Key result
Cardiac autopsies of 12 ICU-naïve COVID-19 patients revealed widespread platelet and fibrin thrombi, perivascular inflammation, and SARS-CoV-2 viral components in the myocardium.
Why the study?
Myocardial damage contributes to COVID-19 morbidity and mortality, creating a demand to visualize viral components within tissue specimens.
Observational (n=12)
No
Autopsy findings demonstrate direct cardiac involvement in COVID-19, characterized by viral protein localization, microthrombi, and myocardial inflammation, which may contribute to cardiac ischemia and remodeling.
Answers are grounded in this paper and cite their sources.
Supports direct cardiac involvement in non-critical COVID-19; hypothesis-generating and should not yet change practice.
Coronavirus disease-19 (COVID-19) is caused by the newly discovered coronavirus, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). While the lung remains the primary target site of COVID-19 injury, damage to myocardium, and other organs also contribute to the morbidity and mortality of this disease. There is also increasing demand to visualize viral components within tissue specimens. Here we discuss the cardiac autopsy findings of 12 intensive care unit (ICU) naïve and PCR-positive COVID-19 cases using a combination of histological, Immunohistochemical/immunofluorescent and molecular techniques. We performed SARS-CoV-2 qRT-PCR on fresh tissue from all cases; RNA-ISH and IHC for SARS-CoV-2 were performed on selected cases using FFPE tissue from heart. Eight of these patients also had positive post-mortem serology for SARS-CoV-2. Histopathologic changes in the coronary vessels and inflammation of the myocardium as well as in the endocardium were documented which support the reports of a cardiac component to the viral infection. As in the pulmonary reports, widespread platelet and fibrin thrombi were also identified in the cardiac tissue. In keeping with vaccine-induced activation of virus-specific CD4 + and CD8 + T cells, and release of cytokines such as interferon-gamma (IFNγ), we observed similar immune cellular distribution and cytokines in these patients. Immunohistochemical and immunofluorescent localisation for the viral Spike (S-protein) protein and the nucleocapsid protein (NP) were performed; presence of these aggregates may possibly contribute to cardiac ischemia and even remodelling.
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Chong et al. (2021) conducted an observational in COVID-19 (n=12). SARS-CoV-2 infection was evaluated on Cardiac histopathologic changes and viral detection. Cardiac autopsies of 12 ICU-naïve COVID-19 patients revealed widespread platelet and fibrin thrombi, perivascular inflammation, and SARS-CoV-2 viral components in the myocardium.
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