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Cardiomyopathy of the aging human heart. Myocyte loss and reactive cellular hypertrophy
G Olivetti1, M Melissari, J M Capasso
1Department of Pathology, University of Parma, Italy.
Insights
Aging human hearts lose millions of myocyte nuclei annually, leading to enlarged remaining cells. This cellular remodeling contributes to reduced heart function and potential failure in older adults.
Area of Science:
- Cardiovascular Science
- Gerontology
- Cardiac Physiology
Background:
- The aging process significantly impacts cardiac structure and function.
- Understanding age-related changes in the human myocardium is crucial for addressing cardiovascular health in the elderly.
Purpose of the Study:
- To investigate the effects of aging on the human myocardium.
- To quantify age-related changes in myocyte number, size, and ventricular mass.
Main Methods:
- Analysis of 67 human hearts from individuals aged 17-90 years, excluding cardiovascular disease deaths.
- Utilized regression analysis to assess changes in myocyte nuclei count and cell volume.
- Measured left and right ventricular weights to determine cardiac mass changes.
Main Results:
- A significant loss of myocyte nuclei was observed: 38 million/year in the left ventricle and 14 million/year in the right ventricle.
- Remaining myocytes increased in volume (110 microns3/yr for left, 118 microns3/yr for right ventricle).
- Despite cellular hypertrophy, ventricular weights decreased (0.70 g/yr for left, 0.21 g/yr for right ventricle).
Conclusions:
- Age-related myocyte loss and compensatory hypertrophy represent the structural basis for diminished cardiac reserve.
- These changes contribute to myocardial dysfunction and heart failure in the elderly population.
Abstract:
To determine the effects of aging on the human myocardium, 67 hearts were obtained from individuals who died from causes other than cardiovascular disease. The age interval examined was 17-90 years. Regression analysis demonstrated that the aging process was characterized by a loss of 38 million and 14 million myocyte nuclei/yr in the left and right ventricular myocardium, respectively. This loss in muscle mass was accompanied by a progressive increase in myocyte cell volume per nucleus in both ventricles. Left ventricular myocytes enlarged by 110 microns3/yr, whereas right ventricular myocytes increased by 118 microns3/yr, resulting in a preservation of ventricular wall thickness. However, the cellular hypertrophic response was unable to maintain normal cardiac mass. Left and right ventricular weights decreased by 0.70 and 0.21 g/yr, respectively. In conclusion, loss of cells and enlargement of the remaining myocytes may represent the structural basis for the reduced compensatory capacity of the aged heart and together may contribute to the development of myocardial dysfunction and failure in the elderly.