glycogen and Heart-Valve-Diseases

We determined representative enzyme activities of glycogenolysis (glycogen phosphorylase) glycolysis (d-glyceraldehyde-3-phosphate dehydrogenase, GAPDH), beta 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 energy-supplying 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.

Topics: 3-Hydroxyacyl CoA Dehydrogenases; Cardiomyopathy, Dilated; Citric Acid Cycle; Creatine Kinase; Energy Metabolism; Enzymes; Fatty Acids; Glycogen; Glycolysis; Heart Valve Diseases; Heart Ventricles; Humans; Isoenzymes; L-Lactate Dehydrogenase; Lactates; Lactic Acid; Middle Aged; Myocardium; Phosphocreatine

Topics: Adolescent; Adult; Aged; Glycogen; Heart Valve Diseases; Humans; Middle Aged; Myocardium; Prognosis

Topics: Cardiac Surgical Procedures; Cardiopulmonary Bypass; Creatine Kinase; Female; Glycogen; Heart Arrest, Induced; Heart Valve Diseases; Humans; Isoenzymes; Male; Metoprolol; Myocardium; Propranolol

Topics: Creatine Kinase; Female; Glucose; Glycogen; Heart Arrest, Induced; Heart Valve Diseases; Humans; Hypothermia, Induced; Male; Middle Aged; Myocardium; Random Allocation

We report observations on ultrastructural and cytochemical changes in the myocardium after hypothermic protection in 21 patients who underwent cardiac operation. Two general categories of hypothermic protection were studied. (1) topical cooling during anoxic arrest and moderate general hypothermia (10 patients with aortic valve replacement, Group 1) and (2) intermittent perfusion during moderate general hypothermia combined with topical cooling (11 patients with multiple valve replacement, Group II). Transmural left ventricular biopsies were taken at the start of the cardiopulmonary bypass and shortly after the end of aortic cross-clamping. In Group I (cross-clamp time, 51 +/- 12 minutes) only minor pathologic changes of the myocardial fine structure were found, with no differences among the left ventricular layers. In most mitochondria, structure remained intact but the mitochondrial granules disappeared. Cytochrome-c-oxidase activity was unchanged. In Group II (total cross-clamp time, 83 +/- 16 minutes) the subendocardium was well preserved. Slight subcellular damage comparable with that of resulting from topical cooling was seen in all hearts even after a total cross-clamp period of 106 minutes. Cytochrome-c-oxidase activity was unchanged. In the subepicardium, however, a positive correlation was found between the severity of ultrastructural damage and total cross-clamp time (p less than 0.05). Matrix clearing, damage to the cristae and the mitochondrial membranes, and nuclear abnormalities occurred when the aorta was cross-clamped for morethan 60 minutes. Cytochrome-c-oxidase activities decreased in these samples. It is concluded that: (1) no significant subcellular injury was found in hearts cooled topically during 1 hour of anoxic arrest; and (2) in hearts protected by intermittent perfusion during moderate general hypothermia and additional external cooling, the subendocardium was well preserved for anoxic periods of up to 106 minutes. However, after 60 minutes of aortic cross-clamping subcellular damage increased progressively in the subepicardium.

Topics: Aged; Aortic Valve; Cardiopulmonary Bypass; Chromatin; Electron Transport Complex IV; Female; Glycogen; Heart Valve Diseases; Heart Valve Prosthesis; Humans; Hypothermia, Induced; Male; Middle Aged; Mitochondria, Heart; Mitral Valve; Myocardial Contraction; Myocardium; Myofibrils; Time Factors

Topics: Adult; Aortic Valve Insufficiency; Aortic Valve Stenosis; Biopsy; Cardiomyopathies; Cell Membrane; Cytoplasmic Granules; Desmosomes; Endocardium; Endoplasmic Reticulum; Female; Glycogen; Golgi Apparatus; Heart Valve Diseases; Heart Ventricles; Humans; Male; Microscopy, Electron; Mitochondria; Mitral Valve Insufficiency; Myocardium; Myofibrils; Sarcoplasmic Reticulum; Temperature

Topics: Animals; Collagen; Endocarditis; Endocarditis, Bacterial; Fluorescent Antibody Technique; Glycogen; Heart Atria; Heart Defects, Congenital; Heart Valve Diseases; Heart Valves; Hemagglutination Tests; Humans; Immune Sera; Inclusion Bodies; Lipids; Microscopy, Electron; Mitochondria; Myocardium; Papillary Muscles; Rabbits; Rheumatic Heart Disease; Staining and Labeling

Topics: Alkaline Phosphatase; Blood Cells; Blood Chemical Analysis; Clinical Enzyme Tests; Glycogen; Heart Diseases; Heart Valve Diseases; Heart Valves; Humans; Lipids; Neutrophils; Oxidoreductases; Peroxidases