Background/Purpose: In early atherogenesis inflammation drives and co-localizes with intimal calcification. In chronic, advanced plaques inflammation and calcification are inversely correlated and spatially distinct; advanced calcification is considered a stabilizing physiologic process rendering plaques less prone to rupture. We evaluated the role of inflammation, biologic treatments and cardiac risk factors on the de-novo generation and progression of advanced, calcified coronary plaques (CP) in patients with rheumatoid arthritis (RA).

Methods: Ninety-nine participants with a baseline non-invasive evaluation of coronary anatomy with computed tomography angiography (CCTA) underwent a repeat assessment within 83±3.6 months. Coronary lesions were counted and defined as non-calcified (NCP), mixed (MP) or calcified (CP). The prevalence, number, stenotic severity and burden of individual CP plaques was recorded. Patients were classified into three groups according to plaque disposition: CP-negative (no CP at any time), CP-positive (CP present at both times), and new-CP (absent at baseline, present at follow-up). A Multinomial logistic regression model evaluated predictors independently associated with patient classification into the CP-positive or New-CP groups compared to the CP negative group.

Results: CP prevalence was higher at follow-up compared to baseline (42.3% vs. 19.8%, p<0.001, table 1); 21 of 99 (21%) patients developed new CP lesions. In the CP-positive group, 43% of the lesions at follow-up were unchanged from baseline,16% derived from progression of MP, 3% from NCP and 23% were incident CP lesions. In the New-CP group, 73% of lesions were incident CP, 13% derived from NCP and 13% from MP. CP-positive patients were older, with greater baseline hyperlipidemia and higher inflammatory burden [area under the curve for c-reactive protein (AUC-CRP), p=0.008] compared to the CP-negative ones (table 2). New CP subjects were older, had greater frequency of baseline erosions, higher inflammatory burden (p=0.002) and lengthier biologic exposure (p=0.015) vs. the CP-negative group.

Conclusion: Higher inflammatory burden promotes generation, maturation and early calcification of coronary plaques in patients with RA. Higher duration of biologic exposure, through systemic and/ or local inflammatory control, fosters advanced calcification and stabilization of atherosclerotic plaques.