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Circulation, Vol 83, 504-514, Copyright © 1991 by American Heart Association
J Schaper, R Froede, S Hein, A Buck, H Hashizume, B Speiser, A Friedl and N Bleese
This study was designed to determine the morphological correlate of chronic
heart failure. Myocardial tissue from eight patients undergoing
transplantation surgery because of end-stage dilated cardiomyopathy was
investigated by electron microscopy and immunocytochemistry using
monoclonal antibodies against elements of the cytoskeleton: desmin,
tubulin, vinculin, and vimentin. The tissue showed hypertrophy, atrophy of
myocytes, and an increased amount of fibrosis. Ultrastructural changes
consisted of enlargement and varying shape of nuclei, numerous very small
mitochondria, proliferation of T tubules, and accumulation of lipid
droplets and glycogen. The most obvious ultrastructural alteration was the
decrease of myofilaments, ranging from rarefication to complete absence of
sarcomeres in cells filled with unspecified cytoplasm. Immunocytochemistry
showed that desmin was localized at the Z lines. In diseased myocardium,
the amount of desmin was increased, but it was disorderly arranged. Tubulin
formed a fine network throughout the myocytes and was significantly
increased in cardiomyopathic hearts. Vinculin, a protein closely associated
with the cytoskeleton, occurred not only at the sarcolemma and the
intercalated disc but also within the myocardial cells. Ultrastructural
changes and alterations of the cytoskeleton were severe in about one third
of all cells. About one third of all cells showed moderately severe
changes, and the remaining cells were normal. Vimentin was present in the
interstitial cells and was increased in relation to the increase of
fibrosis. We conclude that the increase of fibrosis, the degeneration of
hypertrophied myocardial cells, and the alterations of the cytoskeleton are
the morphological correlates of reduced myocardial function in chronic
heart failure.
ARTICLES
Impairment of the myocardial ultrastructure and changes of the cytoskeleton in dilated cardiomyopathy
Department of Experimental Cardiology, Max-Planck-Institute for Physiological and Clinical Research, Nauheim, FRG.
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C.F. Vahl, T. Kloss, Y. Yang, M. Castell, A. Mehrkens, R. deSimone, L. Schaffer, and S. Hagl Surgical treatment of oligosymptomatic mitral valve incompetence? Eur. J. Cardiothorac. Surg., November 1, 1999; 16(5): 524 - 532. [Abstract] [Full Text] [PDF]
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H. F. Clemo, B. S. Stambler, and C. M. Baumgarten Persistent Activation of a Swelling-Activated Cation Current in Ventricular Myocytes From Dogs With Tachycardia-Induced Congestive Heart Failure Circ. Res., July 27, 1998; 83(2): 147 - 157. [Abstract] [Full Text] [PDF]
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M. Maeda, E. Holder, B. Lowes, S. Valent, and R. D. Bies Dilated Cardiomyopathy Associated With Deficiency of the Cytoskeletal Protein Metavinculin Circulation, January 7, 1997; 95(1): 17 - 20. [Abstract] [Full Text]
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