Novel Approach for In Vivo Detection of Vulnerable Coronary Plaques Using Molecular 3-T CMR Imaging With an Albumin-Binding Probe.


Journal

JACC. Cardiovascular imaging
ISSN: 1876-7591
Titre abrégé: JACC Cardiovasc Imaging
Pays: United States
ID NLM: 101467978

Informations de publication

Date de publication:
02 2019
Historique:
received: 26 07 2017
revised: 18 10 2017
accepted: 18 10 2017
pubmed: 24 1 2018
medline: 14 1 2020
entrez: 24 1 2018
Statut: ppublish

Résumé

This study sought to investigate the potential of the noninvasive albumin-binding probe gadofosveset-enhanced cardiac magnetic resonance (GE-CMR) for detection of coronary plaques that can cause acute coronary syndromes (ACS). ACS are frequently caused by rupture or erosion of coronary plaques that initially do not cause hemodynamically significant stenosis and are therefore not detected by invasive x-ray coronary angiography (XCA). A total of 25 patients with ACS or symptoms of stable coronary artery disease underwent GE-CMR, clinically indicated XCA, and optical coherence tomography (OCT) within 24 h. GE-CMR was performed approximately 24 h following a 1-time application of gadofosveset-trisodium. Contrast-to-noise ratio (CNR) was quantified within coronary segments in comparison with blood signal. A total of 207 coronary segments were analyzed on GE-CMR. Segments containing a culprit lesion in ACS patients (n = 11) showed significant higher signal enhancement (CNR) following gadofosveset-trisodium application than segments without culprit lesions (n = 196; 6.1 [3.9 to 16.5] vs. 2.1 [0.5 to 3.5]; p < 0.001). GE-CMR was able to correctly identify culprit coronary lesions in 9 of 11 segments (sensitivity 82%) and correctly excluded culprit coronary lesions in 162 of 195 segments (specificity 83%). Additionally, segmented areas of thin-cap fibroatheroma (n = 22) as seen on OCT demonstrated significantly higher CNR than segments without coronary plaque or segments containing early atherosclerotic lesions (n = 185; 9.2 [3.3 to 13.7] vs. 2.1 [0.5 to 3.4]; p = 0.001). In this study, we demonstrated for the first time the noninvasive detection of culprit coronary lesions and thin-cap fibroatheroma of the coronary arteries in vivo by using GE-CMR. This method may represent a novel approach for noninvasive cardiovascular risk prediction.

Sections du résumé

OBJECTIVES
This study sought to investigate the potential of the noninvasive albumin-binding probe gadofosveset-enhanced cardiac magnetic resonance (GE-CMR) for detection of coronary plaques that can cause acute coronary syndromes (ACS).
BACKGROUND
ACS are frequently caused by rupture or erosion of coronary plaques that initially do not cause hemodynamically significant stenosis and are therefore not detected by invasive x-ray coronary angiography (XCA).
METHODS
A total of 25 patients with ACS or symptoms of stable coronary artery disease underwent GE-CMR, clinically indicated XCA, and optical coherence tomography (OCT) within 24 h. GE-CMR was performed approximately 24 h following a 1-time application of gadofosveset-trisodium. Contrast-to-noise ratio (CNR) was quantified within coronary segments in comparison with blood signal.
RESULTS
A total of 207 coronary segments were analyzed on GE-CMR. Segments containing a culprit lesion in ACS patients (n = 11) showed significant higher signal enhancement (CNR) following gadofosveset-trisodium application than segments without culprit lesions (n = 196; 6.1 [3.9 to 16.5] vs. 2.1 [0.5 to 3.5]; p < 0.001). GE-CMR was able to correctly identify culprit coronary lesions in 9 of 11 segments (sensitivity 82%) and correctly excluded culprit coronary lesions in 162 of 195 segments (specificity 83%). Additionally, segmented areas of thin-cap fibroatheroma (n = 22) as seen on OCT demonstrated significantly higher CNR than segments without coronary plaque or segments containing early atherosclerotic lesions (n = 185; 9.2 [3.3 to 13.7] vs. 2.1 [0.5 to 3.4]; p = 0.001).
CONCLUSIONS
In this study, we demonstrated for the first time the noninvasive detection of culprit coronary lesions and thin-cap fibroatheroma of the coronary arteries in vivo by using GE-CMR. This method may represent a novel approach for noninvasive cardiovascular risk prediction.

Identifiants

pubmed: 29361487
pii: S1936-878X(17)31152-X
doi: 10.1016/j.jcmg.2017.10.026
pii:
doi:

Substances chimiques

Albumins 0
Contrast Media 0
Organometallic Compounds 0
Gadolinium AU0V1LM3JT
gadofosveset trisodium XM33Q67UVH

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

297-306

Subventions

Organisme : British Heart Foundation
ID : PG/10/44/28343
Pays : United Kingdom
Organisme : British Heart Foundation
ID : RG/12/1/29262
Pays : United Kingdom

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Auteurs

Leif-Christopher Engel (LC)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany; Berlin Institute of Health, Berlin, Germany.

Ulf Landmesser (U)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany; Berlin Institute of Health, Berlin, Germany; DZHK (German Centre for Cardiovascular Research), Partner Site, Berlin, Germany.

Kevin Gigengack (K)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Thomas Wurster (T)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Constantina Manes (C)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Georg Girke (G)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Milosz Jaguszewski (M)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Carsten Skurk (C)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

David M Leistner (DM)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Alexander Lauten (A)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Andreas Schuster (A)

Department of Cardiology, Royal North Shore Hospital, The Kolling Institute, Northern Clinical School, University of Sydney, Sydney, Australia; Department of Cardiology and Pulmonology, German Centre for Cardiovascular Research Deutsches Zentrum für Herz-Kreislauf-Forschung e.V. (DZHK) Partner Site, Göttingen, Germany.

Bernd Hamm (B)

Klinik für Radiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany.

Rene M Botnar (RM)

Division of Imaging Sciences and Biomedical Engineering, King's College London, London, United Kingdom; Pontificia Universidad Católica de Chile Escuela de Ingeniería, Santiago, Chile.

Marcus R Makowski (MR)

Klinik für Radiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany. Electronic address: marcus.makowski@charite.de.

Boris Bigalke (B)

Klinik für Kardiologie, Charité Campus Benjamin Franklin, Universitätsmedizin Berlin, Berlin, Germany. Electronic address: boris.bigalke@charite.de.

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Classifications MeSH