Morphological and morphometric changes in the myocardium of the heart under conditions of experimental hyperparathyroidism
DOI:
https://doi.org/10.5281/zenodo.18871423Keywords:
mineral metabolism; myocardium; cardiomyocytes; fibrosis; myocardial remodeling.Abstract
Experimental hyperparathyroidism is accompanied by profound disturbances of mineral metabolism, primarily
hypercalcemia 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 muscle
under conditions of experimental hyperparathyroidism. The experimental model was reproduced in laboratory animals
by sustained induction of hyperparathyroid state. Myocardial samples were subjected to histological and morphometric
analysis using standard staining techniques with subsequent quantitative assessment of cardiomyocyte diameter,
interstitial space, and fibrotic component volume fraction. Morphological examination revealed pronounced dystrophic
and vacuolar degeneration of cardiomyocytes, fragmentation and lysis of myofibrils, focal necrobiotic changes, and
marked microcirculatory disturbances, including vascular congestion and perivascular edema. Expansion of the interstitial
connective tissue and activation of fibroblastic elements were also observed. Morphometric analysis demonstrated a
significant increase in cardiomyocyte diameter, thickening of myocardial fibers, and a statistically significant elevation in
the relative area of fibrotic components compared to controls (p < 0.05).
These findings indicate that mineral metabolism imbalance in hyperparathyroidism induces structural remodeling of the
myocardium characterized by hypertrophic and fibrotic changes. Such remodeling forms the morphological substrate
for the development of heart failure and cardiac rhythm disturbances. The results expand current understanding of
cardiovascular complications associated with hyperparathyroidism and highlight the importance of early pathogenetic
correction of mineral imbalance to prevent myocardial damage.
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