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Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats
This study reports pathological and molecular features in 41 cases of feline restrictive cardiomyopathy (RCM). Grossly, there were patchy or diffuse areas of endocardial thickening affecting the left ventricle. The more common patchy endocardial lesions occurred as large trabecular or irregular broa...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Ltd.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7094507/ https://www.ncbi.nlm.nih.gov/pubmed/27392420 http://dx.doi.org/10.1016/j.jcpa.2016.06.003 |
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author | Kimura, Y. Karakama, S. Hirakawa, A. Tsuchiaka, S. Kobayashi, M. Machida, N. |
author_facet | Kimura, Y. Karakama, S. Hirakawa, A. Tsuchiaka, S. Kobayashi, M. Machida, N. |
author_sort | Kimura, Y. |
collection | PubMed |
description | This study reports pathological and molecular features in 41 cases of feline restrictive cardiomyopathy (RCM). Grossly, there were patchy or diffuse areas of endocardial thickening affecting the left ventricle. The more common patchy endocardial lesions occurred as large trabecular or irregular broad bands of fibrous tissue bridging the left ventricular free wall and ventricular septum. Microscopically, regardless of the gross pattern, the thickened endocardium contained various numbers of stellate, spindle-shaped or elongated mesenchymal cells surrounded by fibrous connective tissue. Immunohistochemical findings were indicative of smooth muscle differentiation in mesenchymal cells. These cells proliferated vigorously and produced alcian blue-positive ground substance and collagen fibres; it was considered that the mesenchymal cells contributed to the formation of the endocardial lesions. In addition, multiple left ventricular ‘false tendons’ were invariably included within the trabecular or broad fibrous bands, providing a framework for formation of those bands. Evidence of endocarditis or endomyocarditis was lacking in all 41 cases, and no viral genomes were detected in any of the DNA or RNA samples obtained from 14 of the hearts. These observations suggest that any relationship between feline RCM and a virus-induced inflammatory response seems unlikely. |
format | Online Article Text |
id | pubmed-7094507 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Elsevier Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-70945072020-03-25 Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats Kimura, Y. Karakama, S. Hirakawa, A. Tsuchiaka, S. Kobayashi, M. Machida, N. J Comp Pathol Article This study reports pathological and molecular features in 41 cases of feline restrictive cardiomyopathy (RCM). Grossly, there were patchy or diffuse areas of endocardial thickening affecting the left ventricle. The more common patchy endocardial lesions occurred as large trabecular or irregular broad bands of fibrous tissue bridging the left ventricular free wall and ventricular septum. Microscopically, regardless of the gross pattern, the thickened endocardium contained various numbers of stellate, spindle-shaped or elongated mesenchymal cells surrounded by fibrous connective tissue. Immunohistochemical findings were indicative of smooth muscle differentiation in mesenchymal cells. These cells proliferated vigorously and produced alcian blue-positive ground substance and collagen fibres; it was considered that the mesenchymal cells contributed to the formation of the endocardial lesions. In addition, multiple left ventricular ‘false tendons’ were invariably included within the trabecular or broad fibrous bands, providing a framework for formation of those bands. Evidence of endocarditis or endomyocarditis was lacking in all 41 cases, and no viral genomes were detected in any of the DNA or RNA samples obtained from 14 of the hearts. These observations suggest that any relationship between feline RCM and a virus-induced inflammatory response seems unlikely. Elsevier Ltd. 2016 2016-07-05 /pmc/articles/PMC7094507/ /pubmed/27392420 http://dx.doi.org/10.1016/j.jcpa.2016.06.003 Text en © 2016 Elsevier Ltd. All rights reserved. Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active. |
spellingShingle | Article Kimura, Y. Karakama, S. Hirakawa, A. Tsuchiaka, S. Kobayashi, M. Machida, N. Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats |
title | Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats |
title_full | Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats |
title_fullStr | Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats |
title_full_unstemmed | Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats |
title_short | Pathological Features and Pathogenesis of the Endomyocardial Form of Restrictive Cardiomyopathy in Cats |
title_sort | pathological features and pathogenesis of the endomyocardial form of restrictive cardiomyopathy in cats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7094507/ https://www.ncbi.nlm.nih.gov/pubmed/27392420 http://dx.doi.org/10.1016/j.jcpa.2016.06.003 |
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