Heart failure and mitochondrial dysfunction: research methods in experiment and clinical practice

Heart failure is the leading cause of death, frequent hospitalizations, and poor quality of life. The fundamental mechanisms involved in the occurrence and progression of heart failure are currently not precisely defined. Mitochondria play a key role in the processes of cellular metabolism, performing many biological functions. The functional activity of mitochondria is inextricably linked to their structure. In cardiovascular diseases, in conditions of repeated hypoxia/reoxygenation of tissues, as well as under the influence of subclinical inflammation processes, pathological restructuring of the cardiomyocyte mitochondriome occurs. Studies conducted to date suggest that mitochondria may be the key to understanding the onset and progression of chronic heart failure (CHF). An analysis of the literature demonstrates that the study of mitochondria in patients with CHF is an urgent topic, and the number of publications in the PubMed/MEDLINE system concerning research in this area is progressively increasing, 100 publications on this topic have been found in the eLibrary system. In this review, we reviewed modern methods for evaluating the structure and function of mitochondria in experimental and clinical studies and analyzed the possibility of using these research methods in patients with cardiovascular diseases. It is shown that, despite a fairly wide range of possibilities for studying the structural and functional state of mitochondria of cardiomyocytes in CHF, the estimated indirect signs of mitochondrial dysfunction are surrogate markers, the degree of informativity of which must be studied in comparison with the actual state of the cardiomyocytes mitochondrial ultrastructure, the clinical picture of the disease and the prognosis of patients. The necessity of conducting clinical studies aimed at studying the association of direct ultrastructural characteristics of cardiomyocytes mitochondria with indirect signs of mitochondrial dysfunction with the clinical course and outcomes of CHF is actualized, which will allow us to obtain fundamentally new fundamental knowledge about the mechanisms of development and progression of the pathophysiological phenomenon of CHF, to assess the degree of informativeness of markers of mitochondrial dysfunction in patients with CHF, which will serve as the basis for the widespread introduction of these diagnostic methods into real clinical practice.