Complicated Carotid Artery Plaques as a Cause of Cryptogenic Stroke.


Journal

Journal of the American College of Cardiology
ISSN: 1558-3597
Titre abrégé: J Am Coll Cardiol
Pays: United States
ID NLM: 8301365

Informations de publication

Date de publication:
10 11 2020
Historique:
received: 21 05 2020
revised: 25 08 2020
accepted: 08 09 2020
entrez: 6 11 2020
pubmed: 7 11 2020
medline: 17 2 2021
Statut: ppublish

Résumé

The underlying etiology of ischemic stroke remains unknown in up to 30% of patients. This study explored the causal role of complicated (American Heart Association-lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS). CAPIAS (Carotid Plaque Imaging in Acute Stroke) is an observational multicenter study that prospectively recruited patients aged older than 49 years with acute ischemic stroke that was restricted to the territory of a single carotid artery on brain magnetic resonance imaging (MRI) and unilateral or bilateral CAP (≥2 mm, NASCET [North American Symptomatic Carotid Endarterectomy Trial] <70%). CAP characteristics were determined qualitatively and quantitatively by high-resolution, contrast-enhanced carotid MRI at 3T using dedicated surface coils. The pre-specified study hypotheses were that that the prevalence of complicated CAP would be higher ipsilateral to the infarct than contralateral to the infarct in CS and higher in CS compared with patients with cardioembolic or small vessel stroke (CES/SVS) as a combined reference group. Patients with large artery stroke (LAS) and NASCET 50% to 69% stenosis served as an additional comparison group. Among 234 recruited patients, 196 had either CS (n = 104), CES/SVS (n = 79), or LAS (n = 19) and complete carotid MRI data. The prevalence of complicated CAP in patients with CS was significantly higher ipsilateral (31%) to the infarct compared with contralateral to the infarct (12%; p = 0.0005). Moreover, the prevalence of ipsilateral complicated CAP was significantly higher in CS (31%) compared with CES/SVS (15%; p = 0.02) and lower in CS compared with LAS (68%; p = 0.003). Lipid-rich and/or necrotic cores in ipsilateral CAP were significantly larger in CS compared with CES/SVS (p < 0.05). These findings substantiate the role of complicated nonstenosing CAP as an under-recognized cause of stroke. (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT01284933).

Sections du résumé

BACKGROUND
The underlying etiology of ischemic stroke remains unknown in up to 30% of patients.
OBJECTIVES
This study explored the causal role of complicated (American Heart Association-lesion type VI) nonstenosing carotid artery plaques (CAPs) in cryptogenic stroke (CS).
METHODS
CAPIAS (Carotid Plaque Imaging in Acute Stroke) is an observational multicenter study that prospectively recruited patients aged older than 49 years with acute ischemic stroke that was restricted to the territory of a single carotid artery on brain magnetic resonance imaging (MRI) and unilateral or bilateral CAP (≥2 mm, NASCET [North American Symptomatic Carotid Endarterectomy Trial] <70%). CAP characteristics were determined qualitatively and quantitatively by high-resolution, contrast-enhanced carotid MRI at 3T using dedicated surface coils. The pre-specified study hypotheses were that that the prevalence of complicated CAP would be higher ipsilateral to the infarct than contralateral to the infarct in CS and higher in CS compared with patients with cardioembolic or small vessel stroke (CES/SVS) as a combined reference group. Patients with large artery stroke (LAS) and NASCET 50% to 69% stenosis served as an additional comparison group.
RESULTS
Among 234 recruited patients, 196 had either CS (n = 104), CES/SVS (n = 79), or LAS (n = 19) and complete carotid MRI data. The prevalence of complicated CAP in patients with CS was significantly higher ipsilateral (31%) to the infarct compared with contralateral to the infarct (12%; p = 0.0005). Moreover, the prevalence of ipsilateral complicated CAP was significantly higher in CS (31%) compared with CES/SVS (15%; p = 0.02) and lower in CS compared with LAS (68%; p = 0.003). Lipid-rich and/or necrotic cores in ipsilateral CAP were significantly larger in CS compared with CES/SVS (p < 0.05).
CONCLUSIONS
These findings substantiate the role of complicated nonstenosing CAP as an under-recognized cause of stroke. (Carotid Plaque Imaging in Acute Stroke [CAPIAS]; NCT01284933).

Identifiants

pubmed: 33153580
pii: S0735-1097(20)37186-2
doi: 10.1016/j.jacc.2020.09.532
pii:
doi:

Banques de données

ClinicalTrials.gov
['NCT01284933']

Types de publication

Clinical Trial Journal Article Multicenter Study Observational Study Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

2212-2222

Commentaires et corrections

Type : CommentIn
Type : CommentIn
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Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Author Relationship With Industry This work was supported by the Vascular Dementia Research Foundation and the German Research Foundation (DFG) as part of the Munich Cluster for Systems Neurology (EXC 2145 SyNergy). Dr. Schindler was supported by a grant from the German Research Foundation (DFG) (SCHI 1394/1-1). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.

Auteurs

Anna Kopczak (A)

Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany.

Andreas Schindler (A)

Department of Radiology, University Hospital, LMU Munich, Munich, Germany; Department of Radiology, Trauma Center Murnau, Murnau, Germany.

Anna Bayer-Karpinska (A)

Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Klinikum Fürstenfeldbruck, Neurology, Fürstenfeldbruck, Germany.

Mia L Koch (ML)

Department of Neurology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany.

Dominik Sepp (D)

Department of Neuroradiology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany.

Julia Zeller (J)

Department of Neurology and Stroke, and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.

Christoph Strecker (C)

Department of Neurology and Neurophysiology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Johann-Martin Hempel (JM)

Department of Diagnostic and Interventional Neuroradiology, University of Tübingen, Tübingen, Germany.

Chun Yuan (C)

Department of Radiology, University of Washington, Seattle, Washington.

Rainer Malik (R)

Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany.

Frank A Wollenweber (FA)

Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Department of Neurology, Helios Dr Horst-Schmidt-Kliniken, Wiesbaden, Germany.

Tobias Boeckh-Behrens (T)

Department of Neuroradiology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany.

Clemens C Cyran (CC)

Department of Radiology, University Hospital, LMU Munich, Munich, Germany.

Andreas Helck (A)

Department of Radiology, University Hospital, LMU Munich, Munich, Germany; Radiology and Neuroradiology Zurich, Hirslanden/Klinik im Park, Zurich, Switzerland.

Andreas Harloff (A)

Department of Neurology and Neurophysiology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, Freiburg, Germany.

Ulf Ziemann (U)

Department of Neurology and Stroke, and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.

Sven Poli (S)

Department of Neurology and Stroke, and Hertie Institute for Clinical Brain Research, University of Tübingen, Tübingen, Germany.

Holger Poppert (H)

Department of Neurology, Klinikum rechts der Isar, Technical University of Munich (TUM), Munich, Germany; Department of Neurology, Helios Klinikum München West, Munich, Germany.

Martin Dichgans (M)

Institute for Stroke and Dementia Research, University Hospital, LMU Munich, Munich, Germany; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Electronic address: martin.dichgans@med.uni-muenchen.de.

Tobias Saam (T)

Department of Radiology, University Hospital, LMU Munich, Munich, Germany; Radiologisches Zentrum Rosenheim, Rosenheim, Germany.

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