Special Issue "COVID-19-Associated Myocarditis and Cardiac Pathology"

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "SARS-CoV-2 and COVID-19".

Deadline for manuscript submissions: 31 October 2021.

Special Issue Editor

Dr. Xavier Clemente-Casares
E-Mail Website
Guest Editor
Department of Medical Microbiology and Immunology, University of Alberta, Alberta, AB T6G 2R3, Canada
Interests: immune cell composition of the heart; immune responses during adult and neonatal viral myocarditis; progression of viral myocarditis towards autoimmunity

Special Issue Information

Dear Colleagues,

Since the early stages of the COVID-19 pandemic, medical reports have highlighted the devastating effects of this “respiratory disease” on the heart. The most severe COVID-19 cases are often associated with cardiovascular symptoms, including elevated troponin in serum, arrhythmias and reduced heart function. These can result from the viral infection of many bodily systems, including the lungs or the vasculature. However, the magnificent work by various groups of scientists searching for the presence of the virus in the hearts of patients and pre-clinical models has demonstrated that SARS-CoV-2 is capable of infecting cardiomyocytes and causing myocarditis. Nevertheless, many questions remain regarding the complex interactions between the virus and the heart.

The virus interactions with cardiomyocytes and the cardiac immune system, whether resident or recruited, are essential determinants of acute viral susceptibility and effective viral clearance. Pre-existing cardiovascular disease is a risk factor for COVID-19 susceptibility and mortality, yet the reasons for this are not well understood.  The elucidation of these processes is critical to the evaluation of risk and interventions in susceptible patients.

Another critical unknown is the long-term effect of coronavirus infection on heart function. While the COVID-19 pandemic has taken an enormous toll in the form of lives, the number of survivors from asymptomatic and severe cases vastly outnumber those. Our experience with pre-clinical animal models of viral myocarditis, and some hints from the clinic, bring forth a frightful prediction. Whether acute or chronic, immunological or viral, the heart damage derived from a viral infection can be associated with, sometimes deadly, long-term alterations in the heart.

Hence, in this Special Issue on “COVID-19-Associated Myocarditis and Cardiac Pathology”, we propose to the research community to address aspects of the acute and long-term effects of COVID-19 infection and heart health.

Dr. Xavier Clemente-Casares
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • SARS-CoV-2
  • coronaviruses
  • cardiomyocyte infection
  • cardiomyocyte injury
  • viral myocarditis
  • COVID-19-associated myocardial infarct or cardiomyopathy
  • post-COVID-19 cardiac alterations

Published Papers (2 papers)

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Research

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Article
Multisystem Inflammatory Syndrome Following SARS-CoV-2 Infection in Children: One Year after the Onset of the Pandemic in a High-Incidence Area
Viruses 2021, 13(10), 2022; https://0-doi-org.brum.beds.ac.uk/10.3390/v13102022 - 07 Oct 2021
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Abstract
SARS-CoV-2 infection in children can trigger cardiovascular manifestations potentially requiring an intensive treatment and defining a new entity named Multisystem Inflammatory Syndrome in Children (MIS-C), whose features partially overlap with Kawasaki Disease (KD). A cross-sectional study including all diagnoses of MIS-C and KD [...] Read more.
SARS-CoV-2 infection in children can trigger cardiovascular manifestations potentially requiring an intensive treatment and defining a new entity named Multisystem Inflammatory Syndrome in Children (MIS-C), whose features partially overlap with Kawasaki Disease (KD). A cross-sectional study including all diagnoses of MIS-C and KD from April 2020 to May 2021 in our metropolitan area was conducted evaluating clinical, laboratory (including immunological response, cytokines, and markers of myocardial damage), and cardiac (coronary and non-coronary) features at onset of the diseases. Evolution of ventricular dysfunction, valve regurgitations, and coronary lesions was documented. The severity of the disease was also considered based on the need for inotropic support and ICU admission. Twenty-four MIS-C were diagnosed (14 boys, median age 82 months): 13/24 cases (54.17%) presented left ventricular dysfunction, 12/24 (50%) required inotropic support, and 10/24 (41.67%) developed coronary anomalies (CALs). All patients received steroids and IVIG at a median time of 5 days (IQR1:4, IQR3:6.5) from onset of fever and heart function normalized 6 days (IQR1: 5, IQR3: 7) after therapy, while CALs persisted in one. One patient (12.5%) required infliximab because of refractory disease and still presented CALs 18 days after therapy. During the same study period, 15 KD were diagnosed: none had ventricular dysfunction, while 7/15 (46.67%) developed CALs. Three out of 15 patients (20%) still presented CALs 46 days from onset. Compared to KD, MIS-C pts have significantly higher IL8 and similar lymphocytes subpopulations. Despite a more severe presentation and initial cardiac findings compared to KD, the myocardial injury in MIS-C has a rapid response to immunomodulatory treatment (median time 6 days), in terms of ventricular function, valve regurgitations, and troponin. Incidence of CALs is similar at onset, but it tends to regress in most of the cases of MIS-C differently than in KD where CALs persist in up to 40% in the subacute stage after treatment. Full article
(This article belongs to the Special Issue COVID-19-Associated Myocarditis and Cardiac Pathology)
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Review

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Review
Myocardial Damage by SARS-CoV-2: Emerging Mechanisms and Therapies
Viruses 2021, 13(9), 1880; https://0-doi-org.brum.beds.ac.uk/10.3390/v13091880 - 21 Sep 2021
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Abstract
Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can [...] Read more.
Evidence is emerging that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can infect various organs of the body, including cardiomyocytes and cardiac endothelial cells in the heart. This review focuses on the effects of SARS-CoV-2 in the heart after direct infection that can lead to myocarditis and an outline of potential treatment options. The main points are: (1) Viral entry: SARS-CoV-2 uses specific receptors and proteases for docking and priming in cardiac cells. Thus, different receptors or protease inhibitors might be effective in SARS-CoV-2-infected cardiac cells. (2) Viral replication: SARS-CoV-2 uses RNA-dependent RNA polymerase for replication. Drugs acting against ssRNA(+) viral replication for cardiac cells can be effective. (3) Autophagy and double-membrane vesicles: SARS-CoV-2 manipulates autophagy to inhibit viral clearance and promote SARS-CoV-2 replication by creating double-membrane vesicles as replication sites. (4) Immune response: Host immune response is manipulated to evade host cell attacks against SARS-CoV-2 and increased inflammation by dysregulating immune cells. Efficiency of immunosuppressive therapy must be elucidated. (5) Programmed cell death: SARS-CoV-2 inhibits programmed cell death in early stages and induces apoptosis, necroptosis, and pyroptosis in later stages. (6) Energy metabolism: SARS-CoV-2 infection leads to disturbed energy metabolism that in turn leads to a decrease in ATP production and ROS production. (7) Viroporins: SARS-CoV-2 creates viroporins that lead to an imbalance of ion homeostasis. This causes apoptosis, altered action potential, and arrhythmia. Full article
(This article belongs to the Special Issue COVID-19-Associated Myocarditis and Cardiac Pathology)
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