Background/Purpose: Early atherosclerotic lesions appear as non-calcified plaques (NCP) on a non-invasive coronary artery evaluation by computed tomography angiography (CCTA). Advanced, more vulnerable lesions appear as mixed/ partially calcified plaques (MP) or calcified plaques (CP). We evaluated the role of inflammation, medication exposure and cardiac risk factors (CRFs) on NCP generation and progression in RA patients with a follow-up evaluation of coronary anatomy with CCTA.

Methods: Ninety-nine participants underwent a repeat CCTA assessment within 83±3.6 months. All coronary lesions were counted and characterized as NCP, MP, or CP; prevalence, number, stenotic severity and burden of individual NCP plaques on both baseline and follow-up scans was recorded. Patients were subsequently classified into four groups according to plaque disposition: NCP-negative (no NCP at any time), NCP-positive (NCP present at both times), disappearing-NCP (present at baseline, absent at follow-up), or new-NCP (absent at baseline, present at follow-up). A Multinomial logistic regression model evaluated predictors independently associated with classification of patients into the respective NCP groups compared to the NCP-negative group.

Results: Overall NCP prevalence was lower at follow-up compared to the baseline assessment (26.5% vs. 52.4%, p<0.001, table 1); 21 of 99 (21%) patients showed disappearance or development of new NCP lesions. In the NCP-positive group, 68% of the follow-up NCP plaques derived from original NCP lesions, with the vast majority (93%) displaying identical stenotic severity and burden; 29% were incident NCP plaques. Of baseline NCP lesions, 18% receded. In the disappearing group, 75% of the original NCP plaques receded, whereas 16% transitioned to more stable calcified plaques (CP). Patients in the NCP-positive group displayed lower cumulative inflammatory burden [area under the curve for c-reactive protein (AUC-CRP), p=0.016] and longer duration of statin exposure compared to the NCP-negative ones (table 2, p=0.046). NCP disappearance was mostly predicted by lengthier statin exposure (p=0.04).

Conclusion: Lower inflammatory burden and longer statin exposure inhibit NCP growth or progression to more advanced, vulnerable plaques. Lengthier statin exposure may further induce regression of such early atherosclerotic lesions.