Faculty, Staff and Student Publications

Language

English

Publication Date

4-1-2021

Journal

JACC: Basic to Translational Science

DOI

10.1016/j.jacbts.2021.01.002

PMID

33681537

PMCID

PMC7909907

PubMedCentral® Posted Date

February 2021

PubMedCentral® Full Text Version

Post-print

Abstract

There is ongoing debate as to whether cardiac complications of coronavirus disease-2019 (COVID-19) result from myocardial viral infection or are secondary to systemic inflammation and/or thrombosis. We provide evidence that cardiomyocytes are infected in patients with COVID-19 myocarditis and are susceptible to severe acute respiratory syndrome coronavirus 2. We establish an engineered heart tissue model of COVID-19 myocardial pathology, define mechanisms of viral pathogenesis, and demonstrate that cardiomyocyte severe acute respiratory syndrome coronavirus 2 infection results in contractile deficits, cytokine production, sarcomere disassembly, and cell death. These findings implicate direct infection of cardiomyocytes in the pathogenesis of COVID-19 myocardial pathology and provides a model system to study this emerging disease.

Keywords

cardiomyocyte, coronavirus disease 2019, engineered heart tissue, myocarditis, severe acute respiratory syndrome coronavirus 2

Published Open-Access

yes

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