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Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases

Educational Objective
To understand the association of cardiac infection with SARS-CoV-2 in confirmed COVID-19 autopsy cases
1 Credit CME
Key Points

Question  Can severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) be documented in cardiac tissue of coronavirus disease 2019 (COVID-19) autopsy cases?

Findings  In this cohort study of 39 autopsy cases of patients with COVID-19, cardiac infection with SARS-CoV-2 was found to be frequent but not associated with myocarditislike influx of inflammatory cells into the myocardium.

Meaning  Among individuals with cardiac infection, overt myocarditis was not observed in the acute phase, but the long-term consequences of this cardiac infection needs to be studied.

Abstract

Importance  Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) can be documented in various tissues, but the frequency of cardiac involvement as well as possible consequences are unknown.

Objective  To evaluate the presence of SARS-CoV-2 in the myocardial tissue from autopsy cases and to document a possible cardiac response to that infection.

Design, Setting, and Participants  This cohort study used data from consecutive autopsy cases from Germany between April 8 and April 18, 2020. All patients had tested positive for SARS-CoV-2 in pharyngeal swab tests.

Exposures  Patients who died of coronavirus disease 2019.

Main Outcomes and Measures  Incidence of SARS-CoV-2 positivity in cardiac tissue as well as CD3+, CD45+, and CD68+ cells in the myocardium and gene expression of tumor necrosis growth factor α, interferon γ, chemokine ligand 5, as well as interleukin-6, -8, and -18.

Results  Cardiac tissue from 39 consecutive autopsy cases were included. The median (interquartile range) age of patients was 85 (78-89) years, and 23 (59.0%) were women. SARS-CoV-2 could be documented in 24 of 39 patients (61.5%). Viral load above 1000 copies per μg RNA could be documented in 16 of 39 patients (41.0%). A cytokine response panel consisting of 6 proinflammatory genes was increased in those 16 patients compared with 15 patients without any SARS-CoV-2 in the heart. Comparison of 15 patients without cardiac infection with 16 patients with more than 1000 copies revealed no inflammatory cell infiltrates or differences in leukocyte numbers per high power field.

Conclusions and Relevance  In this analysis of autopsy cases, viral presence within the myocardium could be documented. While a response to this infection could be reported in cases with higher virus load vs no virus infection, this was not associated with an influx of inflammatory cells. Future investigations should focus on evaluating the long-term consequences of this cardiac involvement.

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Article Information

Corresponding Author: Dirk Westermann, MD, University Heart and Vascular Centre Hamburg, Department of Cardiology, Martinistr. 52, 20246 Hamburg, Germany (d.westermann@uke.de).

Accepted for Publication: June 29, 2020.

Published Online: July 27, 2020. doi:10.1001/jamacardio.2020.3551

Author Contributions: Drs Westermann and Lindner had full access to all of the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Lindner, Scherschel, Westermann.

Acquisition, analysis, or interpretation of data: Lindner, Fitzek, Bräuninger, Aleshcheva, Edler, Meißner, Kirchhof, Escher, Schultheiss, Blankenberg, Püschel, Westermann.

Drafting of the manuscript: Lindner, Westermann.

Critical revision of the manuscript for important intellectual content: Fitzek, Bräuninger, Aleshcheva, Edler, Meißner, Scherschel, Kirchhof, Escher, Schultheiss, Blankenberg, Püschel, Westermann.

Statistical analysis: Lindner, Westermann.

Obtained funding: Lindner, Aleshcheva, Westermann.

Administrative, technical, or material support: Lindner, Bräuninger, Aleshcheva, Edler, Meißner, Scherschel, Escher, Püschel, Westermann.

Supervision: Escher, Schultheiss, Blankenberg, Westermann.

Conflict of Interest Disclosures: Dr Kirchhof reports grants and nonfinancial support for basic, translational, and clinical research projects from European Union, British Heart Foundation, Leducq Foundation, Medical Research Council (UK), and German Centre for Cardiovascular Research; and is an inventor on 2 patents held by University of Birmingham (Atrial Fibrillation Therapy WO 2015140571, Markers for Atrial Fibrillation WO 2016012783) outside the submitted work. Dr Escher reported personal fees from IKDT Berlin outside the submitted work. Dr Blankenberg reports grants and personal fees from Abbott Diagnostics, Bayer, Siemens, and Thermo Fisher; grants from Singulex; and personal fees from AstraZeneca, Amgen, Medtronic, Pfizer, Roche, Novartis, Abbott, and Siemens DX outside the submitted work. Dr Westermann reported personal fees from AstraZeneca, Bayer, Novartis, and Medtronic outside the submitted work. No other disclosures were reported.

Funding/Support: This study was supported by the grant to Drs Westermann and Lindner from the Deutsche Herzstiftung and by the German Center of Cardiovascular Research (DZHK).

Role of the Funder/Sponsor: The funders had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication.

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