<abstract xmlns="http://www.w3.org/1999/xhtml"><p>Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV-2. As several patients confirmed with the new SARS-CoV-2 are known with cardiovascular disease (CVD) and data from the literature show negative prognosis and a higher risk of complications, this subgroup of subjects represents a particular situation. Therefore, an adequate understanding of the mechanisms involved in myocardial injury and interaction between COVID-19 and CVD is essential for optimal further management. Studies have proved that in COVID-19 patient myocarditis is determined via three pathological mechanisms of cardiomyocyte injury: direct viral cell entry and binding to ACE2, vasculitis-mediated injury, and systemic inflammatory response leading to pro-inflammatory cytokine discharge. Studies show that the incidence of myocarditis in patients with SARS-CoV-2 is relatively low, 4.8%, but myocardial damage occurs in more than 25% of critical cases in the form of acute fulminant myocarditis with severe hemodynamic degradation, or develops when the severity of SARS-CoV-2 infection intensifies. The mortality rate in myocarditis from COVID-19 infection ranges between 50–70%, with poorer prognosis and a higher risk of complications in CVD patients. As in all of these cases increased troponin and natriuretic peptide levels proved to be a negative prognostic factor, for risk stratification and prompt treatment, cardiac biomarkers should be evaluated in all patients with COVID-19.</p></abstract>

Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV-2. As several patients confirmed with the new SARS-CoV-2 are known with cardiovascular disease (CVD) and data from the literature show negative prognosis and a higher risk of complications, this subgroup of subjects represents a particular situation. Therefore, an adequate understanding of the mechanisms involved in myocardial injury and interaction between COVID-19 and CVD is essential for optimal further management. Studies have proved that in COVID-19 patient myocarditis is determined via three pathological mechanisms of cardiomyocyte injury: direct viral cell entry and binding to ACE2, vasculitis-mediated injury, and systemic inflammatory response leading to pro-inflammatory cytokine discharge. Studies show that the incidence of myocarditis in patients with SARS-CoV-2 is relatively low, 4.8%, but myocardial damage occurs in more than 25% of critical cases in the form of acute fulminant myocarditis with severe hemodynamic degradation, or develops when the severity of SARS-CoV-2 infection intensifies. The mortality rate in myocarditis from COVID-19 infection ranges between 50–70%, with poorer prognosis and a higher risk of complications in CVD patients. As in all of these cases increased troponin and natriuretic peptide levels proved to be a negative prognostic factor, for risk stratification and prompt treatment, cardiac biomarkers should be evaluated in all patients with COVID-19.

Myocardial Injury and Myocarditis in SARS-CoV-2 Patients

“George Emil Palade” University of Medicine

Journal of Interdisciplinary Medicine

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

{"article-title":"Myocardial Injury and Myocarditis in SARS-CoV-2 Patients"}

Myocarditis is one of the relatively common complications of respiratory infection with SARSCoV-2. As several patients confirmed with the new SARS-CoV-2 are...

Myocardial Injury and Myocarditis in SARS-CoV-2 Patients

Publicado en línea: 20 oct 2020

Páginas: 101 - 104

Recibido: 20 jun 2020

Aceptado: 19 jul 2020

DOI: https://doi.org/10.2478/jim-2020-0019

Palabras clave
SARS-CoV-2, myocarditis, ACE2 receptors, cardiovascular disease, cardiac biomarkers

© 2020 Camelia Libenciuc et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Myocardial Injury and Myocarditis in SARS-CoV-2 Patients

Publicado en línea: 20 oct 2020

Páginas: 101 - 104

Recibido: 20 jun 2020

Aceptado: 19 jul 2020

DOI: https://doi.org/10.2478/jim-2020-0019

Palabras claveSARS-CoV-2, myocarditis, ACE2 receptors, cardiovascular disease, cardiac biomarkers

© 2020 Camelia Libenciuc et al., published by Sciendo

This work is licensed under the Creative Commons Attribution-NonCommercial-NoDerivatives 3.0 License.

Palabras clave
SARS-CoV-2, myocarditis, ACE2 receptors, cardiovascular disease, cardiac biomarkers