researchers highlight two different profiles

you will also be interested

[EN VIDÉO] Where does SARS-CoV-2 really come from?
Almost two years after the start of the Covid epidemic, the exact origin of the SARS-CoV-2 virus is still unknown.

Fulminant myocarditis is a weird illness and severe, mainly affecting young individuals. She is responsible for a inflammation and myocardial dysfunction associated with significant mortality. viral infection SARS-CoV-2 can lead to fulminant myocarditis, most of the time integrating into a syndrome multisystem inflammatory disease, initially described in children (MIS-C) and later in adults (MIS-A). Recommended treatments are corticosteroids and the immunoglobulins intravenous. However, some adults with fulminant myocarditis do not meet the diagnostic criteria for MIS-A established by the Center for Disease Control and Prevention (fever prolonged rash, conjunctivitisneurological and digestive deterioration, thrombocytopenia and marked inflammatory syndrome), suggesting that there are several phenotypes fulminant myocarditis related to COVID-19.

Under the direction of doctors Marc Pineton de Chambrun, Guillaume Hékimian and Guy Gorochov, teams from the intensive care-resuscitation department of the Pitié-Salpêtrière hospital, in collaboration with researchers from Inserm and Sorbonne University, at the Center for Immunology and Infectious Diseases (CIMI-Paris) wanted better characterize fulminant myocarditis associated with infection by virus SARS-CoV-2 in adults.

They conducted a retrospective study on 38 patients who met or did not meet the MIS-A criteria admitted to intensive care at the La Pitié-Salpêtrière Heart Institute hospital for fulminant myocarditis secondary to SARS-CoV-2 infection between May 2020 and June 2021 The results of this study will be published on July 26, 2022 in the journal Journal of the American College of Cardiology (JAC).

The group of patients who did not meet the MIS-A criteria (group MIS-A-) had a more recent SARS-CoV-2 infection (median time to onset after start of symptom Covid-19: 3 days), a PCR SARS-CoV-2 more frequently positive, more severe myocarditis that more frequently require the use of extracorporeal circulatory assistance by venoarterial ECMO (Extracorporeal Membrane Oxygenation is an assistance technique that ensures all or part of the blood circulation used in emergency) and higher hospital mortality. In the other group of patients with these criteria (MIS-A-+), heart failure presented later (median time to onset after proven Covid-19: 32 days) and was less severe, the virus was typically undetectable at this stage and the best prognosis.

Biomarkers to distinguish two phenotypes

These two phenotypes were also associated with different immunological profiles. innate responses interferon alpha (early participant in the antiviral response) and interleukin(IL)-8 (chemokine that allows the recruitment of polynuclear neutrophils) were strongly increased in MIS-A- patients, compared to MIS-A+.

MIS-A+ patients had particularly high blood levels of IL-22 and IL-17. These cytokines play an important physiological role in the barriers mucous membranes and skin and are produced by the lymphocytes Rh17. IL-17 is a cytokine proinflammatory implicated in several chronic inflammatory diseases.

In summary, MIS-A myocarditis occurs at the same time as immune response early against replication viral. An interesting point: 54% of MIS-A- patients expressed antibody individuals (the antibody anti-RNA polymerase III), which have already been associated with recurrent fulminant viral myocarditis. In comparison, MIS-A+ forms are associated with a delayed and exacerbated Th17-type lymphocyte-specific response. The targets of this Th17 response and the possibility of cross-reactions between viruses and antigens the myocardium remains to be determined.

Therefore, this study shows that COVID-19-associated fulminant myocarditis represents a heterogeneous entity encompassing 2 patient phenotypes that differ in clinical, immunobiological, and prognostic criteria. Suggests that IL-17, IL-22, interferon and antibodies RNA polymerase III could be used as a biomarker to distinguish these two phenotypes.

the vaccines against Covid-19 would also be associated with a risk of myocarditis and pericarditis. While these cardiological side effects are very rare, it would be important to determine if these biomarkers could also help diagnose them early. Finally, IL-17 inhibitors, currently available on the market, seem to be an interesting therapeutic route in MIS-A+ patients.

Are you interested in what you just read?


Add Comment