Prognostic value of autoantibodies to cardiomyocyte proteins in the diagnosis of chronic physical overexertion

Abstract

Relevance. In conditions of ever-increasing volume of training loads, the frequency of cases of chronic physical overstrain (CPO) among athletes is increasing. It determines the importance of early diagnosis of the formed pathology of the cardiovascular system in order to prevent its further development. The aim of the study was to study the dynamics of autoantibodies to cardiomyocyte proteins using an experimental model of CPO and to determine the prospects of a laboratory method for the determination of autoantibodies for early diagnosis of pathomorphological changes in the heart. Materials and Methods. The study was conducted on male white rats. A treadmill was used to model CPO. In animals, the heart rate was measured, electrical phenomena in the heart were recorded. The content of hemoglobin and erythrocytes was determined in the blood. The level of cardiospecific autoantibodies (auto-AB) to troponin I, to alpha-actin 1, and to the heavy chain of beta-myosin 7B was measured. Heart mass was measured and histomorphological assessment of the state of cardiomyocytes was carried out. Results and Discussion. While modeling CPO, a decrease in body weight of the animals, the development of anemia, and cardiac hypertrophy were recorded. A decrease in body weight by more than 30 % was recorded from days 25 to 35 of the modeled CPO. A decrease in the number of erythrocytes in the blood was noted on day 25 with a peak fall on days 30-35. The mass of heart of animals in the dynamics of 0-15-35 days was 0.39±0.003; 0.41±0.001; 0.44±0.005 g/100 g, respectively. On day 25, sinus tachycardia was recorded in 2 % of the animals. On days 30 and 35, in 10 % of the studied rats, a violation of the processes of repolarization of the left ventricle by the type of subepicardial ischemia was recorded. On the 25th day, fibrosis of the perivascular region was visualized, passing into the interstitial field between the myofibrils. Reticulate structures of connective tissue fibers between cardiomyocytes were found. The period of 30-35 days was characterized by even greater severity of pathomorphological changes: myocardial hypertrophy, moderate myocardial dystrophy, interstitial and perivascular fibrosis. An increase in the number of detectable auto-ABs to cardiomyocyte proteins was noted on the 10th day of the experiment. A multiple increase in autoantibodies to cardiomyocyte proteins was recorded earlier than functional disorders in the heart and morphological changes in cardiomyocytes were detected. Conclusion. The laboratory method for determining auto-ABs to myocardial proteins can be the earliest of the complex methods for diagnosing disorders that are formed in the body in conditions of adaptation to intense and prolonged physical exertion.