Open AccessComparative analysis of myocardial enzyme activities of the energy‐supplying metabolism in patients with dilative cardiomyopathies and valve diseases
Author(s) -
Klein H. H.,
Spaar U.,
Schlepple H.,
Wiegand V.,
Kreuzer H.
Publication year - 1986
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960090506
Subject(s) - glycolysis , citrate synthase , medicine , creatine kinase , lactate dehydrogenase , endocrinology , creatine , citric acid cycle , metabolism , enzyme , glycogen phosphorylase , glycogenolysis , dehydrogenase , biochemistry , glycogen , cardiology , chemistry
We determined representative enzyme activities of glycogenolysis (glycogen phosphorylase) glycolysis (d‐glyceraldehyde‐3‐phosphate dehydrogenase, GAPDH), β oxidation of free fatty acids (1‐3‐hydroxyacyl CoA dehydrogenase, HADH), citric acid cycle (citrate synthase, CS), lactate fermentation (lactate dehydrogenase LDH), and creatine phosphate metabolism (creatine kinase, CK) in left ventricular samples of 36 patients to investigate if the metabolic capacities of the energysupplying pathways are differently affected in different heart diseases. There were 17 patients with mitral valve diseases (MVD), 8 patients with aortic valve diseases (AVD), and 11 patients who suffered from dilative cardiomyopathies (DCM). The main metabolic characteristic on the level of enzymatic organization in patients with DCM was an increased ratio of GAPDH/HADH activities and a decreased ratio of HADH/CS activities compared to the valve‐diseased patients. This result indicates that the capacity of glucose oxidation is enhanced at the expense of fatty acid metabolism in patients with DCM. Furthermore, we determined significantly lower myocardial CK activities in this group of patients, most probably reflecting a diminished content of myofibrils. Citrate synthase activity was lowest in patients with AVD. Although we cannot rule out that the impaired left ventricular function is in part responsible for the shift of the capacities of the energy‐supplying metabolism in patients with DCM, we favor the assumption that it is a specific feature of this myocardial disease.