OBJECTIVES:To explore incidence and progression of coronary atherosclerosis and identify determinants thereof in patients with rheumatoid arthritis. We specifically evaluated the impact of inflammation, cardiac risk factors, duration of medication exposure and their interactions on coronary plaque progression. METHODS:One hundred-one participants with a baseline coronary computed tomography angiography underwent follow-up assessment in 83±3.6 months. Plaque burden was reported as segment involvement score (SIS) describing the number of coronary segments with plaque and segment stenosis score (SSS) characterizing the cumulative plaque stenosis over all evaluable segments. Plaque composition was defined as non-calcified (NCP), mixed (MP) or calcified (CP). Coronary artery calcium (CAC) was quantified by the Agatston method. RESULTS:Total plaque increased in 48% of patients; progression was predicted by older age, higher cumulative inflammation and total prednisone dose (p<0.05). CAC progressors were older, more obese, hypertensive, with higher cumulative inflammation compared to non-progressors (p<0.05). Longer exposure to biologics associated with lower likelihood of NCP progression, lesion remodeling and constrained CAC change in patients without baseline calcification independently of inflammation, prednisone dose, or statin exposure (all p<0.05). Longer statin treatment further restricted NCP progression and attenuated the effect of inflammation on plaque and CAC increase (p<0.05). Stringent systolic blood pressure control further weakened the effect of inflammation on total plaque progression. CONCLUSION:Inflammation was a consistent and independent predictor of coronary atherosclerosis progression in RA; it should therefore be specifically targeted towards mitigating cardiovascular risk. BDMARDs, statins and blood pressure control may further constrain plaque progression directly or indirectly.