2023
DOI: 10.1002/jmri.28668
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Low Prevalence of Late Myocardial Injury on Cardiac MRI Following COVID‐19 Infection

Abstract: BackgroundThe prevalence of abnormal cardiac magnetic resonance imaging (MRI) findings indicative of myocardial injury in patients who recovered from coronavirus disease 2019 (COVID‐19) is currently unclear, with a high variability in the reported prevalence.PurposeTo assess the prevalence of myocardial injury after a COVID‐19 infection.Study TypeProspective, bicentric study.SubjectsSeventy consecutive patients who recovered from COVID‐19 and were previously hospitalized. Mean age was 57 years and 39% of the p… Show more

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(1 citation statement)
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“…Importantly, it is well known that angiotensin-converting enzyme 2 plays a central role in the processes of inflammation, oxidative stress, vasoconstriction and fibrosis [18], as well as the affinity of SARS-CoV 2 virus to angiotensin-converting enzyme 2 receptor with the hyperactivation of the renin-angiotensin-aldosterone system, thereby promoting the inflammation process [19]. The mixed effect of the direct viral effect and the inflammation process with cytokine storm, endothelitis and thrombosis occurring at different stages in the evolution of the disease represent the substrate for cardiac injury [10] Subsequently, some patients recovering from COVID-19 may develop long-term consequences with a variable prevalence at different time points [20]. For example, post-COVID lymphocytic and eosinophilic myocarditis was reported between one and five months following the acute infection, with SARS-CoV-2 ribonucleic acid (RNA) being detected in association with parvovirus B19 DNA [21].…”
Section: Acute and Delayed Myocardial Injurymentioning
confidence: 99%
“…Importantly, it is well known that angiotensin-converting enzyme 2 plays a central role in the processes of inflammation, oxidative stress, vasoconstriction and fibrosis [18], as well as the affinity of SARS-CoV 2 virus to angiotensin-converting enzyme 2 receptor with the hyperactivation of the renin-angiotensin-aldosterone system, thereby promoting the inflammation process [19]. The mixed effect of the direct viral effect and the inflammation process with cytokine storm, endothelitis and thrombosis occurring at different stages in the evolution of the disease represent the substrate for cardiac injury [10] Subsequently, some patients recovering from COVID-19 may develop long-term consequences with a variable prevalence at different time points [20]. For example, post-COVID lymphocytic and eosinophilic myocarditis was reported between one and five months following the acute infection, with SARS-CoV-2 ribonucleic acid (RNA) being detected in association with parvovirus B19 DNA [21].…”
Section: Acute and Delayed Myocardial Injurymentioning
confidence: 99%