The study of standard and specific therapy effects on patients with angina and type 2 diabetes can provide a rationale for the individualization of therapy aimed at reducing the "residual" cardiovascular risk associated with systemic inflammation. The purpose of the study was to analyze changes in the levels of new biomarkers of P-Selectin and Galectin-3 inflammation in patients with stable angina depending on the therapy. Materials and methods. 89 patients with angina and with or without type 2 diabetes mellitus were examined. The levels of P-selectin, Galectin-3 and hs-CRP were assessed in all patients. Results and discussion. The level of plasma Galectin-3 was 12.2±5.5 ng/ml, P-Selectin 90.0±46.5 ng/ml and hs-CRP 6.2±4.2 mg/l in the group of examined patients with verified stable angina. No correlation was found between the plasma levels of P-Selectin and hs-CRP in the examined patients (r= -0.131, p=0.284).The levels of P-Selectin and Galectin-3 in patients with stable angina were interrelated, but vary significantly at the individual level, which created the prerequisites for personalization of therapeutic goals for reducing the systemic inflammatory response. In patients with CABG, the level of P-Selectin was significantly higher (127.9±23.5, p<0.05). In the group of patients with IHD who received aspirin therapy at a dose of 75 mg/s, the level of P-Selectin did not differ significantly compared to patients who did not receive antiplatelet therapy. There was a decrease in the level of Galectin-3 in patients who received aspirin monotherapy, but this trend did not reach the level of reliability. In patients treated with clopidogrel at a dose of 75 mg, the P-Selectin level was significantly lower in comparison with patients who did not receive antiplatelet drugs and patients receiving monotherapy with aspirin (66.4±25.6 ng/ml, 97.2±19.3 ng/ml and 81.5±29.1 ng/ml, respectively, p<0.05). In patients who received DAT, the level of P-Selectin (57.9±28.1 ng/ml) was significantly lower than in patients who did not receive antiplatelet drugs and received aspirin monotherapy. In the group of patients with angina who received anticoagulant therapy, the P-Selectin level was significantly lower than in patients who did not receive anticoagulant therapy (73.1±21.1 ng/ml and 95.6±22.3 ng/ml, respectively, p<0.05). Conclusions. Clopidogrel therapy, in contrast to aspirin, leads to a decrease in the level of P-Selectin, which reflects a decrease in the activity of the platelet component of the systemic inflammatory response in atherosclerosis. The use of RAS blockers is also accompanied by a decrease in the systemic inflammatory response.
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