This clinicopathologic study describes the age-related and disease-related histopathologic changes in cardiac myocytes, highlighting the progression of hypertrophy and cardiosclerosis in cardiomyopathy.
Myocyte maturation and disease patterns warrant cautious histopathologic interpretation; leaves open need for prospective validation before clinical application.
Age-associated changes in histopathologic and ultrastructural aspects of cardiac myocytes were systematically compared with clinical problems. The study material consisted of 1,515 endomyocardial biopsies; 150 normal and 50 diseased cardiac myocytes from pediatric autopsy specimens; 34 intraoperative endomyocardial biopsy specimens from the left ventricle and 28 surgical biopsy specimens from the right or left atrium. The following results were obtained: The myocytes developed to adult size by the age of 15 years. Thereafter, the size did not change up to the age of 59. Short-term hemodynamic overloading to the ventricle caused reactive hyperfunction and hypertrophy of myocytes. Stable hypertrophy resulted in long-term overloading. In cardiomyopathy, compensated or stable hypertrophy occurred, but progression to decompensated or gradual exhaustion and progressive cardiosclerosis (Meerson) took place. Progress of endocardial thickening was often observed during the course of the disease. In the right and left atrial myocardium, extremely advanced pathology was observed and changes were related to the duration of the disease rather than to the severity of the hemodynamics.
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Sekiguchi et al. (1986) studied this question.
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