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Patterns of Increased Cardiomyocyte Ploidy in Myocardial Hypertrophy of Various Origins
T V Sukhacheva1,2, R A Serov3, A I Kim3
1A. N. Bakulev Center for Cardiovascular Surgery, Ministry of Health of the Russian Federation, Moscow, Russia. sukhachevat@gmail.com.
Insights
Cardiomyocyte (CMC) polyploidy drives hypertrophic growth in heart conditions like hypertrophic cardiomyopathy (HCM) and tetralogy of Fallot (TF). HCM hypertrophy stems from polyploidization, while TF involves increased multinucleated CMCs.
Area of Science:
- Cardiovascular Biology
- Cell Biology
- Pathology
Background:
- Cardiomyocyte (CMC) ploidy is linked to hypertrophic growth potential.
- Understanding CMC ploidy and size changes is crucial in pediatric and adult cardiovascular diseases.
Purpose of the Study:
- To investigate alterations in CMC ploidy and interventricular septum size in hypertrophic cardiomyopathy (HCM) and tetralogy of Fallot (TF).
- To compare these changes between patient groups and healthy controls, and across different age groups.
Main Methods:
- Analysis of cardiomyocyte ploidy and cell size in patient samples.
- Comparison of cellular metrics between patients with HCM, TF, and control individuals.
- Assessment of the proportion of mononucleated and multinucleated cardiomyocytes.
Main Results:
- CMC ploidy was 1.5-2 fold higher in HCM and TF patients compared to controls, irrespective of age.
- CMC size increased by 1.3-2 times in HCM and TF patients, with a more significant increase in HCM.
- Multinucleated CMCs were less frequent in HCM but nearly doubled in TF patients.
Conclusions:
- Myocardial hypertrophy in HCM is primarily driven by polyploidy in mononucleated CMCs.
- In tetralogy of Fallot, increased myocardial hypertrophy is associated with a higher proportion of multinucleated CMCs.
Abstract:
An increase in the ploidy of cardiomyocytes (CMCs) determines the potential for their hypertrophic growth. We analyzed the changes in CMC ploidy and size of the interventricular septum in patients with hypertrophic cardiomyopathy (HCM) and tetralogy of Fallot (TF). The ploidy of CMCs in children and adult patients with HCM and children with TF was 1.5-2-fold higher than in individuals without cardiovascular pathology, and it did not change with age. The size of the CMCs was also larger by 1.3-2 times in patients with HCM and TF, compared to the control groups. However, the increase in CMCs size was more significant in HCM than in TF. The proportion of multinucleated CMCs was significantly lower in patients with HCM compared to controls and was by almost 2 times higher in patients with TF. Thus, myocardial hypertrophy in HCM is mainly due to the polyploidy of mononucleated CMCs, whereas in TF, the proportion of multinucleated CMCs increases.
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