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Nuclear size of myocardial cells in end-stage cardiomyopathies
S M Yan1, N Finato, C Di Loreto
1Department of Pathology, University of Udine, Italy.
Insights
Cardiomyopathy increases heart cell nuclear size through DNA changes or simple enlargement. Nuclear growth mechanisms differ between myocytes and interstitial cells in heart failure.
Area of Science:
- Cardiovascular Biology
- Cell Biology
- Genetics
Background:
- Cardiomyopathies, including ischemic and dilated forms, are leading causes of heart failure.
- Alterations in cellular structure, particularly nuclear morphology, are associated with disease progression.
- Understanding nuclear changes in heart muscle cells is crucial for diagnosing and treating cardiac conditions.
Purpose of the Study:
- To investigate changes in nuclear size within myocardial cells.
- To explore the relationship between nuclear size and DNA ploidy in normal and cardiomyopathic human hearts.
Main Methods:
- Analysis of 46 explanted hearts from patients with ischemic or dilated cardiomyopathy and 10 control hearts.
- Evaluation of 100 fibroblasts and 200 myocytes per ventricle using image cytometry.
- Measurement of nuclear area and DNA content to determine ploidy classes.
Main Results:
- Cardiomyopathic hearts showed increased nuclear size in both myocytes and interstitial cells.
- Myocyte nuclear area increased 1.2-fold in ischemic and 1.5-fold in dilated cardiomyopathy compared to controls.
- Nuclear enlargement in myocytes correlated with increased DNA content, indicating polyploidization.
Conclusions:
- Nuclear size increase in cardiomyopathy occurs via DNA content increase or independent hypertrophy.
- Myocyte nuclear growth involves hypertrophy, polyploidization, and multinucleation.
- Interstitial cell nuclear growth primarily involves hypertrophy without DNA content alteration.
Objective:
To determine the alteration of nuclear size in myocardial cells and the relationship between nuclear size and DNA ploidy classes in normal and cardiomyopathic human hearts.
Study Design:
The study group consisted of 46 hearts obtained at biopsy. These patients had undergone cardiac transplantation for intractable congestive heart failure (18 cases with ischemic cardiomyopathy and 28 cases with idiopathic dilated cardiomyopathy). Another 10 hearts were collected at autopsy and used as control hearts according to preautopsy, autopsy and histology criteria. One hundred fibroblasts and 200 myocytes were evaluated in each ventricle. The nuclear area and DNA content were estimated using image cytometry.
Results:
End-stage ischemic and dilated cardiomyopathies were characterized by an increase in nuclear size of both the myocyte and nonmyocyte population. The nuclear area of interstitial cells increased about 30% in cardiomyopathic hearts. Augmentation of average nuclear area of myocytes was 1.2-fold in the ischemic group and about 1.5-fold in the dilated group as compared with the control group. Also, a tendency was found for the coefficient of variation of average nuclear area to decrease in the interstitial cell population and increased in the myocyte population in cardiomyopathic situations. Furthermore, the nuclear area of myocytes enlarged as augmentation of nuclear DNA content. The relative nuclear areas of myocytes can be presented as: 2c:4c:8c:16c :32c:64c = 1:1.65:2.75:4.60:7.25:9.18.
Conclusion:
The increase in nuclear size follows either one of two different processes: the first does not involve an increase in DNA content, whereas the second is concomitant with an incremental increase in DNA content. In the first instance, the enlargement of nuclear size is limited. In the second, augmentation of nuclear size can become very impressive. In end-stage ischemic and dilated cardiomyopathies, the nuclear growth of myocytes and interstitial cells may be due to different mechanisms. Enlargement of the nuclear area of myocytes represents a complex process, including simple nuclear hypertrophy, polyploidization and multinucleation. The main pattern of nuclear growth of interstitial cells is nuclear hypertrophy without an increase in DNA content.