Background TNFa is a pivotal cytokine in the pathophysiology and progression of both RA and atherosclerosis. Addition of TNFa inhibitors (TNFi) to disease modifying agents (DMARDs) superiorly controls clinical inflammation and radiographic progression in RA. Non-invasive, accurate evaluation of coronary plaque is feasible with computed tomography angiography (CTA); it reliably defines plaque presence, burden, severity and composition as non-calcified (NCP), mixed (MP), or densely calcified (CP). Importantly, MP presence has been correlated with higher risk of future clinical events.
Objectives To evaluate whether TNFi therapy is associated with lower plaque prevalence, burden, or different plaque composition compared to DMARD-treated patients, and whether good RA response is required for the tentative benefit.
Methods One hundred and fifty CAD-naïve subjects with RA, 60 on DMARDs alone and 90 on TNFi, underwent CTA. A standard 15-segment American Heart Association (AHA) model was used for plaque evaluation. Involved segments, stenosis severity score (sum of stenosis score of each segment, averaged over all 15 segments/patient) and plaque burden score (sum of the plaque amount per each segment averaged over all 15 segments/patient) were evaluated. Disease activity score (DAS28-3v-CRP) less than 3.2 defined good disease control. Non parametric and Fisher’s exact tests compared continuous and categorical variables respectively among groups.
Results Good responders (R) to either therapy displayed differences in proportions of involved segments, stenosis severity, and plaque burden scores, especially for MP and CP compared to non-responders (NR- table 1). Good responders had similar proportions of involved segments, and quantitative plaque measures for MP and CP regardless of type of therapy. However, TNFi-NR, had significantly lower prevalence of segments involved with MP (p=0.01), lower adjusted stenosis severity (p=0.01) and burden scores (p=0.05) for MP compared to DMARD-NR. Additionally, TNFi-NR, had higher prevalence, stenosis scores (p=0.05), and burden scores (p=0.05) for the lower risk CP.
Conclusions Treatment with TNFi may have a quantitative atheroprotective effect, particularly against high risk MP, independent of good clinical RA response.
Disclosure of Interest None Declared
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