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Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19)
Myocardial damage with a consequent rise in cardio-specific troponin level is a frequent phenomenon in severe cases of coronavirus disease 2019 (COVID-19). Its causes are capillary endothelial cell dysfunction, associated carditis, low oxygenization, and increased sympathetic tone, which all worsen...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer Healthcare
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018688/ https://www.ncbi.nlm.nih.gov/pubmed/33811310 http://dx.doi.org/10.1007/s40119-021-00216-8 |
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author | Medvegy, Mihály Simonyi, Gábor |
author_facet | Medvegy, Mihály Simonyi, Gábor |
author_sort | Medvegy, Mihály |
collection | PubMed |
description | Myocardial damage with a consequent rise in cardio-specific troponin level is a frequent phenomenon in severe cases of coronavirus disease 2019 (COVID-19). Its causes are capillary endothelial cell dysfunction, associated carditis, low oxygenization, and increased sympathetic tone, which all worsen myocardial stiffness and microvascular dysfunction (MD). They lead to severe myocardial dysfunction, arrhythmia, acute congestive heart failure, and a significant rise in death cases. During COVID-19, no specific cardiological treatment is started. As adjuvant therapy, anxiolytics in COVID-19 are widely used, but not in all anxious patients who had been infected with coronavirus. Anxiolytics can be useful to moderate MD and immunosuppressive effect of anxiety. The favorable effects of trimetazidine (TMZ) and Coenzyme Q(10) (CoQ(10)) in the treatment of myocardial ischemia and heart failure had previously been proven, and also their anti-inflammatory effects had been suspected; however, they have not yet been used in COVID-19 cases. TMZ promotes glucose-mediated ATP production, which requires less oxygen, which explains its advantageous cardiac effects. Since it lowers serum and myocardial tissue proinflammatory cytokine levels and inhibits myocardial macrophage infiltration, it was suspected that TMZ might represent a novel therapeutic agent to prevent and treat sepsis-induced myocardial dysfunction. CoQ(10) plays an important role in cellular ATP production; however, its concentration is decreased in cardiovascular diseases and in influenza patients. Due to its anti-inflammatory effect, CoQ(10) has been suspected to have a key therapeutic target in influenza infection. We suggest considering these medicines to alleviate myocardial damage and inflammation in COVID-19. |
format | Online Article Text |
id | pubmed-8018688 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Springer Healthcare |
record_format | MEDLINE/PubMed |
spelling | pubmed-80186882021-04-06 Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) Medvegy, Mihály Simonyi, Gábor Cardiol Ther Commentary Myocardial damage with a consequent rise in cardio-specific troponin level is a frequent phenomenon in severe cases of coronavirus disease 2019 (COVID-19). Its causes are capillary endothelial cell dysfunction, associated carditis, low oxygenization, and increased sympathetic tone, which all worsen myocardial stiffness and microvascular dysfunction (MD). They lead to severe myocardial dysfunction, arrhythmia, acute congestive heart failure, and a significant rise in death cases. During COVID-19, no specific cardiological treatment is started. As adjuvant therapy, anxiolytics in COVID-19 are widely used, but not in all anxious patients who had been infected with coronavirus. Anxiolytics can be useful to moderate MD and immunosuppressive effect of anxiety. The favorable effects of trimetazidine (TMZ) and Coenzyme Q(10) (CoQ(10)) in the treatment of myocardial ischemia and heart failure had previously been proven, and also their anti-inflammatory effects had been suspected; however, they have not yet been used in COVID-19 cases. TMZ promotes glucose-mediated ATP production, which requires less oxygen, which explains its advantageous cardiac effects. Since it lowers serum and myocardial tissue proinflammatory cytokine levels and inhibits myocardial macrophage infiltration, it was suspected that TMZ might represent a novel therapeutic agent to prevent and treat sepsis-induced myocardial dysfunction. CoQ(10) plays an important role in cellular ATP production; however, its concentration is decreased in cardiovascular diseases and in influenza patients. Due to its anti-inflammatory effect, CoQ(10) has been suspected to have a key therapeutic target in influenza infection. We suggest considering these medicines to alleviate myocardial damage and inflammation in COVID-19. Springer Healthcare 2021-04-02 2021-06 /pmc/articles/PMC8018688/ /pubmed/33811310 http://dx.doi.org/10.1007/s40119-021-00216-8 Text en © The Author(s) 2021 https://creativecommons.org/licenses/by-nc/4.0/Open Access This article is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License, which permits any non-commercial use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by-nc/4.0/ (https://creativecommons.org/licenses/by-nc/4.0/) . |
spellingShingle | Commentary Medvegy, Mihály Simonyi, Gábor Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) |
title | Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) |
title_full | Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) |
title_fullStr | Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) |
title_full_unstemmed | Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) |
title_short | Supplementary Therapeutic Possibilities to Alleviate Myocardial Damage Due to Microvascular Dysfunction in Coronavirus Disease 2019 (COVID-19) |
title_sort | supplementary therapeutic possibilities to alleviate myocardial damage due to microvascular dysfunction in coronavirus disease 2019 (covid-19) |
topic | Commentary |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8018688/ https://www.ncbi.nlm.nih.gov/pubmed/33811310 http://dx.doi.org/10.1007/s40119-021-00216-8 |
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