Susceptibility Vessel Sign in Deep Perforating Arteries in Patients with Recent Small Subcortical Infarcts.


Journal

Journal of stroke and cerebrovascular diseases : the official journal of National Stroke Association
ISSN: 1532-8511
Titre abrégé: J Stroke Cerebrovasc Dis
Pays: United States
ID NLM: 9111633

Informations de publication

Date de publication:
Jan 2021
Historique:
received: 09 09 2020
revised: 05 10 2020
accepted: 15 10 2020
pubmed: 4 11 2020
medline: 5 1 2021
entrez: 3 11 2020
Statut: ppublish

Résumé

Recent small subcortical infarcts (RSSI) are considered an acute manifestation of cerebral small vessel disease. Paramagnetic signals in perforating arteries supplying RSSI may be detected on T2*-relaxation derived sequences on MRI and is defined as susceptibility vessel sign (SVS). We aimed to study the prevalence of SVS in patients with RSSI, and explore whether its identification is related to cerebral small vessel disease markers. We selected patients with RSSI identified on MRI during admission from a single-center stroke registry. The main demographic and clinical features, including vascular risk factors, were collected. Radiological features of RSSI and cerebral small vessel disease [white matter hyperintensities in deep and periventricular regions, enlarged perivascular spaces, lacunae, microbleeds, and brain atrophy] were described using validated qualitative scores. The presence of SVS was assessed on T2*gradient-echo or other susceptibility-weighted imaging. We compared the clinical and radiological features of patients with or without SVS in uni- and multivariate models. Out of 210 patients with an RSSI on an MRI, 35 (17%) showed SVS. The proportion of SVS+ patients was similar in different susceptibility imaging modalities (p=.64). Risk factor profiles and clinical course were similar in SVS+ and SVS- patients. SVS+ patients had a higher grade of deep white matter hyperintensities and brain atrophy, more lacunae (p=.001, p=.034, p=.022, respectively), and a similar degree of the rest of radiological variables, compared to SVS- patients. In the multivariate analysis, the grade of deep white matter hyperintensities was the only independent factor associated with SVS [OR 3.1 (95% CI, 1.5-6.4)]. SVS in patients with RSSI is uncommon and related to a higher grade of deep white matter hyperintensities. Pathophysiological mechanisms underlying the deposition of hemosiderin in the path of occluded perforating arteries are uncertain and might include endothelial dysfunction or embolic mechanisms.

Identifiants

pubmed: 33142246
pii: S1052-3057(20)30833-8
doi: 10.1016/j.jstrokecerebrovasdis.2020.105415
pii:
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

105415

Informations de copyright

Copyright © 2020 Elsevier Inc. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors declared no potential conflicts of interest concerning the research, authorship, and/or publication of this article.

Auteurs

Salvatore Rudilosso (S)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Electronic address: srudilos@clinic.cat.

Marta Olivera (M)

Department of Neurology, Hospital Clínic of Barcelona, Spain.

Diana Esteller (D)

Department of Neurology, Hospital Clínic of Barcelona, Spain.

Carlos Laredo (C)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.

Sergio Amaro (S)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.

Laura Llull (L)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.

Arturo Renú (A)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.

Víctor Obach (V)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.

Víctor Vera (V)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain.

Alejandro Rodríguez (A)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain.

Jordi Blasco (J)

Department of Radiology, Hospital Clínic, University of Barcelona, Barcelona, Spain.

Antonio López-Rueda (A)

Department of Radiology, Hospital Clínic, University of Barcelona, Barcelona, Spain.

Xabier Urra (X)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain. Electronic address: xurra@clinic.cat.

Ángel Chamorro (Á)

Comprehensive Stroke Center, Department of Neuroscience, Hospital Clinic, University of Barcelona, Villarroel 170, 08036 Barcelona, Spain; August Pi i Sunyer Biomedical Research Institute (IDIBAPS), Barcelona, Spain.

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