Karpouzas GA, et al. - One hundred-one individuals with a baseline coronary CT angiography were recruited in order to investigate the incidence and progression of coronary atherosclerosis and recognize determinants thereof in patients with rheumatoid arthritis. Total plaque rose in 48% of patients. Coronary artery calcium (CAC) progressors were elderly, more obese, hypertensive, with higher cumulative inflammation in contrast with non-progressors. In individuals without baseline calcification, longer exposure to biologics correlated with a lower probability of non-calcified plaque progression (NCP), lesion remodeling and constrained CAC change, independently of inflammation, prednisone dose, or statin exposure. Longer statin treatment additionally restrained NCP progression and attenuated the impact of inflammation on plaque and CAC progression. Stringent systolic blood pressure control moreover reduced the impact of inflammation on total plaque progression. Hence, inflammation was a constant and independent predictor of coronary atherosclerosis progression in RA and it should, hence, be particularly taken into account towards alleviating cardiovascular risk. BDMARDs, statins and blood pressure control may additionally restrain plaque progression straight or discursively.