Characterisation of cardiac pathology in 23 autopsies of lethal COVID-19.


Journal

The journal of pathology. Clinical research
ISSN: 2056-4538
Titre abrégé: J Pathol Clin Res
Pays: England
ID NLM: 101658534

Informations de publication

Date de publication:
07 2021
Historique:
revised: 23 02 2021
received: 17 01 2021
accepted: 10 03 2021
pubmed: 11 4 2021
medline: 22 6 2021
entrez: 10 4 2021
Statut: ppublish

Résumé

While coronavirus disease 2019 (COVID-19) primarily affects the respiratory tract, pathophysiological changes of the cardiovascular system remain to be elucidated. We performed a retrospective cardiopathological analysis of the heart and vasculature from 23 autopsies of COVID-19 patients, comparing the findings with control tissue. Myocardium from autopsies of COVID-19 patients was categorised into severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) positive (n = 14) or negative (n = 9) based on the presence of viral RNA as determined by reverse transcriptase polymerase chain reaction (RT-PCR). Control tissue was selected from autopsies without COVID-19 (n = 10) with similar clinical sequelae. Histological characteristics were scored by ordinal and/or categorical grading. Five RT-PCR-positive cases underwent in situ hybridisation (ISH) for SARS-CoV-2. Patients with lethal COVID-19 infection were mostly male (78%) and had a high incidence of hypertension (91%), coronary artery disease (61%), and diabetes mellitus (48%). Patients with positive myocardial RT-PCR died earlier after hospital admission (5 versus 12 days, p < 0.001) than patients with negative RT-PCR. An increased severity of fibrin deposition, capillary dilatation, and microhaemorrhage was observed in RT-PCR-positive myocardium than in negatives and controls, with a positive correlation amongst these factors All cases with increased cardioinflammatory infiltrate, without myocyte necrosis (n = 4) or with myocarditis (n = 1), were RT-PCR negative. ISH revealed positivity of viral RNA in interstitial cells. Myocardial capillary dilatation, fibrin deposition, and microhaemorrhage may be the histomorphological correlate of COVID-19-associated coagulopathy. Increased cardioinflammation including one case of myocarditis was only detected in RT-PCR-negative hearts with significantly longer hospitalisation time. This may imply a secondary immunological response warranting further characterisation.

Identifiants

pubmed: 33837673
doi: 10.1002/cjp2.212
pmc: PMC8185365
doi:

Substances chimiques

RNA, Viral 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

326-337

Informations de copyright

© 2021 The Authors. The Journal of Pathology: Clinical Research published by The Pathological Society of Great Britain and Ireland & John Wiley & Sons, Ltd.

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Auteurs

Jasmin D Haslbauer (JD)

Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Basel, Switzerland.

Alexandar Tzankov (A)

Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Basel, Switzerland.

Kirsten D Mertz (KD)

Institute of Pathology, Cantonal Hospital Baselland, Liestal, Switzerland.

Nathalie Schwab (N)

Institute of Pathology, Cantonal Hospital Baselland, Liestal, Switzerland.

Ronny Nienhold (R)

Institute of Pathology, Cantonal Hospital Baselland, Liestal, Switzerland.

Raphael Twerenbold (R)

Cardiology, University Hospital Basel, University of Basel, Basel, Switzerland.

Gregor Leibundgut (G)

Cardiology, Cantonal Hospital Baselland, Liestal, Switzerland.

Anna K Stalder (AK)

Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Basel, Switzerland.

Matthias Matter (M)

Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Basel, Switzerland.

Katharina Glatz (K)

Pathology, Institute of Medical Genetics and Pathology, University Hospital Basel, University of Basel, Basel, Switzerland.

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Classifications MeSH