DNA content, ploidy level and number of nuclei in the human heart after myocardial infarction

Cardiac hypertrophy due to a prolonged functional activity is associated with an increase of cell size and polyploidization of the myocyte nuclei. Myocardial infarction is characterized by loss of myocytes. Increased load and as a consequence hypertrophic growth of the surviving myocardium has to be...

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Bibliographic Details
Published inCardiovascular research Vol. 36; no. 1; pp. 45 - 51
Main Authors HERGET, G. W, NEUBURGER, M, PLAGWITZ, R, ADLER, C. P
Format Journal Article
LanguageEnglish
Published Oxford Oxford University Press 01.10.1997
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Summary:Cardiac hypertrophy due to a prolonged functional activity is associated with an increase of cell size and polyploidization of the myocyte nuclei. Myocardial infarction is characterized by loss of myocytes. Increased load and as a consequence hypertrophic growth of the surviving myocardium has to be expected. The aim of this study was to investigate the response of cardiomyocytes after infarction. Biochemical and cytophotometric analysis was performed on myocyte and connective tissue nuclei to determine whether the human heart after myocardial infarction is accompanied by an increase in the ploidy level, DNA content and in the number of nuclei. A total of 15 hearts obtained from autopsy material was studied, among them 8 after myocardial infarction. The number of nuclei was measured by indirect computation. We found a decrease of 4c and no significant difference of 2c nuclei in infarcted hearts. DNA ploidy level (> 8c) as well as the proportion of aneuploid myocyte nuclei were increased in infarcted hearts. DNA concentration and total DNA content were increased in the hearts after myocardial infarction. Numerical ratio of connective tissue nuclei/myocyte nuclei, total number of nuclei, number of myocyte nuclei and number of connective tissue nuclei were increased in infarcted hearts. Polyploidization and nuclear hyperplasia of myocytes may represent an adaptive response of the myocardium to an ischemic injury.
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ISSN:0008-6363
1755-3245
DOI:10.1016/S0008-6363(97)00140-5