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Review
. 2021 Jan 26;77(3):314-325.
doi: 10.1016/j.jacc.2020.11.031.

Pathological Evidence for SARS-CoV-2 as a Cause of Myocarditis: JACC Review Topic of the Week

Rika Kawakami  1 , Atsushi Sakamoto  1 , Kenji Kawai  1 , Andrea Gianatti  2 , Dario Pellegrini  2 , Ahmed Nasr  2 , Bob Kutys  1 , Liang Guo  1 , Anne Cornelissen  1 , Masayuki Mori  1 , Yu Sato  1 , Irene Pescetelli  2 , Matteo Brivio  2 , Maria Romero  1 , Giulio Guagliumi  2 , Renu Virmani  1 , Aloke V Finn  3
Affiliations
Review

Pathological Evidence for SARS-CoV-2 as a Cause of Myocarditis: JACC Review Topic of the Week

Rika Kawakami et al. J Am Coll Cardiol. .

Abstract

To investigate whether severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2)-induced myocarditis constitutes an important mechanism of cardiac injury, a review was conducted of the published data and the authors' experience was added from autopsy examination of 16 patients dying of SARS-CoV-2 infection. Myocarditis is an uncommon pathologic diagnosis occurring in 4.5% of highly selected cases undergoing autopsy or endomyocardial biopsy. Although polymerase chain reaction-detectable virus could be found in the lungs of most coronavirus disease-2019 (COVID-19)-infected subjects in our own autopsy registry, in only 2 cases was the virus detected in the heart. It should be appreciated that myocardial inflammation alone by macrophages and T cells can be seen in noninfectious deaths and COVID-19 cases, but the extent of each is different, and in neither case do such findings represent clinically relevant myocarditis. Given its extremely low frequency and unclear therapeutic implications, the authors do not advocate use of endomyocardial biopsy to diagnose myocarditis in the setting of COVID-19.

Keywords: COVID-19; SARS-CoV-2; cardiovascular disease; heart.

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Conflict of interest statement

Author Disclosures This study was supported by the CVPath Institute, a 501(c)(3) foundation. CVPath Institute has received institutional research support from R01 HL141425 Leducq Foundation Grant, 480 Biomedical, 4C Medical, 4Tech, Abbott, Accumedical, Amgen, Biosensors, Boston Scientific, Cardiac Implants, Celonova, Claret Medical, Concept Medical, Cook, CSI, DuNing, Inc, Edwards LifeSciences, Emboline, Endotronix, Envision Scientific, Lutonix/Bard, Gateway, Lifetech, Limflo, MedAlliance, Medtronic, Mercator, Merill, Microport Medical, Microvention, Mitralign, MitrAssist, NAMSA, Nanova, Neovasc, NIPRO, Novogate, Occulotech, OrbusNeich Medical, Phenox, Profusa, Protembis, Qool, Recor, Senseonics, Shockwave, Sinomed, Spectranetics, Surmodics, Symic, Vesper, W.L. Gore, and Xeltis. Dr. Cornelissen has received research grants from University Hospital RWTH Aachen. Dr. Guagliumi has received institutional research grants from Abbott Vascular, Boston Scientific, and Infraredx; and has served as a consultant for Abbott Vascular and Boston Scientific. Dr. Virmani has received honoraria from Abbott Vascular, Biosensors, Boston Scientific, Celonova, Cook Medical, Cordis, CSI, Lutonix Bard, Medtronic, OrbusNeich Medical, CeloNova, SINO Medical Technology, Recor Medical, Terumo Corporation, W. L. Gore, and Spectranetics; and has served as a consultant for Abbott Vascular, Boston Scientific, Celonova, Cook Medical, Cordis, CSI, Edwards Lifesciences, Lutonix Bard, Medtronic, OrbusNeich Medical, ReCore, Sinomedical Technology, Spectranetics, Surmodics, Terumo Corporation, W. L. Gore, and Xeltis. Dr. Finn has received honoraria from Abbott Vascular, Biosensors, Boston Scientific, Celonova, Cook Medical, CSI, Lutonix Bard, Sinomed, and Terumo Corporation; and has served as a consultant to Amgen, Abbott Vascular, Boston Scientific, Celonova, Cook Medical, Lutonix Bard, and Sinomed. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Figures

None
Graphical abstract
Figure 1
Figure 1
Myocardial Inflammatory Cell Infiltrates in Cases of Traumatic Death, COVID-19, and Myocarditis Representative low and high power of hematoxylin and eosin images, and immunostains for CD3 and CD68 from cases of traumatic death (control) (A to D and P), COVID-19 (E to H), and myocarditis (I to L). Bar graphs represent total inflammatory (i.e., CD3 and CD68) cell counts in control subjects and COVID-19 cases (n = 5 each) (M, N, and O). A photomicrograph of single-cell necrosis with CD3 and CD68 staining is shown in P. CD3 = cluster of differentiation 3; CD68 = cluster of differentiation 68; COVID-19 = coronavirus disease-2019; SARS-CoV-2 = severe acute respiratory syndrome-coronavirus-2.
Central Illustration
Central Illustration
Histological Evidence of Myocarditis in COVID-19 Infection and Numbers of Infiltrated Inflammatory Cells in Myocardium in COVID-19 Autopsy Hearts Without Myocarditis and in Non–COVID-19 Myocarditis According to published data on pathological evidence for myocarditis in subjects with coronavirus disease-2019 (COVID-19), the rate of myocarditis is 4.5%. In our experience with 16 COVID-19 autopsy cases, no case met diagnostic criteria for myocarditis. In a comparison of inflammatory cells in the myocardium of subjects dying from traumatic versus COVID-19 deaths (but without a diagnosis of myocarditis), there were less cluster of differentiation (CD) 3–positive cells in COVID-19 cases and more CD68-positive cells.
See this image and copyright information in PMC

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