Myocardial perfusion in cardiac amyloidosis.

Amyloidosis Extracellular volume Infiltration Ischaemia Magnetic resonance imaging Perfusion

Journal

European journal of heart failure
ISSN: 1879-0844
Titre abrégé: Eur J Heart Fail
Pays: England
ID NLM: 100887595

Informations de publication

Date de publication:
21 Jan 2024
Historique:
revised: 07 11 2023
received: 13 06 2023
accepted: 27 12 2023
medline: 22 1 2024
pubmed: 22 1 2024
entrez: 22 1 2024
Statut: aheadofprint

Résumé

Cardiac involvement is the main driver of clinical outcomes in systemic amyloidosis and preliminary studies support the hypothesis that myocardial ischaemia contributes to cellular damage. The aims of this study were to assess the presence and mechanisms of myocardial ischaemia using cardiovascular magnetic resonance (CMR) with multiparametric mapping and histopathological assessment. Ninety-three patients with cardiac amyloidosis (CA) (light-chain amyloidosis n = 42, transthyretin amyloidosis n = 51) and 97 without CA (three-vessel coronary disease [3VD] n = 47, unobstructed coronary arteries n = 26, healthy volunteers [HV] n = 24) underwent quantitative stress perfusion CMR with myocardial blood flow (MBF) mapping. Twenty-four myocardial biopsies and three explanted hearts with CA were analysed histopathologically. Stress MBF was severely reduced in patients with CA with lower values than patients with 3VD, unobstructed coronary arteries and HV (CA: 1.04 ± 0.51 ml/min/g, 3VD: 1.35 ± 0.50 ml/min/g, unobstructed coronary arteries: 2.92 ± 0.52 ml/min/g, HV: 2.91 ± 0.73 ml/min/g; CA vs. 3VD p = 0.011, CA vs. unobstructed coronary arteries p < 0.001, CA vs. HV p < 0.001). Myocardial perfusion abnormalities correlated with amyloid burden, systolic and diastolic function, structural parameters and blood biomarkers (p < 0.05). Biopsies demonstrated abnormal vascular endothelial growth factor staining in cardiomyocytes and endothelial cells, which may be related to hypoxia conditions. Amyloid infiltration in intramural arteries was associated with severe lumen reduction and severe reduction in capillary density. Cardiac amyloidosis is associated with severe inducible myocardial ischaemia demonstrable by histology and CMR stress perfusion mapping. Histological evaluation indicates a complex pathophysiology, where in addition to systolic and diastolic dysfunction, amyloid infiltration of the epicardial arteries and disruption and rarefaction of the capillaries play a role in contributing to myocardial ischaemia.

Identifiants

pubmed: 38247182
doi: 10.1002/ejhf.3137
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Informations de copyright

© 2024 The Authors. European Journal of Heart Failure published by John Wiley & Sons Ltd on behalf of European Society of Cardiology.

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Auteurs

Liza Chacko (L)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Tushar Kotecha (T)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Adam Ioannou (A)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Niket Patel (N)

Royal Free Hospital NHS Foundation Trust, London, UK.

Ana Martinez-Naharro (A)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Yousuf Razvi (Y)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Rishi Patel (R)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Paolo Massa (P)

Department of Experimental, Diagnostic and Specialty Medicine, University of Bologna, IRCCS Sant'Orsola Hospital, Bologna, Italy.

Lucia Venneri (L)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

James Brown (J)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Aldostefano Porcari (A)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

Kristopher Knott (K)

Institute of Cardiovascular Science, University College London, London, UK.
Barts Heart Centre, London, UK.

Charlotte Manisty (C)

Institute of Cardiovascular Science, University College London, London, UK.

Daniel Knight (D)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Tim Lockie (T)

Royal Free Hospital NHS Foundation Trust, London, UK.

Roby Rakhit (R)

Royal Free Hospital NHS Foundation Trust, London, UK.

Helen Lachmann (H)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

Ashutosh Wechelakar (A)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

Carol Whelan (C)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Markella Ponticos (M)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

James Moon (J)

Institute of Cardiovascular Science, University College London, London, UK.
Barts Heart Centre, London, UK.

Arantxa González (A)

Division of Cardiovascular Sciences, University of Navarra, Pamplona, Spain.

Janet Gilbertson (J)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

Mattia Riefolo (M)

Pathology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Department of Medical and Surgical Sciences (DIMEC), Alma Mater Studiorum University of Bologna, Bologna, Italy.

Ornella Leone (O)

Pathology Unit, IRCCS Azienda Ospedaliero-Universitaria di Bologna, Bologna, Italy.
Department of Medical and Surgical Sciences (DIMEC), Alma Mater Studiorum University of Bologna, Bologna, Italy.

Hui Xue (H)

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

Philip Hawkins (P)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

Peter Kellman (P)

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

Julian Gillmore (J)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.

Marianna Fontana (M)

National Amyloidosis Centre, Division of Medicine, University College London, Royal Free Hospital, London, UK.
Royal Free Hospital NHS Foundation Trust, London, UK.

Classifications MeSH