Cardiac recovery from COVID-19-associated fulminant myocarditis by extracorporeal biventricular assist.

We report a case of cardiac recovery from coronavirus disease 2019 (COVID-19)-associated fulminant myocarditis in a 48-year-old woman diagnosed with COVID-19 infection 4 days before, whose hemodynamic collapse were resuscitated first with venoarterial extracorporeal membranous oxygenation, followed by escalation to extracorporeal biventricular assist devices (ex-BiVAD) using two centrifugal pumps and an oxygenator. She was likely to be multisystem inflammatory syndrome in adults (MIS-A) negative. Cardiac contractility gradually recovered after the 9th day of ex-BiVAD support, and the patient was successfully weaned from ex-BiVAD on the 12th day of support. Due to postresuscitation encephalopathy, she was transferred to the referral hospital for rehabilitation with recovered cardiac function. The histopathology of the myocardial tissue showed smaller amounts of lymphocytes and more infiltration of macrophages. It is important to recognize two phenotypes of MIS-A+ or MIS-A-, with distinct manifestations and outcomes. It is also important to refer urgently such patients with COVID-19-associated fulminant myocarditis, showing different histopathology from usual viral myocarditis, with evolution toward refractory cardiogenic shock to a center with capability for advanced mechanical support to avoid a too-late cannulation. Learning objective: We should recognize the clinical course and histopathology of the multisystem inflammatory syndrome in adults phenotype of coronavirus disease 2019-associated fulminant myocarditis. We should urgently refer such patients with evolution toward refractory cardiogenic shock to a center with capability for advanced mechanical support, such as venoarterial extracorporeal membrane oxygenation, Impella (Abiomed, Danvers, MA, USA), and extracorporeal biventricular assist devices.

Elevated Myl9 reflects the Myl9-containing microthrombi in SARS-CoV-2-induced lung exudative vasculitis and predicts COVID-19 severity.

The mortality of coronavirus disease 2019 (COVID-19) is strongly correlated with pulmonary vascular pathology accompanied by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection-triggered immune dysregulation and aberrant activation of platelets. We combined histological analyses using field emission scanning electron microscopy with energy-dispersive X-ray spectroscopy analyses of the lungs from autopsy samples and single-cell RNA sequencing of peripheral blood mononuclear cells to investigate the pathogenesis of vasculitis and immunothrombosis in COVID-19. We found that SARS-CoV-2 accumulated in the pulmonary vessels, causing exudative vasculitis accompanied by the emergence of thrombospondin-1-expressing noncanonical monocytes and the formation of myosin light chain 9 (Myl9)-containing microthrombi in the lung of COVID-19 patients with fatal disease. The amount of plasma Myl9 in COVID-19 was correlated with the clinical severity, and measuring plasma Myl9 together with other markers allowed us to predict the severity of the disease more accurately. This study provides detailed insight into the pathogenesis of vasculitis and immunothrombosis, which may lead to optimal medical treatment for COVID-19.

An autopsy case report of fulminant myocarditis: Following mRNA COVID-19 vaccination.

There have been few case reports on fatal outcomes in patients with acute myocarditis after mRNA coronavirus disease 2019 (COVID-19) vaccination. In most cases of myocarditis after mRNA COVID-19 vaccination, the myocarditis is mild, and the prognosis is good. Here we report an autopsy case of fulminant myocarditis following mRNA COVID-19 vaccination. Learning objective: The global distribution of the mRNA coronavirus disease 2019 vaccine requires consideration of appropriate treatment for postvaccination myocarditis. Eosinophil-mediated immunological injury to cardiomyocytes can be involved in the cause of fulminant inflammation from the pathological findings of postvaccination myocarditis.

Fatal disseminated mucormycosis associated with COVID-19.

Secondary fungal infections are a critical problem that accompany immunosuppressive therapy for severe coronavirus disease 2019 (COVID-19). We report a fatal case of COVID-19 with disseminated mucormycosis diagnosed during autopsy. A 58-year-old man with diabetes was hospitalized for severe COVID-19 and treated with remdesivir, systemic steroids and tocilizumab. Following treatment, he was provided extracorporeal membrane oxygenation support. However, he died of multiple organ failure accompanied by pulmonary and kidney infarction, as revealed by computed tomography. Autopsy revealed that the infarction was caused by thromboangiitis due to mucormycosis in the brain, lungs, heart, liver and kidneys. Therefore, the diagnosis of disseminated mucormycosis was established. Disseminated mucormycosis is a rare complication of COVID-19. Although its early diagnosis is difficult, the disease progresses rapidly. Hence, we propose that immunosuppressive treatment for COVID-19 should be administered with caution considering the risk of developing severe opportunistic infections, such as mucormycosis.

Lung Pathology of Mutually Exclusive Co-infection with SARS-CoV-2 and Streptococcus pneumoniae.

Postmortem lung pathology of a patient in Japan with severe acute respiratory syndrome coronavirus 2 infection showed diffuse alveolar damage as well as bronchopneumonia caused by Streptococcus pneumoniae infection. The distribution of each pathogen and the accompanying histopathology suggested the infections progressed in a mutually exclusive manner within the lung, resulting in fatal respiratory failure.