Beyond troponins: Emerging diagnostic significance of novel markers in NSTEMI
DOI:
https://doi.org/10.21542/gcsp.2024.33Abstract
Objective: This study aims to comprehensively analyze a multiple-marker panel consisting of 55 morphofunctional and biochemical markers in 123 patients diagnosed with non-ST-segment elevation myocardial infarction (NSTEMI). The goal of this study was to identify novel pathogenetic landmarks and diagnostic predictors associated with NSTEMI.
Methods: The study includes 123 patients diagnosed with NSTEMI based on ESC Guidelines criteria. Clinical characteristics, morphofunctional markers, and serum levels of 53 biochemical markers related to inflammation, oxidative stress, endothelial dysfunction, cellular injury, hemostasis, and myocardial remodeling were assessed. A control group of 47 healthy individuals was included for comparison.
Results: NSTEMI patients exhibited an activated inflammatory status, oxidative stress, and endothelial dysfunction. Notable increases in inflammation markers, alterations in adipokines, and changes in oxidative stress markers were observed. Endothelial dysfunction markers indicated vascular remodeling and dysfunction. Cellular injury markers, including cMyBP-C, suggested myocardial necrotic injury. Hemostasis markers showed impaired anticoagulant systems, and ECM remodeling markers indicated increased matrix metalloproteinases.
Conclusion: The multiple-marker panel provides insights into novel pathogenetic entities associated with NSTEMI. Markers such as MPO, MMP-8, E-selectin, PhA2, Ang 2, FE, MF, and cMyBP-C demonstrate potential diagnostic and prognostic value. This comprehensive analysis enhances our understanding of NSTEMI pathogenesis and offers potential targets for therapeutic interventions.
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Copyright (c) 2024 Amit Varshney, Vidya S. Ram, Pankaj Kumar

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This is an open access article distributed under the terms of the Creative Commons Attribution license CC BY 4.0, which permits unrestricted use, distribution and reproduction in any medium, provided the original work is properly cited.