Hypothyroidism causes a number of histological changes in almost all tissues and cells of the body of a mammal, which is accompanied by numerous clinical and functional disorders. This is due to the multifaceted and multifunctional role of thyroid hormones (thyroxine and triiodothyronine) in the body of mammals. Striated cardiac muscle tissue and its main structural unit (contractile cardiomyocyte) is one of the most frequently involved tissues in the histopathological process in hypothyroidism. In addition, hypothyroidism can be considered as one of the main risk factors for the development of cardiovascular diseases (heart failure, coronary heart disease, cardiac arrhythmias), so the study of histopathological changes in cardiac muscle tissue is of great theoretical and practical importance. To date, there are no studies evaluating histopathological ultrastructural changes in contractile cardiomyocytes in certain forms of hypothyroidism, in particular in overt acquired primary hypothyroidism. The purpose of this study is to investigate the histopathological changes in the nucleus and contractile apparatus of cardiomyocytes in the conditions of experimental modeling of overt acquired primary hypothyroidism. Materials and Methods: male Chinchilla rabbits aged 12-14 months and weighing 3.1-3.5 kg (n=10), were divided into 2 equal groups. 1) The experimental group (n=5), where overt primary hypothyroidism was induced by oral administration of the antithyroid drug thiamazole (10 mg/kg for 4 weeks). 2) The animals of the control group (n=5) received placebo and were in a state of normothyroidism. Transmission electron microscopy (TEM) was used to study ultrastructural changes in contractile cardiomyocytes. Results and Conclusion: Based on the results of electron microscopic study, we detected numerous ultrastructural changes in the nucleus and contractile apparatus of cardiomyocytes: the nucleus (wrinkling, uneven contours of the nucleus and emergence of karyolemma invaginations, chromatin condensation); in the contractile apparatus (thinning of myofibrils, emergence of areas of myofibrils overcontraction with contractures). These ultrastructural changes in cardiomyocytes underlie the disruption of myocardial contractility, as well as an increase in dystrophic and apoptotic changes with the gradual development of heart failure, which is a frequent companion of untreated overt acquired primary hypothyroidism.