Pathological features of COVID-19-associated myocardial injury: a multicentre cardiovascular pathology study

Author:

Basso Cristina1ORCID,Leone Ornella2ORCID,Rizzo Stefania1ORCID,De Gaspari Monica1,van der Wal Allard C3,Aubry Marie-Christine4,Bois Melanie C4ORCID,Lin Peter T4ORCID,Maleszewski Joseph J4ORCID,Stone James R5ORCID

Affiliation:

1. Cardiovascular Pathology, Azienda Ospedaliera, Department of Cardiac, Thoracic and Vascular Sciences and Public Health, University of Padua, Padua, Italy

2. Cardiovascular and Cardiac Transplant Pathology Unit, Department of Pathology, Sant’Orsola-Malpighi University Hospital, Bologna, Italy

3. Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands

4. >Department of Pathology, Mayo Clinic, Rochester, MN, USA

5. Department of Pathology, Massachusetts General Hospital and Harvard Medical School, Boston, MA, USA

Abstract

Abstract Aims Coronavirus disease 2019 (COVID-19) due to severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) has been associated with cardiovascular features of myocardial involvement including elevated serum troponin levels and acute heart failure with reduced ejection fraction. The cardiac pathological changes in these patients with COVID-19 have yet to be well described. Methods and results In an international multicentre study, cardiac tissue from the autopsies of 21 consecutive COVID-19 patients was assessed by cardiovascular pathologists. The presence of myocarditis, as defined by the presence of multiple foci of inflammation with associated myocyte injury, was determined, and the inflammatory cell composition analysed by immunohistochemistry. Other forms of acute myocyte injury and inflammation were also described, as well as coronary artery, endocardium, and pericardium involvement. Lymphocytic myocarditis was present in 3 (14%) of the cases. In two of these cases, the T lymphocytes were CD4 predominant and in one case the T lymphocytes were CD8 predominant. Increased interstitial macrophage infiltration was present in 18 (86%) of the cases. A mild pericarditis was present in four cases. Acute myocyte injury in the right ventricle, most probably due to strain/overload, was present in four cases. There was a non-significant trend toward higher serum troponin levels in the patients with myocarditis compared with those without myocarditis. Disrupted coronary artery plaques, coronary artery aneurysms, and large pulmonary emboli were not identified. Conclusions In SARS-CoV-2 there are increased interstitial macrophages in a majority of the cases and multifocal lymphocytic myocarditis in a small fraction of the cases. Other forms of myocardial injury are also present in these patients. The macrophage infiltration may reflect underlying diseases rather than COVID-19.

Publisher

Oxford University Press (OUP)

Subject

Cardiology and Cardiovascular Medicine

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