Reference: Ali Razaghi, Attila Szakos, Riham Al-Shakarji, Mikael Björnstedt & Laszlo Szekely (2022) Morphological changes without histological myocarditis in hearts of COVID-19 deceased patients, Scandinavian Cardiovascular Journal, 56:1, 166-173, DOI: 10.1080/14017431.2022.2085320 https://doi.org/10.1080/14017431.2022.2085320
Link to full downloadable pdf.
No evidence of specific myocarditis pathology:
“To detect the presence of the Sars-Cov-2 virus in the heart of Covid-19 patients, RNAscope was conducted. However, replicating [the] SARS-CoV-2 virus was not detected in the heart of Covid-19 patients (Figure 6). In contrast, the presence of replicating the Sars-CoV-2 virus was readily detected in the lung tissue in the same individuals (Figure 7)… RNA in situ hybridization could not detect virus replication in the heart of Covid-19 victims. The negative RNA in situ hybridization coupled with the positive localization in the lung does favor the hypothesis of a systemic mechanism for the cardiac changes. Furthermore, any sign of virus-induced cytopathic effects or any antiviral lymphocytic reaction typical for viral myocarditis was not detected in any cases. Also, signs of antiviral inflammation were not observed.”
“Histological examination of Covid-19 heart victims (37 cases) revealed subtle to severe signs of acute myocardial hypoxia in all cases. Three patients had AMI [acute myocardial infarction] due to Covid-19 independent coronary thrombosis. All patients showed signs of endothelial activation and half of them showed prolonged signs of severe cardiac hypoxia. The presence of Sars-CoV-2 virus, virus-induced tissue damage, or virus induced inflammatory response was not detected in any of the heart tissues. Particularly, lymphocyte infiltration, as a hallmark of myocarditis, was not seen in any cases of this study. Thus, any sign of histological myocarditis was not proved in our Covid-19 victims’ cohort of the study. These findings are mostly congruent with the hypothesis that most cardiac damage is due to generalized hypoxia, and endothelial leakage is likely due to the presence of circulating endothelium activating factor, e.g. VEGF, originating outside of the heart, most probabl[y] from the hypoxic part of the Covid-19 lungs.”
Abstract, with overview of design: