Multi-marker panel in patients with NSTEMI: pillars of pathogenesis and diagnostics
Keywords:NSTEMI, multi-marker panel, pathogenesis, diagnostics
Aim. Assessment within the multi-marker panel applied to patients with NSTEMI of admission levels of the main markers of cardiovascular pathology in order to disentangle the pathogenetic interface and identify diagnostic predictors. Material and methods. The research was carried out on a group of 87 patients with NSTEMI, exposed to angioplas-ty, in which the admission values of 2 morphofunctional markers of endothelial dysfunction were determined, as well as the serum levels of 53 biochemical markers with reference to: inflammation, oxidative stress, endothelial dysfunction, cell injury, hemostasis disorder, myocardial and extracellular matrix (ECM) remodeling. The control group has consisted of 40 apparently healthy people.Results. The analysis of the multi-makrer panel revealed significant deviations of the majority of the explored markers compared to the control level. Endothelial dysfunction was marked by the increase of thickness of the medial-intima complex of the carotid artery and the decrease of the flow-mediated dilation of brachial artery in association with a 7694% raise of endothelial cell fragments (EF), phospholipase A2 (PhA2) and angiopoietin 2 (Ang 2). Among 16 markers of inflammation, the elevation of myeloperoxidase (MPO) by 156% is remarkable as a specific marker of NETosis. Activated oxidative stress is the result of the impairment of the antioxidant defense, and hemostasis disorder must be underlined by double increase of fibrin monomers (FM). From a pathogenetic point of view, the multiple increase (more than 8 times) of cardiac myosin-binding protein (cMyBP-C) is important and understandable, and the markers of myocardial and ECM remodeling basically demonstrated an activation of several types of metalloproteinases. Conclusion. From the spectrum of the multi-marker panel applied to patients with NSTEMI, markers with plausible diagnostic value due to inteligibly reflected pathogenetic mechanism are highlighted as: MPO, PhA2, Ang 2, EF, FM, and cMyBP-C.
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