Loss of Myofibrils in Cardiomyocytes as a Morphological Indicator of Reduced Compensatory Capabilities of Hypertrophied Myocardium

The functioning of the ventricular myocardium in hypertrophic cardiomyopathy (HCM) under high hemodynamic load leads to depletion of its resources and is associated with the risk of developing a dilated stage. In patients with HCM, the cardiomyocytes of the interventricular septum are hypertrophied,...

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Bibliographic Details
Published in:Bulletin of experimental biology and medicine 2024-11, Vol.178 (1), p.130-138
Main Authors: Sukhacheva, T. V., Serov, R. A., Bockeria, L. A.
Format: Article
Language:English
Subjects:
Adult
Biomedical and Life Sciences
Biomedicine
Biopsy
Cardiomyocytes
Cardiomyopathy
Cardiomyopathy, Hypertrophic - diagnostic imaging
Cardiomyopathy, Hypertrophic - pathology
Cardiomyopathy, Hypertrophic - physiopathology
Cell Biology
Disease
Echocardiography
Female
Heart
Heart surgery
Hemodynamics
Humans
Internal Medicine
Laboratory Medicine
Male
Middle Aged
Morphology
Myocardium
Myocardium - metabolism
Myocardium - pathology
Myocardium - ultrastructure
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
Myocytes, Cardiac - ultrastructure
Myofibrils
Myofibrils - pathology
Myofibrils - ultrastructure
Pathology
Patients
Phenotypes
Ultrastructure
Ventricle
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Summary:The functioning of the ventricular myocardium in hypertrophic cardiomyopathy (HCM) under high hemodynamic load leads to depletion of its resources and is associated with the risk of developing a dilated stage. In patients with HCM, the cardiomyocytes of the interventricular septum are hypertrophied, the proportion of cardiomyocytes in which myofibrils constitute less than 50% of the sarcoplasm volume increases with increasing the cardiomyocyte length and correlates with echocardiographic signs of left ventricular obstruction. These cardiomyocytes are characterized by ultrastructural signs of synthetic activity. In the myocardium of patients with HCM, single cardiomyocytes with “critical” loss of myofibrils and nonspecific degenerative changes corresponding to the picture of irreversible changes in the cardiomyocyte ultrastructure were revealed. The presence of cardiomyocytes with this ultrastructural phenotype is an early marker of exhaustion of the compensatory capabilities of the myocardium in HCM.
ISSN:0007-4888
1573-8221
1573-8221
DOI:10.1007/s10517-024-06295-6