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COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism
COVID-19 has a significant effect upon the cardiovascular system. While a number of different cardiovascular histopathologies have been described at post-mortem examination, the incidence of typical viral myocarditis in COVID-19 positive patients appears very low [1], [2], [3]. In this study, we fur...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8223028/ https://www.ncbi.nlm.nih.gov/pubmed/34174415 http://dx.doi.org/10.1016/j.carpath.2021.107361 |
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author | Fox, Sharon E. Falgout, Lacey Vander Heide, Richard S. |
author_facet | Fox, Sharon E. Falgout, Lacey Vander Heide, Richard S. |
author_sort | Fox, Sharon E. |
collection | PubMed |
description | COVID-19 has a significant effect upon the cardiovascular system. While a number of different cardiovascular histopathologies have been described at post-mortem examination, the incidence of typical viral myocarditis in COVID-19 positive patients appears very low [1], [2], [3]. In this study, we further characterize and quantify the inflammatory cell infiltrate in a COVID-19 study cohort and compare the findings to both an age and disease matched control cohort and a cohort of patients diagnosed with typical inflammatory myocarditis. All study and control cohorts had 1 or more of the comorbidities most commonly associated with severe disease (hypertension, type II diabetes, obesity, or known cardiovascular disease). The results demonstrate a skewed distribution of the number of CD68+ cells in COVID-19 hearts, with upper quantiles showing a significant increase as compared to both matched control hearts, and those with myocarditis. In contrast, hearts from typical inflammatory myocarditis contained increased numbers of CD4+, and CD8+ cells compared to both COVID-19 and control cohorts. In conclusion, the presence of an increased number of CD68+ cells suggests that COVID-19 may incite a form of myocarditis different from typical viral myocarditis, and associated with diffusely infiltrative cells of monocytes/macrophage lineage. |
format | Online Article Text |
id | pubmed-8223028 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Elsevier Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-82230282021-06-25 COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism Fox, Sharon E. Falgout, Lacey Vander Heide, Richard S. Cardiovasc Pathol Original Article COVID-19 has a significant effect upon the cardiovascular system. While a number of different cardiovascular histopathologies have been described at post-mortem examination, the incidence of typical viral myocarditis in COVID-19 positive patients appears very low [1], [2], [3]. In this study, we further characterize and quantify the inflammatory cell infiltrate in a COVID-19 study cohort and compare the findings to both an age and disease matched control cohort and a cohort of patients diagnosed with typical inflammatory myocarditis. All study and control cohorts had 1 or more of the comorbidities most commonly associated with severe disease (hypertension, type II diabetes, obesity, or known cardiovascular disease). The results demonstrate a skewed distribution of the number of CD68+ cells in COVID-19 hearts, with upper quantiles showing a significant increase as compared to both matched control hearts, and those with myocarditis. In contrast, hearts from typical inflammatory myocarditis contained increased numbers of CD4+, and CD8+ cells compared to both COVID-19 and control cohorts. In conclusion, the presence of an increased number of CD68+ cells suggests that COVID-19 may incite a form of myocarditis different from typical viral myocarditis, and associated with diffusely infiltrative cells of monocytes/macrophage lineage. Elsevier Inc. 2021 2021-06-24 /pmc/articles/PMC8223028/ /pubmed/34174415 http://dx.doi.org/10.1016/j.carpath.2021.107361 Text en © 2021 Elsevier Inc. 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 | Original Article Fox, Sharon E. Falgout, Lacey Vander Heide, Richard S. COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
title | COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
title_full | COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
title_fullStr | COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
title_full_unstemmed | COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
title_short | COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
title_sort | covid-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8223028/ https://www.ncbi.nlm.nih.gov/pubmed/34174415 http://dx.doi.org/10.1016/j.carpath.2021.107361 |
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