What we (don’t) know about myocardial injury after COVID-19

European Heart Journal, Volume 42, Issue 19, 14 May 2021, Pages 1879- 1882, https://doi.org/10.1093/eurheartj/ehab145  Published: 13 March 2021

The frequency of cardiac injury among hospitalized patients with acute coronavirus disease 2019 (COVID-19) is estimated at 13–41% as defined by elevated troponin levels.1 Evidence of cardiac involvement in hospitalized COVID-19 patients is significant because cardiac injury is associated with higher mortality.2,3 Multiple mechanisms can lead to cardiac damage, including demand ischaemia, systemic hypoxia, intravascular thrombosis and endotheliitis, and myocarditis. Myocardial inflammation can result from both a systemic inflammatory response4 and, less commonly, direct viral injury. Because of a low rate of histological inflammation associated with the presence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) in the tissue on autopsy or endomyocardial biopsy, some have questioned whether COVID-19-related myocarditis exists. Cardiovascular injury from COVID-19 in children and adolescents is much less common than rates seen in cohorts of older patients and includes a multisystem inflammatory syndrome (termed MIS-C) with higher rates of myocarditis and arterial aneurysms.5

Following recovery from the acute COVID-19 illness, shortness of breath and fatigue may persist. In a recent study, 64% of patients 2–3 months after COVID-19 reported dyspnoea and fatigue, an incidence much higher than after other viral diseases.6 The reasons for ‘long COVID’ are not well understood, but are associated with signs of ongoing inflammation as well as tissue abnormalities of the lungs, heart, and kidneys as identified by magnetic resonance imaging (MRI).7

Cardiovascular magnetic resonance (CMR) is the non-invasive gold standard for the assessment of myocardial tissue pathology, especially myocardial oedema, which is not possible by other imaging modalities. Specifically, CMR is highly accurate to diagnose acute myocarditis when published consensus criteria are used.8 Myocardial oedema assessed with T2-weighted sequences provides a unique role for MRI in the non-invasive cardiac assessment of patients with suspected ongoing inflammation.9

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