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THE ROLE OF HEAT SHOCK PROTEIN HSP-70 IN THE PATHOGENESIS OF MYOCARDIAL INFARCTION AND CHRONIC ISCHEMIC HEART DISEASE
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Coronary heart disease remains a leading cause of morbidity and mortality worldwide. There is an ongoing search for new circulating biomarkers not only to identify preclinical changes but also to monitor the disease course and treatment effectiveness. This study aimed to evaluate the serum concentration of the heat shock protein HSP-70, which has significant prognostic potential in cardiovascular diseases. The aim of the study was to compare HSP-70 levels between groups of patients with stable chronic coronary heart disease and acute myocardial infarction. Materials and methods. The study included 34 patients with myocardial infarction, 30 with chronic ischemic heart disease, 20 healthy controls. HSP-70 concentrations were determined by enzyme-linked immunosorbent assay using FineTest ready-made kits. Results and discussion. The highest levels were observed in patients with chronic ischemic heart disease, while a significant decrease in HSP-70 levels (p<0.001) was recorded in myocardial infarction, demonstrating a paradoxical bidirectional dynamic of HSP-70 levels in various forms of ischemic heart disease. Thus, elevated HSP-70 levels can be considered not only as a marker of adaptation to chronic hypoxia but also as an indicator of ischemic process progression. Conclusion. A comprehensive analysis of the obtained data showed that acute myocardial infarction is characterized by systemic biological suppression of HSP-70 in the blood serum, while chronic ischemic heart disease, in contrast, is associated with HSP-70 hyperproduction. The discovered opposite biological profiles indicate different immunopathophysiological conditions in acute and chronic forms of coronary heart disease and highlight the potential for the comprehensive use of this biomarker to improve diagnostics, risk stratification, and the development of personalized therapeutic strategies for coronary heart disease.
Academy of International Scientific Cooperation
Title: THE ROLE OF HEAT SHOCK PROTEIN HSP-70 IN THE PATHOGENESIS OF MYOCARDIAL INFARCTION AND CHRONIC ISCHEMIC HEART DISEASE
Description:
Coronary heart disease remains a leading cause of morbidity and mortality worldwide.
There is an ongoing search for new circulating biomarkers not only to identify preclinical changes but also to monitor the disease course and treatment effectiveness.
This study aimed to evaluate the serum concentration of the heat shock protein HSP-70, which has significant prognostic potential in cardiovascular diseases.
The aim of the study was to compare HSP-70 levels between groups of patients with stable chronic coronary heart disease and acute myocardial infarction.
Materials and methods.
The study included 34 patients with myocardial infarction, 30 with chronic ischemic heart disease, 20 healthy controls.
HSP-70 concentrations were determined by enzyme-linked immunosorbent assay using FineTest ready-made kits.
Results and discussion.
The highest levels were observed in patients with chronic ischemic heart disease, while a significant decrease in HSP-70 levels (p<0.
001) was recorded in myocardial infarction, demonstrating a paradoxical bidirectional dynamic of HSP-70 levels in various forms of ischemic heart disease.
Thus, elevated HSP-70 levels can be considered not only as a marker of adaptation to chronic hypoxia but also as an indicator of ischemic process progression.
Conclusion.
A comprehensive analysis of the obtained data showed that acute myocardial infarction is characterized by systemic biological suppression of HSP-70 in the blood serum, while chronic ischemic heart disease, in contrast, is associated with HSP-70 hyperproduction.
The discovered opposite biological profiles indicate different immunopathophysiological conditions in acute and chronic forms of coronary heart disease and highlight the potential for the comprehensive use of this biomarker to improve diagnostics, risk stratification, and the development of personalized therapeutic strategies for coronary heart disease.
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Abstract
Funding Acknowledgements
Type of funding sources: None.
Introduction
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