acid-phosphatase and Heart-Valve-Diseases

A study of myocardium of patients with mitral stenosis was performed using ultrahistochemical methods at different stages of disease and in the course of valve replacement operation. A quantitative analysis of degenerative changes was introduced, the results of which correlated with the severity of heart failure. A pronounced heterogeneity in mitochondrial enzyme activity has been detected cytochemically. In some apparently "unaffected" cardiomyocytes an active alterative process was expressed in an increase of sarcolemma permeability for electron-microscopic tracers. An elevated fenestration of membrane barriers was noted at the stages of anoxic heart arrest. Using tannic acid it was possible to demonstrate a penetration of plasma protein-polysaccharide complexes into cell sarcoplasma. There were observed topographic variations in the distribution of acid phosphatase activity.

Topics: Acid Phosphatase; Cell Membrane Permeability; Electron Transport Complex IV; Heart Valve Diseases; Histocytochemistry; Humans; Microscopy, Electron; Mitral Valve; Myocardium; Rheumatic Heart Disease; Succinate Dehydrogenase

Cardiac tissue obtained by left-ventricular endomyocardial biopsy from patients with valvular heart-disease was assayed for marker enzyme activities of subcellular organelles and these were correlated with left ventricular function as assessed by haemodynamic studies. In patients with poor left ventricular function, calcium-dependent adenosine-triphosphatase (A.T.P.ase) activity, predominantly localised to the myofibrils, was strikingly reduced. Activity of lactate dehydrongenase, a cytosol enzyme, was significantly increased in tissue from patients with poor left ventricular function. The activity of enzymes associated with sarcolemma (5'-nucleotidase), mitochondria (glutamate dehydrogenase and monoamine oxidase), microsomes (neutral alpha-glucosidase), and lysosomes (acid phosphatase, N-acetyl-beta-glucosaminidase) was no different in patients with good or poor left ventricular function. It is suggested that reduced myofibrillary A.T.P.ase concentration is the biochemical basis for the impaired ventricular function.

Topics: Acid Phosphatase; Adenosine Triphosphatases; Biopsy; Glucosidases; Glutamate Dehydrogenase; Heart Valve Diseases; Heart Ventricles; Hemodynamics; Hexosaminidases; Humans; L-Lactate Dehydrogenase; Malate Dehydrogenase; Monoamine Oxidase; Myocardium; Nucleotidases