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Z Kardiol. 1987;76 Suppl 3:20-5.

Evidence of myocyte hyperplasia in hypertrophic cardiomyopathy and other disorders with myocardial hypertrophy?

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  • 1Pathology Branch, National Heart, Lung and Blood Institute, Bethesda, Maryland.


A review is presented of the mechanisms that mediate the increase in cardiac mass that occurs in patients with hypertrophic cardiomyopathy. This increase in mass is mediated by an increase in the total mass of the myocytes and the total mass of interstitial fibrous connective tissue. The increase in myocyte mass is the most important of these two components. However, it is not clear at the present time whether this increase is mediated not only by an increase in the size of the cells (hypertrophy), but also by an increase in the numbers of myocytes (hyperplasia) or by a combination of these two factors. Hyperplasia normally occurs during the prenatal phase of cardiac development and stops soon after birth, at which time hypertrophy becomes the main mechanism by which cardiac mass increases. Under certain circumstances, the ability of cardiac myocytes to synthesize DNA and undergo mitotic division can be restored; however, it is uncertain to what extent this results in complete cell division or only in either polyploidy or bi- or multinucleation. It is proposed that in hypertrophic cardiomyopathy, increased hyperplasia of cardiac myocytes occurs early in life and leads to permanently disturbed patterns of cardiac gross anatomy; it is then followed by a phase of progressive hypertrophy after the switch from hyperplastic to hypertrophic growth. It is possible that hyperplasia continues to occur after the usual time of this switch. It is also proposed that the increased number of layers of myocytes in the ventricular septum of patients with hypertrophic cardiomyopathy is a consequence of exaggerated hyperplasia during development.

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