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Atherosclerotic plaque instability increases the risk of stroke. As such, determining the nature of an instability atherosclerotic plaque may speed up qualification for carotid endarterectomy (CEA), thus reducing the risk of acute vascular events. The aim of the study was to determine the diagnostic value of oxidized LDL cholesterol (ox‐LDL), matrix metalloproteinase 9 (MMP‐9) and 8‐hydroxy‐2′‐deoxyguanosine (8‐OHdG) in serum as a prognostic markers of instability atherosclerotic plaques. Serum was collected from 67 patients who underwent CEA in accordance with the qualification criteria. The levels of ox‐LDL, MMP‐9 and 8‐OHdG were assessed by ELISA. The predictive value of the markers was determined based on an ROC curve, and the cut‐off points with the highest sensitivity and specificity were determined. Patients with unstable atherosclerotic plaque had significantly higher serum ox‐LDL, MMP‐9 and 8‐OHdG values. It was found that in patients before CEA, ox‐LDL >31.4 ng/mL was associated with an 82.5% probability of unstable atherosclerotic plaque, MMP‐9 >113.1 ng/mL with 78.6%, and 8‐OHdG >2.15 ng/mL with 64.7%. Multivariate regression analysis found ox‐LDL to be an independent factor associated with plaque instability. Patients with unstable plaques tend to have higher serum levels of ox‐LDL, MMP‐9 and 8‐OHdG compared to those with stable plaques. The optimal cut‐off point for ox‐LDL (AUC 0.86, p <0.0001) was 31.14 ng/mL, with 91.18% sensitivity and 78.79% specificity. The high sensitivity and specificity of ox‐LDL suggests that it can be used as an independent marker of plaque instability. [ABSTRACT FROM AUTHOR]

Atherosclerosis is associated with a haemostatic imbalance characterized by excessive activation of pro‐inflammatory and pro‐coagulant pathways. Non‐vitamin K antagonists oral anticoagulant (NOACs) may reduce the incidence of cardiovascular events, cerebral ischemia, thromboembolic events and atherosclerosis. Chronic inflammation, vascular proliferation and the development of atherosclerosis is also influenced by 25‐hydroxycholesterol (25‐OHC). The aim of the study was to assess the effect of rivaroxaban and dabigatran on the messenger RNA (mRNA) expression of anti‐inflammatory cytokines transforming growth factor β (TGF‐β), interleukin (IL)‐37, IL‐35 as well as of pro‐inflammatory cytokines IL‐18 and IL‐23, in endothelial cells damaged by 25‐OHC. Human umbilical vascular endothelial cells (HUVECs) were treated with 25‐OHC (10 μg/mL), rivaroxaban (100, 500 ng/mL), dabigatran (100, 500 ng/mL), 25‐OHC + rivaroxaban, and 25‐OHC + dabigatran. The mRNA expression of TGF‐β, IL‐37, IL‐35 subunits EBI3 and p35, IL‐18, and IL‐23 was analysed using real‐time polymerase chain reaction (PCR). The results showed that 25‐OHC decreased TGF‐β and IL‐37 mRNA expression and increased EBI3, p35, IL‐18, IL‐23 mRNA expression in endothelial cell as compared to an untreated control (P <.05). Messenger RNA expression of TGF‐β and IL‐37 significantly increased following stimulation with rivaroxaban and dabigatran as compared to an untreated control (P <.01). In HUVECs pre‐treated with oxysterol, rivaroxaban and dabigatran increased mRNA expression of TGF‐β, IL‐37 and decreased mRNA expression of EBI3, p35, IL‐23 and IL‐18 as compared to 25‐OHC (P <.01). Our finding suggests that both rivaroxaban and dabigatran inhibit the inflammatory activation caused by oxysterol in vitro. [ABSTRACT FROM AUTHOR]