Do COVID-19 viral infection and its mRNA vaccine carry an equivalent risk of myocarditis? Review of the current evidence, insights, and future directions

Abstract

According to recent epidemiological analysis, the percentage of world population infected with COVID-19 by end of December 2020 is approximately 12.56%¹. COVID induced acute care and ICU hospitalization rates are around 9.22 (95% CI: 18.73-19.51), and 4.14 (95% CI: 4.10-4.18) per 1000 population¹. Although therapeutic strategies such as antivirals, intravenous immunoglobulins and corticosteroids have shown modest efficacy in reducing the disease progression, they are not disease specific and only temper the immune mediated attack on the systemic tissues. Therefore, clinicians started to rely on mRNA COVID-19 vaccines, which are clinically efficacious in reducing the incidence, disease severity and systemic complications of COVID-19 infections. Nevertheless, usage of COVID-19 mRNA vaccines is also associated with cardiovascular complications such as myocarditis and pericarditis. On the other hand, COVID-19 infections itself are associated with cardiovascular complications such as myocarditis. The underlying signaling pathways for occurrence of COVID-19 and mRNA COVID-19 vaccine induced myocarditis are quite different although there is some overlap in autoimmunity and cross reactivity mechanisms. With media reports highlighting the cardiovascular complications of COVID-19 vaccines such as myocarditis, general population have become more hesitant and uncertain regarding the safety and efficacy of these mRNA vaccines. We plan to review the current literature and provide insights into their pathophysiological mechanisms for myocarditis and offer recommendations for further research studies in this regard. This will hopefully dispel some doubts and encourage more people to be vaccinated for preventing the risk of COVID-19 induced myocarditis and other associated cardiovascular complications.

Keywords: Adaptive immunity; Autoantibodies; Autoimmunity; Autoreactive T-cells; COVID-19 infection; COVID-19 mRNA vaccine; Inflammation; Innate immunity; Myocarditis; Spike protein.