Сучасні медичні технології (Apr 2020)
Relationships between markers of extracellular matrix degradation and systemic inflammatory response among patients with acute myocardial infarction
Abstract
Despite all the preventive, diagnostic and therapeutic possibilities of our time, diseases of the circulatory system are the leading causes of death among adult population both in the world and in Ukraine. Modern consensuses of the European society of Cardiology have recommendations with many years of based-on-evidence experience in the diagnosis of acute myocardial infarction. They note that biomarkers of myocardial necrosis must meet modern requirements of accuracy, reproducibility, and especially sensitivity and specificity. Now, together with classical markers of heart muscle damage, markers reflecting various pathogenetic directions of acute myocardial infarction are increasingly used in clinical practice; they include markers of myocardial dysfunction and markers of inflammatory process activation. Purpose of the study. Identify relationships between markers of the extracellular matrix degradation and systemic inflammatory response among patients with acute myocardial infarction. Materials and methods. Results of the study are based on data from a comprehensive survey of 305 IHD patients: 162 patients with STEMI, 81 individuals with NSTEMI, and the control group consisted of 62 patients with angina pectoris (functional class II and III for 31 people). The sample of patients was carried out in the period from 2015 to January 2018 on the basis of MI «Regional medical center of cardiovascular diseases» of the Zaporizhzhia regional Council. All 305 surveyed people were comparable in age, social status, and gender (with the ratio of men to women was 4 to 1). Results and discussion. The highest level of HS-CRP was in the group of STEMI patients and amounted to 10,91 (9,40–13,43) mg/l and significantly exceeded by 24% the level of this indicator in the group of NSTEMI patients – 8,80 (7,05–10,91) mg/l, (p < 0,05). The level of TNF-αwas significantly higher in the STEMI group of 2,10 (1,53–2,86) pg/ml versus 1,67 (1,09–2,20) pg/ml in the NSTEMI group of patients, (p < 0,05) and the leap rate was 2,4 times higher than the level of 0,89 (0,67–1,55) pg/ml in the group of patients with stable IHD (p < 0,05). In both groups of AMI patients with both STEMI and NSTEMI, there was a significant increase in IL-6 levels compared to the group of patients with stable IHD, where this indicator was 2,26 (1,22–3,66) pg/ml, 5 and 3,2 times, respectively (p < 0,05). The IL-6/IL-10 ratio in the STEMI and NSTEMI groups was 2,78 (1,72–4,68) versus 1,82 (1,49–2,36), respectively, and was significantly 50,8% higher (p < 0,05). Reliable direct links were found between: the levels of MPP-9 and HF-CRP (R = +0,61, p = 0,001), the levels of MPP-9 and TNF-α (R = +0,62, p = 0,001), the level of MPP-9 and the IL-6/IL-10 ratio, the levels of TIMP-2 and CRP (R = +0,50, p = 0,001).
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