ABC | Volume 111, Nº2, August 2018

Original Article Farsky et al Persistent inflammation after stent Arq Bras Cardiol. 2018; 111(2):134-141 Figure 2 – Comparison of the staining of TNF-alpha and IL-6 proteins in different layers of arterial tissue. The analysis was performed comparing three groups: A1 (arteries with stent), A2 (native arteries from patient with a stent in another artery) and A3 (control, patients without previous stent placement). TNF-alpha protein staining was higher in the adipose tissue of group A1 (6.69 ± 3.87 vs 2.27 ± 4.00; p < 0.001) (a), as well as in the intima-media layer (5.16 ± 5.05 vs 1.90 ± 2.27; p = 0.02) (b). The IL-6 protein staining was also higher in the adipose tissue from group A1 than that from group A3 (2.29 ± 1.96 vs 0.28 ± 0.33; p = 0.048) (c). The Kruskall-Wallis test and nonparametric Tukey’s multiple comparisons test were used for statistical analysis. The difference is considered significant for p-values < 0.05. 15 15 20 10 10 5 5 5 0 0 0 1 2 3 4 % of staining % of staining % of staining p < 0.001 p = 0.023 p = 0.048 A1 A2 A3 A1 A2 A3 A1 A2 A3 a) Adipose Tissue - TNF-alfa b) Intima Media - TNF-alfa c) Adipose Tissue - IL6 Figure 3 – Panoramic (left side) and high-power view (right side) of immunostained arterial intima-media layer from individuals with previous stent implantation. Panels A and B show MHCII-positive cells, with morphology of macrophages (arrows), surrounding the lipid core (LC). Panels C and D show a large amount of TNF-alpha in the cytoplasm of inflammatory cells (arrows) and in the lipid core (LC). Panels E and F exhibit fewer inflammatory cells positive for IL-6 protein in similar sites (arrows). are responsible for the production of that cytokine. Those are also MHCII-positive cells, primarily responsible for presenting antigenic peptides to T cells of the immune system. Interleukin-6 is a multifunctional cytokine playing a central role in inflammation and tissue injury. 22 Interleukin-6 activates platelet receptor GPIIb/IIIa and leukocyte-platelet interaction, thus favoring the prothrombotic and atherogenic formation. Previous studies have shown that the increased circulating IL-6 is associated with the risk of coronary restenosis and de novo coronary artery lesions, 23 as well as the severity of stenosis. 24 The increase in IL-6 mRNA and protein has been observed in human arterial atherosclerotic wall. In this study, our data showed a significant higher amount of IL-6 protein in the coronary tissue of patients with previous stent placement than in that of controls, suggesting that local arterial inflammation is intensified by stent placement. 139