Intracranial atherosclerotic disease mechanistic subtypes drive hypoperfusion patterns.


Journal

Journal of neuroimaging : official journal of the American Society of Neuroimaging
ISSN: 1552-6569
Titre abrégé: J Neuroimaging
Pays: United States
ID NLM: 9102705

Informations de publication

Date de publication:
07 2021
Historique:
revised: 21 03 2021
received: 28 02 2021
accepted: 23 03 2021
pubmed: 1 5 2021
medline: 28 9 2021
entrez: 30 4 2021
Statut: ppublish

Résumé

In symptomatic intracranial atherosclerotic stenosis (ICAS), borderzone infarct pattern and perfusion mismatch are associated with increased risk of recurrent strokes, which may reflect the shared underlying mechanism of hypoperfusion distal to the intracranial atherosclerosis. Accordingly, we hypothesized a correlation between hypoperfusion volumes and ICAS infarct patterns based on the respective underlying mechanistic subtypes. We conducted a retrospective analysis of consecutive symptomatic ICAS cases, acute strokes due to subocclusive (50%-99%) intracranial stenosis. The following mechanistic subtypes were assigned based on the infarct pattern on the diffusion-weighted imaging: Branch occlusive disease (BOD), internal borderzone (IBZ), and thromboembolic (TE). Perfusion parameters, obtained concurrently with the MRI, were studied in each group. A total of 42 patients (57% women, mean age 71 ± 13 years old) with symptomatic ICAS received MRI within 24 h of acute presentation. Fourteen IBZ, 11 BOD, and 17 TE patterns were identified. IBZ pattern yielded higher total T ICAS infarct patterns, in keeping with their respective underlying mechanisms, may correlate with distinct perfusion profiles.

Sections du résumé

BACKGROUND AND PURPOSE
In symptomatic intracranial atherosclerotic stenosis (ICAS), borderzone infarct pattern and perfusion mismatch are associated with increased risk of recurrent strokes, which may reflect the shared underlying mechanism of hypoperfusion distal to the intracranial atherosclerosis. Accordingly, we hypothesized a correlation between hypoperfusion volumes and ICAS infarct patterns based on the respective underlying mechanistic subtypes.
METHODS
We conducted a retrospective analysis of consecutive symptomatic ICAS cases, acute strokes due to subocclusive (50%-99%) intracranial stenosis. The following mechanistic subtypes were assigned based on the infarct pattern on the diffusion-weighted imaging: Branch occlusive disease (BOD), internal borderzone (IBZ), and thromboembolic (TE). Perfusion parameters, obtained concurrently with the MRI, were studied in each group.
RESULTS
A total of 42 patients (57% women, mean age 71 ± 13 years old) with symptomatic ICAS received MRI within 24 h of acute presentation. Fourteen IBZ, 11 BOD, and 17 TE patterns were identified. IBZ pattern yielded higher total T
CONCLUSION
ICAS infarct patterns, in keeping with their respective underlying mechanisms, may correlate with distinct perfusion profiles.

Identifiants

pubmed: 33930227
doi: 10.1111/jon.12863
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

686-690

Subventions

Organisme : NINDS NIH HHS
ID : R01 NS084288
Pays : United States

Informations de copyright

© 2021 American Society of Neuroimaging.

Références

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Auteurs

Song J Kim (SJ)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Jose M Morales (JM)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Shadi Yaghi (S)

Department of Neurology, Warren Alpert Medical School, Brown University, Providence, Rhode Island, USA.

Tristan Honda (T)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Fabien Scalzo (F)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Jason D Hinman (JD)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Radoslav Raychev (R)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Latisha K Sharma (LK)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

Edward Feldmann (E)

Department of Neurology, Baystate Health, University of Massachusetts, Springfield, Massachusetts, USA.

Jose G Romano (JG)

Department of Neurology, University of Miami, Miami, Florida, USA.

Shyam Prabhakaran (S)

Department of Neurology, University of Chicago, Chicago, Illinois, USA.

David S Liebeskind (DS)

Department of Neurology, David Geffen School of Medicine, University of California, Los Angeles, California, USA.

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