COVID-19 myocarditis: quantitative analysis of the inflammatory infiltrate and a proposed mechanism *

COVID-19 has a significant effect upon the cardiovascular system. 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 [1-3] . In this study, we further characterize and quantify the inflammatory cell infiltrate in a COVID-19 study cohort and compare the findings to both an age and disease matched control cohort and a cohort of patients diagnosed with typical inflammatory myocarditis. All study and control cohorts had 1 or more of the comorbidities most commonly associated with severe disease (hypertension, type II diabetes, obesity, or known cardiovascular disease). 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. 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. (c) 2021 Elsevier Inc. All rights reserved.

Automated summary

This study characterizes and quantifies the inflammatory cell infiltrate in COVID-19 patients' hearts and compares it with age and disease-matched controls and patients with typical inflammatory myocarditis. The results suggest that COVID-19 may cause a different form of myocarditis characterized by an increased number of CD68+ cells compared to typical viral myocarditis.