COVID-19 and myocarditis: a review of literature

Abstract

Myocarditis has been discovered to be a significant complication of coronavirus disease 2019 (COVID-19), a condition caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus. COVID-19 myocarditis seems to have distinct inflammatory characteristics, which make it unique to other viral etiologies. The incidence of COVID-19 myocarditis is still not clear as a wide range of figures have been quoted in the literature; however, it seems that the risk of developing myocarditis increases with more severe infection. Furthermore, the administration of the mRNA COVID-19 vaccine has been associated with the development of myocarditis, particularly after the second dose. COVID-19 myocarditis has a wide variety of presentations, ranging from dyspnea and chest pain to acute heart failure and possibly death. It is important to catch any cases of myocarditis, particularly those presenting with fulminant myocarditis which can be characterized by signs of heart failure and arrythmias. Initial work up for suspected myocarditis should include serial troponins and electrocardiograms. If myocardial damage is detected in these tests, further screening should be carried out. Cardiac magnetic resonance imagining and endomyocardial biopsy are the most useful tests for myocarditis. Treatment for COVID-19 myocarditis is still controversial; however, the use of intravenous immunoglobulins and corticosteroids in combination may be effective, particularly in cases of fulminant myocarditis. Overall, the incidence of COVID-19 myocarditis requires further research, while the use of intravenous immunoglobulins and corticosteroids in conjunction requires large randomized controlled trials to determine their efficacy.

Long-term effect of SARS-CoV-2 infection on cardiovascular outcomes and all-cause mortality

“…Since arrhythmic events have been reported in patients with no previous clinical history [41] , increased arrhythmic complications should be sought in sequelae of SARS-CoV-2 on the heart. Several mechanisms have now been proposed and myocarditis is plausible [42] , [43] . Although there is a desperate need to understand the pathological mechanisms triggered by the virus, the investigation is challenging due to pauci-symptomatic or asymptomatic cases, which leads to underestimating the real incidence of myocarditis [43] .…”

“…Several mechanisms have now been proposed and myocarditis is plausible [42] , [43] . Although there is a desperate need to understand the pathological mechanisms triggered by the virus, the investigation is challenging due to pauci-symptomatic or asymptomatic cases, which leads to underestimating the real incidence of myocarditis [43] . Whilst the literature in this field has been conflicting at times, one of most comprehensive analysis to date has estimated a prevalence for definite/probable acute myocarditis (AM) of 2.4 per 1000 hospitalizations [44] that increases to 4.1 considering also possible AM cases.…”

“…Overall, the aforementioned characteristics lead to myocardial damage, thus inducing remodeling and fibrosis that contribute to conduction system dysfunction as emerged at echocardiogram evaluation [43] , [48] . Furthermore, nerve inflammation, or inflammatory neuropathy, is involved in the degeneration of ganglia and neuronal fibers increasing the incidence of arrhythmic complications [47] , [49] .…”

Cardiac MRI in post COVID acute myocarditis: A case report

“…Regarding the clinical management of COVID-19-related myocarditis, studies are yet inconclusive to follow a regular treatment option in particular. Nevertheless, intravenous immunoglobulins (IVIG) and corticosteroids in combination have been widely used with an effective outcome so far [11] . Our patient received similar medical treatment in addition to antiarrhythmics and beta-blockers with an uneventful hospital stay.…”

Myocardite à COVID-19 : « à propos d'une série monocentrique de 33 cas »

“…Elle est d'origine ischémique (fracture de la plaque liée au stress inflammatoire, thrombose in situ ou embolie coronaire liée à l'hypercoagulabilité) ou non ischémique (myocardite le plus souvent fulminante) [ 10 , 12 ]. Les biopsies myocardiques (le plus souvent post-mortem) confirment l'existence d'un infiltrat inflammatoire lymphocytaire [ 13 , 14 ].…”