Miocarditis in Patients with COVID-19 Confirmed by Immunohistochemical

Abstract

Aim Despite the regular heart damage in patients with coronavirus pneumonia caused by SARS-Cov-2, a possibility of developing lymphocytic myocarditis as a part of COVID-19 remains unsubstantiated. The aim of this study was to demonstrate a possibility of lymphocytic myocarditis and to study its morphological features in patients with the novel coronavirus infection (COVID-19) with a severe course.Material and methods Postmortem data were studied for 5 elderly patients (74.8±4.4 years; 3 men and 2 women) with the novel coronavirus infection and bilateral, severe polysegmental pneumonia (stage 3–4 by computed tomography). COVID-19 was diagnosed based on the typical clinical presentation and positive polymerase chain reaction test in nasopharyngeal swabs. All patients were treated in different hospitals repurposed for the treatment of patients with COVID-19. A standard histological study was performed with hematoxylin and eosin, toluidine blue, and van Gieson staining. Serial paraffin slices were studied immunohistochemically with antibodies to CD3, СD68, CD20, perforin, and toll-like receptors (TLR) 4 and 9.Results In none of the cases, myocarditis was suspected clinically, added to the diagnosis or indicated as a possible cause of death. IHD and acute myocardial infarction were mentioned as error diagnoses not confirmed by the postmortem examination. The morphological examination of the heart identified signs of lymphocytic myocarditis consistent with Dallas criteria for this diagnosis. Myocardial infiltrate was characterized in detail, and a combined inflammatory damage of endocardium and pericardium was described. The immunohistochemical study with cell infiltrate typing confirmed the presence of CD3-positive Т lymphocytes and the increased expression of TLR-4. A picture of coronaritis, including that with microvascular thrombosis, was found in all cases.Conclusion A possibility for development of lymphocytic viral myocarditis in COVID-19 was confirmed morphologically and immunohistochemically. Specific features of myocarditis in COVID-19 include the presence of coronaritis and a possible combination of myocarditis with lymphocytic endo- and pericarditis.

Anti‐heart antibodies levels and their correlation with clinical symptoms and outcomes in patients with confirmed or suspected diagnosis COVID‐19

“…COVID‐19 has features common to many other viral infections. Thus, we observed increased expression of TLRs especially type 4 and also type 9 in patients with severe (fatal) COVID‐19, which indicates activation of antiviral innate immunity [2]. Inflammatory and immune reactions includes increasing levels of ILs 1, 2, 6, 7, 10, 12, 18, TNF‐α, gamma IFN, VEGF, and other biomarkers [3].…”

Anticardiac antibodies in patients with severe and moderate COVID-19 (correlations with the clinical performance and prognosis)

“…Морфологические особенности миокардита позволяют думать не только о прямом вирусном, но и об ишемическом повреждении миокарда: выявлены васкулит с облитерацией микрососудов, периваскулярный склероз [15]. В нашей серии аутопсий у больных с COVID-19 выявлен лимфоцитарный миокардит с очень сходными характеристиками, включая инфильтрацию CD3+ и CD45+ клетками (при отсутствии CD20+ и NK клеток) и активацию врожденных механизмов противовирусного иммунитета, о чем свидетельствует повышенная экспрессия toll-подобных рецепторов 4-го и 9-го типов [10]. При этом во всех случаях нами подтверждено наличие вирусной РНК в миокарде.…”

“…Перикардит четко коррелировал с общей активностью заболеваниявысотой лихорадки, уровнем воспалительных маркеров, а также тяжестью пневмонии по данным КТ (r=0,64), что позволяет расценивать его как парапневмонический. В то же время сильная корреляция с уровнем АНФ и АтК, лимфоцитарная природа перикардита [10] и наличие вирусного генома в миокарде у этих больных (по нашим данным) говорят о самостоятельном вирусно-иммунном поражении.…”

“…С другой стороны, у больных с тяжелым течением COVID-19 снижается количество CD4+ и CD8+ Т-лимфоцитов, что сближает SARS-Cov-2 с вирусом иммунодефицита человека [9]. Выявляются и общие для многих вирусных инфекций закономерности: у больных с тяжелым (фатальным) течением COVID-19 мы наблюдали повышенную экспрессию toll-подобных рецепторов 9-го и особенно 4-го типов, которая свидетельствует об активации врожденного противовирусного иммунитета [10].…”

Troponina-T e Peptídeo Natriurético tipo B na COVID-19

“…2 O comprometimento miocárdico é um problema cardíaco comum e a miocardite imunológica é uma importante manifestação grave da COVID-19. 3 Portanto, a troponina-T, que é um bom biomarcador de lesão miocárdica, pode ter um bom fator prognóstico para a gravidade da COVID-19. No entanto, deve-se notar que problemas renais também podem induzir alterações da troponina-T 4 Se o paciente tiver um problema renal subjacente, a interpretação da troponina-T em pacientes com COVID-19 deve ser cuidadosa.…”