Patterns of myocardial injury in recovered troponin-positive COVID-19 patients assessed by cardiovascular magnetic resonance.


Journal

European heart journal
ISSN: 1522-9645
Titre abrégé: Eur Heart J
Pays: England
ID NLM: 8006263

Informations de publication

Date de publication:
14 05 2021
Historique:
received: 10 11 2020
revised: 14 12 2020
accepted: 03 02 2021
pubmed: 18 2 2021
medline: 20 5 2021
entrez: 17 2 2021
Statut: ppublish

Résumé

Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients. One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms). During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.

Sections du résumé

BACKGROUND
Troponin elevation is common in hospitalized COVID-19 patients, but underlying aetiologies are ill-defined. We used multi-parametric cardiovascular magnetic resonance (CMR) to assess myocardial injury in recovered COVID-19 patients.
METHODS AND RESULTS
One hundred and forty-eight patients (64 ± 12 years, 70% male) with severe COVID-19 infection [all requiring hospital admission, 48 (32%) requiring ventilatory support] and troponin elevation discharged from six hospitals underwent convalescent CMR (including adenosine stress perfusion if indicated) at median 68 days. Left ventricular (LV) function was normal in 89% (ejection fraction 67% ± 11%). Late gadolinium enhancement and/or ischaemia was found in 54% (80/148). This comprised myocarditis-like scar in 26% (39/148), infarction and/or ischaemia in 22% (32/148) and dual pathology in 6% (9/148). Myocarditis-like injury was limited to three or less myocardial segments in 88% (35/40) of cases with no associated LV dysfunction; of these, 30% had active myocarditis. Myocardial infarction was found in 19% (28/148) and inducible ischaemia in 26% (20/76) of those undergoing stress perfusion (including 7 with both infarction and ischaemia). Of patients with ischaemic injury pattern, 66% (27/41) had no past history of coronary disease. There was no evidence of diffuse fibrosis or oedema in the remote myocardium (T1: COVID-19 patients 1033 ± 41 ms vs. matched controls 1028 ± 35 ms; T2: COVID-19 46 ± 3 ms vs. matched controls 47 ± 3 ms).
CONCLUSIONS
During convalescence after severe COVID-19 infection with troponin elevation, myocarditis-like injury can be encountered, with limited extent and minimal functional consequence. In a proportion of patients, there is evidence of possible ongoing localized inflammation. A quarter of patients had ischaemic heart disease, of which two-thirds had no previous history. Whether these observed findings represent pre-existing clinically silent disease or de novo COVID-19-related changes remain undetermined. Diffuse oedema or fibrosis was not detected.

Identifiants

pubmed: 33596594
pii: 6140994
doi: 10.1093/eurheartj/ehab075
pmc: PMC7928984
doi:

Substances chimiques

Contrast Media 0
Troponin 0
Gadolinium AU0V1LM3JT

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

1866-1878

Subventions

Organisme : British Heart Foundation
ID : FS/20/14/34917
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/CRLF/20/23004
Pays : United Kingdom
Organisme : British Heart Foundation
ID : FS/CRTF/21/24128
Pays : United Kingdom
Organisme : British Heart Foundation
ID : SP/20/2/34841
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn
Type : CommentIn
Type : CommentIn

Informations de copyright

© The Author(s) 2021. Published by Oxford University Press on behalf of the European Society of Cardiology.

Auteurs

Tushar Kotecha (T)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Institute of Cardiovascular Science, University College London, UK.

Daniel S Knight (DS)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Institute of Cardiovascular Science, University College London, UK.

Yousuf Razvi (Y)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.

Kartik Kumar (K)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.

Kavitha Vimalesvaran (K)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.

George Thornton (G)

Institute of Cardiovascular Science, University College London, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Rishi Patel (R)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Liza Chacko (L)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

James T Brown (JT)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Institute of Cardiovascular Science, University College London, UK.

Clare Coyle (C)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Donald Leith (D)

Institute of Cardiovascular Science, University College London, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Abhishek Shetye (A)

Institute of Cardiovascular Science, University College London, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.
University College London Hospitals NHS Trust, London, UK.

Ben Ariff (B)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.

Robert Bell (R)

Institute of Cardiovascular Science, University College London, UK.
University College London Hospitals NHS Trust, London, UK.

Gabriella Captur (G)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Institute of Cardiovascular Science, University College London, UK.

Meg Coleman (M)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.

James Goldring (J)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.

Deepa Gopalan (D)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.

Melissa Heightman (M)

University College London Hospitals NHS Trust, London, UK.

Toby Hillman (T)

University College London Hospitals NHS Trust, London, UK.

Luke Howard (L)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Michael Jacobs (M)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.

Paramjit S Jeetley (PS)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.

Prapa Kanagaratnam (P)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Onn Min Kon (OM)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Lucy E Lamb (LE)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Academic Department of Defence Medicine, Royal Centre for Defence Medicine, Edgbaston, Birmingham, UK.

Charlotte H Manisty (CH)

Institute of Cardiovascular Science, University College London, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Palmira Mathurdas (P)

University College London Hospitals NHS Trust, London, UK.

Jamil Mayet (J)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Rupert Negus (R)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.

Niket Patel (N)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
Institute of Cardiovascular Science, University College London, UK.

Iain Pierce (I)

Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Georgina Russell (G)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Anthony Wolff (A)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.

Hui Xue (H)

National Heart, Lung, and Blood Institute, National Institute of Health, Bethesda, MD, USA.

Peter Kellman (P)

National Heart, Lung, and Blood Institute, National Institute of Health, Bethesda, MD, USA.

James C Moon (JC)

Institute of Cardiovascular Science, University College London, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Thomas A Treibel (TA)

Institute of Cardiovascular Science, University College London, UK.
Barts Heart Centre, Barts Health NHS Trust, W Smithfield, London EC1A 7BE, UK.

Graham D Cole (GD)

Imperial College Healthcare NHS Trust, Du Cane Road, London W12 0HS, UK.
National Heart and Lung Institute, Imperial College London, UK.

Marianna Fontana (M)

Royal Free London NHS Foundation Trust, Pond Street, London NW3 2QG, UK.
National Amyloidosis Centre, Division of Medicine, University College London, UK.

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