[Biopsy of the myocardium in patients with ventricular arrhythmia of unknown etiology].
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Biomedical subjects
Publications and source records attributed to A Rosnowski.
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Besides elastic and collagen fibres, numerous smooth muscle (SM) cells were found in the thickened endocardium in 3 cases of restrictive cardiomyopathy and in 1 case of congenital endocardial fibroelastosis. In 3 other cases of congenital endocardial fibroelastosis, fibroblast-like cells were present besides numerous fibres. The former seemed to originate from SM cells. The authors present their opinion that both in congenital and acquired endocardial fibroelastosis, the lesion develops essentially in the same way. The basic phenomenon consists in increased elastoplastic activity of SM cells. In contrast, the aetiology (stimulus) of higher, elastogenous activity of SM cells remains obscure and seems to be different in individual cases.
Nine cases of subendocardial fat cell accumulation were found in association with various heart diseases in adults. Morphological observations suggest that this lesion results from injury to myocardial cells resulting in accumulation and later extrusion of lipids. This evokes lipidophagy and transforms the phagocytizing macrophage into a preadipocyte-like and in turn adipocyte-like cell. Collagen production around the process depends upon the extent of myocardial damage and the intensity of removal of cell debris.
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The results of endomyocardial biopsy (EMB) are presented in 174 patients. Techniques and apparatus are described. EMB is safe and useful for diagnosing inflammatory myocarditis and as a guide to therapy. Unsuspected lymphocytic myocarditis was found in 17% of patients with dilated cardiomyopathy. The results confirm that the EMB findings in dilated cardiomyopathy are nonspecific and that restrictive cardiomyopathy is not confined to hypereosinophilic states and amyloid heart disease.
Fifty-seven patients with unexplained dilated hearts and congestive heart failure were studied clinically and by endomyocardial biopsy of the left ventricle. Of the patients, 61% had histologic evidence of active lymphocytic myocarditis. The sudden onset of heart failure, often with arrhythmias, if preceded by a viral-like illness indicated a high chance of finding inflammatory infiltration in the biopsy material. No abnormal accumulation of immunoglobulin was found in these patients with dilated cardiomyopathy and myocarditis. Immunosuppressive therapy did not always bring about improvement.
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Morphological lesions were found to be different in arteries and in veins, in 9 cases of Buerger's disease. The arterial lesions were not characteristic and consisted of non-specific inflammation, thrombosis and obliteration which also occur in many other disease. In contrast, in addition to wall infiltration and thrombosis, the veins showed microabscesses and giant cell granulomas, which we believe to be absent in all other known diseases. The affected venous segment exhibited a variety of lesions. In the earliest period, the morphological aspect of inflammation in arteries and veins was fairly similar. In a late periods, that is those of vascular obliteration, the arteries and veins did not show any distinguishing morphological differences.
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Cells from aortas of healthy newborn and adult rabbits were liberated by digestion with trypsin and collagenase. In the same way were obtained free cells from the aortas of rabbits with far advanced experimental atherosclerosis. More than 90 p. 100 of the cells from all groups were viable. Isolated cells were used for electron microscopic examination. In material obtained from aortas of newborn rabbits, endothelial cells, fibroblasts and smooths muscle cells were present. In adult rabbits two kinds of endothelial cells, fibroblasts, several varieties of myocytes and foam cells were found. The bulk of aortic cells isolated from rabbits with experimental atherosclerosis consisted of endothelial cells and smooth myocytes. The cytoplasm of all myocytes contained lipid vacuoles. The lipid-loaded myocytes corresponded to the typical foam cells. Lipid content was relatively scanty in the endothelial cells. The presence of myocytes foam cells like in the aortas of healthy adult rabbits, identical as in material from experimental atherosclerosis, may support the view that these cellular changes so far considered as typical for atherosclerosis are common, and may be treated as an exponent of the natural process of aging of the vascular wall.
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