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Review
. 2022 Aug 26:13:982896.
doi: 10.3389/fneur.2022.982896. eCollection 2022.

The role of cross-sectional imaging of the extracranial and intracranial vasculature in embolic stroke of undetermined source

Affiliations
Review

The role of cross-sectional imaging of the extracranial and intracranial vasculature in embolic stroke of undetermined source

Hediyeh Baradaran et al. Front Neurol. .

Abstract

Despite an extensive workup, nearly one third of ischemic strokes are defined as Embolic Stroke of Undetermined Source (ESUS), indicating that no clear etiologic cause has been identified. Since large vessel atherosclerotic disease is a major cause of ischemic stroke, we focus on imaging of large vessel atherosclerosis to identify further sources of potential emboli which may be contributing to ESUS. For a stroke to be considered ESUS, both the extracranial and intracranial vessels must have <50% stenosis. Given the recent paradigm shift in our understanding of the role of plaque vulnerability in ischemic stroke risk, we evaluate the role of imaging specific high-risk extracranial plaque features in non-stenosing plaque and their potential contributions to ESUS. Further, intracranial vessel-wall MR is another potential tool to identify non-stenosing atherosclerotic plaques which may also contribute to ESUS. In this review, we discuss the role of cross-sectional imaging of the extracranial and intracranial arteries and how imaging may potentially uncover high risk plaque features which may be contributing to ischemic strokes.

Keywords: atherosclerosis; carotid artery disease; carotid artery stenosis; cerebrovascular disease/stroke; magnetic resonance angiography.

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Conflict of interest statement

HK serves as a PI for the NIH-funded ARCADIA trial (NINDS U01NS095869), which receives in-kind study drug from the BMS-Pfizer Alliance for Eliquis® and ancillary study support from Roche Diagnostics; as Deputy Editor for JAMA Neurology; on clinical trial steering/executive committees for Medtronic, Janssen, and Javelin Medical; and on endpoint adjudication committees for AstraZeneca, Novo Nordisk, and Boehringer Ingelheim. He has an ownership interest in TETMedical, Inc. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Though there is no accompanying significant stenosis [(A) maximum intensity projection of contrast-enhanced MRA], this MPRAGE sequence of the proximal right internal carotid artery in a 73-years-old male demonstrates a large T1 hyperintense plaque [(B) arrow]. These findings are compatible with intraplaque hemorrhage, a well-established marker of vulnerable plaque and likely contributor to acute ischemic stroke in this patient.
Figure 2
Figure 2
This 71-years-old patient presenting with an acute left middle cerebral artery territory infarction [arrow (A)] did not have any significant stenosis by North American Symptomatic Carotid Endarterectomy Trial criteria on CT angiography (CTA) and was thought to have an embolic stroke of undetermined source. The CTA (B) does however show a large, predominantly non–calcified plaque up to 5 mm in thickness in the proximal left internal carotid artery [(B) arrow] compatible with a vulnerable plaque, potentially the embolic source of the infarction.
Figure 3
Figure 3
This 62-year old patient presenting with an acute left middle cerebral artery (MCA) infarction on MR (A) had CT angiography [(B) maximum intensity projection] at presentation without evidence of any significant stenosis. Initially thought to have an embolic stroke of undetermined source, he underwent an intracranial vessel wall MR where he was found to have a focal, eccentric T2 hyperintense [(C) white arrow] enhancing [(D) pre-contrast image, (E) post-contrast image, white arrow] plaque, in the distal M1 segment of the left MCA, thought to be the culprit plaque.4.

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