Abstract

Introduction: COVID-19 has a significant effect upon the cardiovascular system including small amounts of myocyte death in some patients resulting in elevated troponin levels. While a number of different cardiovascular histopathologies have been described at post-mortem examination, the incidence of typical viral myocarditis in COVID-19 positive patients appears very low. Hypothesis: We hypothesized that COVID-19 causes a different type of inflammatory cell response that although different, may still cause significant negative effects on the cardiovascular system. Methods: Using immunoperoxidase staining, we characterized and quantified the number of CD3 + , CD4 + , CD8 + , CD68 + staining cells in 10 COVID-19 hearts, 10 hearts matched for age and underlying comorbidities, and 5 hearts with autopsy proven typical inflammatory myocarditis. Results: The results demonstrate a skewed distribution of the number of CD68+ cells in COVID-19 hearts, with upper quantiles showing a significant increase as compared to both matched control hearts, and those with myocarditis. In contrast, hearts from typical inflammatory myocarditis contained increased numbers of CD4+, and CD8+ cells compared to both COVID-19 and control cohorts. . Conclusions: In conclusion, the presence of an increased number of CD68+ cells suggests that COVID-19 may incite a form of myocarditis different from typical viral myocarditis, and associated with diffusely infiltrative cells of monocytes/macrophage lineage.

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