Carotid plaque vulnerability and circle of Willis anatomy predict ipsilateral brain infarcts and long-term mortality in carotid endarterectomy patients

Figures

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  Fig. 1. Flowchart demonstrating the exclusion criteria and number of patients excluded

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  Fig. 2. a, b Multiplanar CT reformats of a voluminous ill-defined cortical-subcortical hypodensity in the right frontal and parietal lobes (blue arrows), corresponding to a subacute middle cerebral artery territorial infarct of a patient with an exulcerated plaque and a carotid score of 4 (70% stenosis of the right internal carotid artery and no stenosis of the contralateral internal carotid artery). Left lateral craniectomy following surgical removal of an old meningioma; b ill-defined cortical-subcortical hypodensity in the right upper parietal lobe (yellow arrows), corresponding to a subacute triple watershed infarct of a patient with a carotid score of 1 (˃90% stenosis of the right internal carotid artery caused by a calcified plaque and 70% stenosis of the contralateral internal carotid artery)

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  Fig. 3. Multiplanar CT reformats perpendicular to the residual lumen of the stenosed right internal carotid artery, with measurement at the site of maximal plaque thickness (green text)

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  Fig. 4. a–d Multiplanar CT reformats perpendicular to the residual lumen of the stenosed right internal carotid artery a–c with plaque density measurements (green regions of interest) in three consecutive axial slices, showing a dominantly lipid-rich plaque with an average density of 15–19 Hounsfield Units. d Contrast filling (red arrows) pointing at an exulceration within a dominantly lipid-rich plaque

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  Fig. 5. a–g Schematic illustration of the circle of Willis (CW) types; a Normal CW segments, demonstrating collateral supply from the anterior (curved thick red arrow) and ipsilateral posterior parts (curved thick yellow arrow) to the index middle cerebral artery during surgery; b Type 0 (severely compromised) CW: both the anterior and ipsilateral posterior parts are incomplete. Non-visualisation of the ipsilateral anterior precommunicating segment and ipsilateral posterior communicating artery was the most common variant; c Type 1 (severely compromised) CW: one part incomplete, the other hypoplastic. Hypoplasia of the anterior communicating artery and non-visualisation of the ipsilateral posterior communicating artery was the most frequent; d Type 2 CW: one part incomplete, the other normal. Non-visualisation of the ipsilateral posterior communicating artery was the most common variant; e Type 3 CW: both the anterior and ipsilateral parts hypoplastic. Hypoplasia of the anterior and ipsilateral posterior communicating arteries was the most frequent; f Type 4 CW: one of the parts hypoplastic. Hypoplasia of the ipsilateral posterior communicating artery was the most common variant; g Type…

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  Fig. 6. a, b Thick slab (14 mm) maximal intensity projections of a type 0 circle of Willis in a patient with left internal carotid artery stenosis. Non-visualization of the right precommunicating segment of the anterior cerebral artery (double yellow arrows). Well-developped anterior communicating artery (blue arrow). Normal left precommunicating segment of the anterior cerebral artery (yellow arrow). Non-visualization of the ipsilateral (left) posterior communicating artery (double green arrows). Normal precommunicating segment of the posterior cerebral arteries (red arrows). Hypoplasia of the contralateral posterior communicating artery, poorly visualized (green arrowhead); b type 1 circle of Willis in a patient with left internal carotid artery stenosis. Hypoplasia of the anterior communicating artery (blue arrow). Non-visualization of the ipsilateral (left) precommunicating segment of the posterior cerebral artery (double red arrows). Well-developped ipsilateral posterior communicating artery (green arrow). Non-visualization of the contralateral posterior communicating artery (double green arrows). Precommunicating segment of the anterior cerebral arteries (yellow arrows). The left…