently associated with an approximately five-fold increase in the odds of CAC progression, despite no association with CAC incidence. These findings suggest that chronic inflammatory disease primarily accelerates established atherosclerotic processes rather than initiating them, underscoring the need for sustained cardiovascular monitoring in this population