Key result
COVID-19 infection is associated with the development of myocarditis, likely driven by direct viral toxicity and systemic immune-mediated mechanisms such as a cytokine storm.
Why the study?
SARS-CoV-2 has a significant impact on the cardiovascular system, motivating a review of worldwide clinical experiences regarding the presentation, diagnosis, and treatment of COVID-19-induced myocarditis.
This review summarizes the clinical presentation, mechanisms, and supportive treatment approaches for COVID-19-induced myocarditis.
May warrant myocarditis monitoring in COVID-19; leaves open need for prospective studies to confirm mechanisms and guide therapy.
Based on the clinical experience, it has been observed that when it comes to the impact of SARS-CoV-2 virus on the cardiovascular system, it is significant. In patients with COVID-19 infection, the development of myocarditis occurs a few days after the onset of fever. The mechanism of myocardial injury alone, as well as most pathologies caused by the SARS-CoV-2 virus, is the subject of research by many experts, but two basic ways can certainly be assumed: a direct toxic effect of SARS-CoV-2 on myocardial cells and another possible way of myocardial injury is to activate the innate immune response by releasing proinflammatory cytokines, as well as to activate the adaptive mechanisms of the autoimmune type by molecular mimicry. The approach to treatment is the same as for other viral myocarditis; it is non-specific, applied supportive treatment, such as anti-inflammatory drugs, low-dose corticosteroid therapy, and immunoglobulins. The aim of this review is to present the previous experiences of physicians around the world on the clinical presentation of myocarditis caused by COVID-19 infection, diagnostic and therapeutic approach in a specific situation of high-risk infection.
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Maričić et al. (2021) conducted a review in COVID-19 associated myocarditis. COVID-19 was evaluated. COVID-19 infection is associated with the development of myocarditis, likely driven by direct viral toxicity and systemic immune-mediated mechanisms such as a cytokine storm.
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