Clinical, morphological and molecular biological examination of the myocardium in COVID-19 patients

Abstract

The presence of coronavirus-associated myocarditis remains controversial despite elevations in cardiac troponin and natriuretic peptide in many patients.Aim. To assess the morphological changes in the myocardium of patients who died due to coronavirus disease 2019 (COVID-19) and compare them with the intravital level of cardiac biomarkers.Material and methods. A total of 420 hospital charts and 77 autopsies of those who died from COVID-19 were analyzed. In 15 of 77 cases (19%) with histologically suspected myocarditis, an immunohistochemical examination of the myocardium with antibodies to CD3, CD45, CD8, CD68, CD34, Ang1, VWF, VEGF, HLA-DR, MHC1, C1q, VP1 of enteroviruses was performed, and in 8 patients with immunohistochemically confirmed myocarditis (10%) — polymerase chain reaction for SARS-CoV-2.Results. Hemorrhage, intramural thrombosis, necrosis of non-coronary origin, myocardial infarction and lymphocytic myocarditis were detected in 43%, 10%, 17%, 19% and 10% of cases, respectively, without coronavirus N and E gene sequences in the myocardium. Dysplasia, hyperplasia and hypertrophy of the vascular endothelium, expression of Ang1, VWF, VEGF, MHC1, C1q, VP1 of enteroviruses were determined in 100, 100, 87, 100, 75 and 62% of cases of myocarditis, respectively. There were no significant correlations between inflammatory biomarkers and myocarditis.Conclusion. The main morphological manifestation of COVID-19 in the myocardium is the so-called endotheliitis with dysplasia and endothelial activation, leading to hemorrhages, intramural thrombosis and necrosis. There is no convincing evidence of a direct involvement of coronavirus in myocarditis induction.

COVID-19 Heart Lesions in Children: Clinical, Diagnostic and Immunological Changes

“…At the same time, no significant association was found between inflammatory markers and morphologically by confirmed myocarditis, and no convincing evidence was obtained on the direct involvement of the SARS-CoV-2 virus in the induction of myocarditis. This fact once again confirms the theory of the pathogenesis of a severe course of COVID-19, based on predominantly immune damage to the vascular endothelium and the formation of microthrombosis [ 48 ].…”

“…There was myocardial damage in the range of 13–41% in hospitalized adult patients with COVID-19 which causes high mortality from cardiovascular complications [ 48 ]. However, current data on the tropism of SARS-CoV-2 to the myocardium is different.…”

Morphological Changes in the Myocardium of Patients with Post-Acute Coronavirus Syndrome: A Study of Endomyocardial Biopsies

“…These changes are associated with the repair of the consequences of cytokine imbalance and angiopathy in the acute phase of coronavirus infection, which leads to post-acute sequelae of SARS-CoV-2 infection (PASC), as evidenced by the decrease in the expression level of endothelial activation markers such as VEGF, VWF, Ang1, and C1q. In our previous study, we showed that the expression levels of these markers increase in the acute phase of coronavirus infection [ 28 ]. This is consistent with the literature data that myocardial damage in the acute phase of the coronavirus infection is due to systemic manifestations of cytokine storm and generalized angiopathy [ 19 , 29 , 30 , 31 ].…”

Clinical and morphological myocardial changes in patients with post-COVID-19 syndrome

“…Кроме того, повреждение эндотелия может привлекать моноциты, активирующие путь комплемента и вызывающие апоптотическое повреждение кардиомиоцитов, инициированное макрофагами [15]. В предыдущих исследованиях мы показали, что основными морфологическими изменениями в остром периоде COVID-19 является эндотелиит и его осложнения в виде тромбозов и кровоизлияний [16,17]. А в ряде исследований наряду с ангиопатией острого периода показано значимое увеличение CD68 + -макрофагов в ткани миокарда в остром периоде COVID-19 [15,18].…”