Morphological and morphometric changes in the myocardium of the heart under conditions of experimental hyperparathyroidism

Experimental hyperparathyroidism is accompanied by profound disturbances of mineral metabolism, primarilyhypercalcemia and phosphorus imbalance, which adversely affect the structural and functional state of the myocardium.The present study aimed to comprehensively evaluate morphological and morphometric alterations in the heart muscleunder conditions of experimental hyperparathyroidism. The experimental model was reproduced in laboratory animalsby sustained induction of hyperparathyroid state. Myocardial samples were subjected to histological and morphometricanalysis using standard staining techniques with subsequent quantitative assessment of cardiomyocyte diameter,interstitial space, and fibrotic component volume fraction. Morphological examination revealed pronounced dystrophicand vacuolar degeneration of cardiomyocytes, fragmentation and lysis of myofibrils, focal necrobiotic changes, andmarked microcirculatory disturbances, including vascular congestion and perivascular edema. Expansion of the interstitialconnective tissue and activation of fibroblastic elements were also observed. Morphometric analysis demonstrated asignificant increase in cardiomyocyte diameter, thickening of myocardial fibers, and a statistically significant elevation inthe relative area of fibrotic components compared to controls (p < 0.05).These findings indicate that mineral metabolism imbalance in hyperparathyroidism induces structural remodeling of themyocardium characterized by hypertrophic and fibrotic changes. Such remodeling forms the morphological substratefor the development of heart failure and cardiac rhythm disturbances. The results expand current understanding ofcardiovascular complications associated with hyperparathyroidism and highlight the importance of early pathogeneticcorrection of mineral imbalance to prevent myocardial damage.