Key result
Failing hearts are linked to decreased cytochemical ATPase activity and ultrastructural degeneration.
Why the study?
The relationship between ultrastructural alterations, ATPase activity, and cardiac function in various heart diseases was not fully characterized.
Observational
Answers are grounded in this paper and cite their sources.
Caution against inferring function from ATPase intensity in biopsies; leaves open links to outcomes in heart disease.
Ultrastructural localization and intensity of ATPase activity were studied in myocardial cells from biopsies with reference to fine-structural alterations and cardiac functions in patients with various heart diseases. ATPase activity was found to be intense in the sarcoplasmic reticulum (SR), the matrices of the mitochondria (Mt), on the myofilaments (Mf) and along the gap-junctions of intercalated discs in the control myocardial cells. ATPase activity was more intense in cardiac myocytes from well-functioning or ultrastructurally well preserved hearts. In failing and degenerating hearts, ATPase activity was decreased. ATPase activity was more intense in clinically-improving than in clinically-worsening patients. However, the localized pattern of ATPase activity was similar in each heart disease. These results suggest that cytochemical observation of ATPase activity can reflect not only fine structural changes in cardiac myocytes, but also the metabolic state in the diseased heart, and is valuable therefore from the standpoint of clinical medicine.
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Takeyama et al. (1987) conducted an observational in Various heart diseases. Failing and degenerating hearts vs. Well-functioning or ultrastructurally well preserved hearts was evaluated on Ultrastructural localization and intensity of ATPase activity. Cytochemical ATPase activity was decreased in failing and degenerating hearts compared to well-functioning hearts, reflecting fine structural changes and metabolic state.
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