Identification, Prognosis, and Management of Patients with Carotid Artery Near Occlusion
Allan J. Foxa,
Michael Eliasziwd,
Peter M. Rothwelle,
Matthias H. Schmidtc,
Charles P. Warlowf,
Henry J.M. Barnettb for the North American Symptomatic Carotid Endarterectomy Trial and European Carotid Surgery Trial Groups
a Department of Medical Imaging, Sunnybrook and Women’s College Health Sciences Center, University of Toronto, Toronto
b John P. Robarts Research Institute, London, Ontario, Canada
c Department of Diagnostic Imaging, IWK Health Centre, and Department of Radiology, Dalhousie University, Halifax, Nova Scotia, Canada
d Departments of Community Health Sciences and Clinical Neurosciences, University of Calgary, Calgary, Alberta, Canada
e Stroke Prevention Research Unit, University Department of Clinical Neurology, Radcliffe Infirmary, University of Oxford, Oxford, United Kingdom
f Department of Clinical Neurosciences, Western General Hospital, University of Edinburgh, Edinburgh, United Kingdom
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FIG 1. Near occlusion with collapsed lumen. Lateral common carotid angiogram shows the thin collapsed lumen (arrows) of the ICA above a prominent internal carotid stenosis at the carotid bulb (not shown).
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FIG 2. Progression of stenosis to near occlusion.
A, Anterioposterior angiogram shows ulcerated stenosis of the left carotid bulb. The normal ICA (larger arrow) beyond the stenosis is about twice the diameter of the ipsilateral distal ECA (smaller arrow).
B, Anterioposterior angiogram about 1 year later shows progression of stenosis to near occlusion with the left ICA (larger arrow) reduced in diameter in comparison to previous angiogram and close to the diameter of the ECA (smaller arrow).
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FIG 3. Progression of near occlusion to occlusion.
A, Lateral carotid angiogram shows ulcerated stenosis causing near occlusion with ICA diameter beyond the stenosis (larger arrow), reduced in diameter to be smaller than the distal ECA diameter (smaller arrow). It should be about twice that diameter.
B, Lateral carotid angiogram of the same carotid as A about 8 months later shows that the near occlusion has progressed to occlusion.
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FIG 4. Collaterals (cross-filling and dilution) and late arrival of ICA to the head.
A, Anterioposterior right carotid angiogram, head view, contralateral to left near occlusion shows exuberant cross-filling to left middle cerebral branches and even slightly down the supraclinoid carotid (arrow) to supply the anterior choroidal artery.
B, Lateral left carotid angiogram, late arterial neck and head view, shows delay in ICA filling intracranially, and abrupt dilution contrast in the supraclinoid carotid (arrow) above the origin of a fetal-type posterior cerebral artery. This dilution indirectly demonstrates the excellent collateral already shown in A, not opacified here. It also shows the supraclinoid carotid site of the "watershed" between the right carotid source and the extremely severe left carotid stenosis.
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FIG 5. Delayed ICA filling and intracranial dilution from collaterals.
A, Lateral carotid angiogram (neck view) shows delayed ICA filling (larger arrow) beyond the nearly occluded bulb stenosis.
B, There is dilution of contrast of middle cerebral branches (small arrows) intracranially, implying inflow of unopacified blood from circle of Willis collateral sources.
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FIG 6. Decreased diameter of the ipsilateral ICA compared with the normal opposite carotid artery.
A, Anterioposterior right carotid angiogram shows the diameter of the normal ICA (arrow).
B, Anterioposterior left carotid angiogram done with the same magnification (same position of radiograph tube and image intensifier; same field of view) as the right in A showing decreased diameter of the left ICA (arrow).
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FIG 7. Reduced ICA diameter compared with ECA. ICA diameter (larger arrow) is slightly less than distal ECA (small arrow), implying gross reduction of expected diameter. This implies that the ICA is much narrower than it should be.
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FIG 8. Kaplan-Meier event-free survival from ipsilateral stroke for patients with near occlusion.
A, The 3-year intention-to-treat risk of ipsilateral stroke in NASCET patients was 17.9% for medically treated and 11.4% for surgically treated. The 3-year risk of ipsilateral stroke for medically treated NASCET patients who continued to receive medical therapy throughout the duration of the trial (on-treatment) was 27.3%.
B, The 3-year intention-to-treat risk of ipsilateral stroke in ECST patients was 11.1% for medically treated and 10.5% for surgically treated. The 3-year risk of ipsilateral stroke for medically treated ECST patients who continued to receive medical therapy throughout the duration of the trial (on-treatment) was 11.6%.
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FIG 9. Kaplan-Meier event-free survival from ipsilateral stroke for patients with near occlusion, pooled data from the NASCET and ECST. The 3-year intention-to-treat risk of ipsilateral stroke in was 15.1% for medically treated and 10.9% for surgically treated. The 3-year risk of ipsilateral stroke for medically treated patients who continued to receive medical therapy throughout the duration of the trial (on-treatment) was 18.3%.
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FIG 10. Kaplan-Meier event-free survival from ipsilateral stroke for patients with severe stenosis but without near occlusion, pooled data from the NASCET and ECST. The 3-year intention-to-treat risk of ipsilateral stroke in was 26.0% for medically treated and 8.2% for surgically treated. The 3-year risk of ipsilateral stroke for medically treated patients who continued to receive medical therapy throughout the duration of the trial (on-treatment) was 29.3%.
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