Comparison of Magnetic Resonance Analysis of Myocardial Scarring With Biomarker Release Following S-T Elevation Myocardial Infarction.


Journal

Heart, lung & circulation
ISSN: 1444-2892
Titre abrégé: Heart Lung Circ
Pays: Australia
ID NLM: 100963739

Informations de publication

Date de publication:
Mar 2019
Historique:
received: 14 06 2017
revised: 23 01 2018
accepted: 07 02 2018
pubmed: 13 3 2018
medline: 12 3 2019
entrez: 13 3 2018
Statut: ppublish

Résumé

Late gadolinium enhancement (LGE) with cardiac magnetic resonance (CMR) is commonly assumed to represent myocardial fibrosis; however, comparative human histological data are limited, and there is no consensus on the most accurate method for LGE quantitation. We evaluated the relationship between CMR assessment of regional fibrosis and infarct size assessment using serial biomarkers after ST elevation acute myocardial infarction (STEMI). Ninety-three patients treated for STEMI (59±10 years, 86% male) underwent CMR 6 months after infarction. Infarct size was quantified by CMR-LGE using manual and range of semi-automated thresholds (range: 2-10 standard deviations [SD]) above reference myocardium and the full width-half maximum (FWHM) technique, and compared with the rise in serum biomarkers. The agreement between CMR and biomarker in the identification of large infarcts based on peak troponin (TnI) levels was also analysed. Quantification methods had a strong influence on the infarct size assessment with CMR-LGE. Significant correlations were observed between LGE and biomarkers across all of the signal intensity thresholds. Whilst there was a wide variation with respect to the estimation of total LGE size (from 6.8±7.7 to 32.1±11.3 grams), the variation in the correlation with peak troponin level was much smaller (r-values ranging from 0.670 to 0.876). There was good agreement between CMR-LGE and biomarker assessment of infarct size; the best agreement between CMR-LGE and large infarction using a threshold of 8SD for peak TnI>50ng/mL (Cohen's kappa (κ)=0.722), and a threshold of 4SD for peak TnI >95ng/mL (κ=0.761). The correlation between CMR-LGE quantification of infarct size and biomarker release following STEMI at a range of semi-automated thresholds was consistently strong, with good agreement between measures across a range of thresholds.

Sections du résumé

BACKGROUND BACKGROUND
Late gadolinium enhancement (LGE) with cardiac magnetic resonance (CMR) is commonly assumed to represent myocardial fibrosis; however, comparative human histological data are limited, and there is no consensus on the most accurate method for LGE quantitation. We evaluated the relationship between CMR assessment of regional fibrosis and infarct size assessment using serial biomarkers after ST elevation acute myocardial infarction (STEMI).
METHODS METHODS
Ninety-three patients treated for STEMI (59±10 years, 86% male) underwent CMR 6 months after infarction. Infarct size was quantified by CMR-LGE using manual and range of semi-automated thresholds (range: 2-10 standard deviations [SD]) above reference myocardium and the full width-half maximum (FWHM) technique, and compared with the rise in serum biomarkers. The agreement between CMR and biomarker in the identification of large infarcts based on peak troponin (TnI) levels was also analysed.
RESULTS RESULTS
Quantification methods had a strong influence on the infarct size assessment with CMR-LGE. Significant correlations were observed between LGE and biomarkers across all of the signal intensity thresholds. Whilst there was a wide variation with respect to the estimation of total LGE size (from 6.8±7.7 to 32.1±11.3 grams), the variation in the correlation with peak troponin level was much smaller (r-values ranging from 0.670 to 0.876). There was good agreement between CMR-LGE and biomarker assessment of infarct size; the best agreement between CMR-LGE and large infarction using a threshold of 8SD for peak TnI>50ng/mL (Cohen's kappa (κ)=0.722), and a threshold of 4SD for peak TnI >95ng/mL (κ=0.761).
CONCLUSIONS CONCLUSIONS
The correlation between CMR-LGE quantification of infarct size and biomarker release following STEMI at a range of semi-automated thresholds was consistently strong, with good agreement between measures across a range of thresholds.

Identifiants

pubmed: 29526416
pii: S1443-9506(18)30070-2
doi: 10.1016/j.hlc.2018.02.007
pii:
doi:

Substances chimiques

Biomarkers 0
Troponin 0

Types de publication

Journal Article Randomized Controlled Trial

Langues

eng

Sous-ensembles de citation

IM

Pagination

397-405

Informations de copyright

Crown Copyright © 2018. Published by Elsevier B.V. All rights reserved.

Auteurs

Benedict T Costello (BT)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia.

Dion Stub (D)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia; Western Health, Melbourne, Vic, Australia.

James Hare (J)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia.

Andris H Ellims (AH)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia.

Xinyu Wang (X)

Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia; Peking University Third Hospital, Beijing, China.

Karen Smith (K)

Ambulance Victoria, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia; University of Western Australia, Perth, WA, Australia.

Stephen Bernard (S)

The Alfred Hospital, Melbourne, Vic, Australia; Ambulance Victoria, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia.

Ziad Nehme (Z)

Ambulance Victoria, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia.

Michael Stephenson (M)

Ambulance Victoria, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia.

Janet E Bray (JE)

The Alfred Hospital, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia.

Peter Cameron (P)

The Alfred Hospital, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia.

Bill Barger (B)

Ambulance Victoria, Melbourne, Vic, Australia.

Ian T Meredith (IT)

Monash University, Melbourne, Vic, Australia; Monash Medical Centre, Melbourne, Vic, Australia.

David M Kaye (DM)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia; Monash University, Melbourne, Vic, Australia.

Leah Iles (L)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia.

Andrew J Taylor (AJ)

The Alfred Hospital, Melbourne, Vic, Australia; Baker IDI Heart Diabetes Institute, Melbourne, Vic, Australia. Electronic address: a.taylor@alfred.org.au.

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Classifications MeSH