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Enzyme histochemistry of endomyocardial biopsies in idiopathic dilated cardiomyopathy
H R Figulla1, A Bardosi, K Dechant
1Department of Internal Medicine, University of Göttingen, FRG.
Insights
Idiopathic dilated cardiomyopathy (DCM) shows elevated NADH-TR activity, suggesting mitochondrial dysfunction. However, enzyme levels don't correlate with clinical data, indicating they aren't the primary cause of heart impairment in DCM.
Area of Science:
- Cardiology
- Biochemistry
- Pathology
Background:
- Idiopathic dilated cardiomyopathy (DCM) etiology remains unknown.
- Understanding enzyme activity in DCM is crucial for disease differentiation.
- Previous studies lack comprehensive enzyme histochemistry analysis in DCM.
Purpose of the Study:
- To differentiate idiopathic dilated cardiomyopathy (DCM) using enzyme histochemistry.
- To investigate enzyme activity alterations in the left ventricle of DCM patients.
- To correlate enzyme levels with clinical and histomorphometric data.
Main Methods:
- Enzyme histochemistry and semiquantitative analysis of endomyocardial biopsies.
- Assessed staining intensities for NADH-TR, succinate dehydrogenase, cytochrome c oxidase, lactate dehydrogenase, and acid phosphatase (aPh).
- Compared 40 DCM patients with 5 control specimens.
Main Results:
- Elevated nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR) activity in DCM patients suggests impaired mitochondrial oxidative phosphorylation.
- Lysosomal enzyme acid phosphatase (aPh) intensity was higher in DCM patients with preserved left ventricular ejection fraction.
- No concrete relationship found between enzyme histochemical intensity and anamnestic, hemodynamic, or histomorphometric data.
Conclusions:
- Enzyme concentrations tested are not solely responsible for functional myocardial impairment in DCM.
- Demonstrated interindependence of structural, hemodynamic, and enzyme parameters in DCM.
- Further research needed to elucidate the complex etiology of idiopathic dilated cardiomyopathy.
Abstract:
The etiology of idiopathic dilated cardiomyopathy (DCM) is yet unknown; this study aimed at further differentiation of the disease by means of enzyme histochemistry. Endomyocardial biopsies from the left ventricle of 40 DCM patients and 5 control specimens had enzymes examined histochemically and semiquantitatively and analyzed according to staining intensities of nicotinamide adenine dinucleotide tetrazolium reductase (NADH-TR), succinate dehydrogenase, cytochrome c oxidase, lactate dehydrogenase and acid phosphatase (aPh). In DCM, the NADH-TR activity was elevated as compared to controls, indicating impaired mitochondrial oxidative phosphorylation. However, a concrete relation of enzyme histochemical intensity to anamnestic, hemodynamic or histomorphometric data could not be determined, except for the fact that the intensity of the lysosomal enzyme aPh was elevated in DCM patients with a relatively high left ventricular ejection fraction. The results demonstrate an interindependence of structural, hemodynamic and historical parameters as well as enzyme concentrations in DCM. Thus, a pathological change in the enzyme concentrations tested here cannot be responsible for the functional myocardial impairment in DCM.