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Ischemic stroke
Original research
Comparative analysis between 1-D, 2-D and 3-D carotid web quantification
  1. Catarina Perry da Camara1,2,
  2. Raul G Nogueira1,
  3. Alhamza R Al-Bayati1,
  4. Leonardo Pisani1,
  5. Mahmoud Mohammaden1,
  6. Jason W Allen3,
  7. Fadi Nahab4,
  8. Marta Olive Gadea1,5,
  9. Michael R Frankel1,
  10. Diogo C Haussen1
  1. 1Marcus Stroke & Neuroscience Center, Grady Memorial Hospital, Emory University School of Medicine, Atlanta, Georgia, USA
  2. 2Department of Neuroradiology, Centro Hospitalar Universitário Lisboa Central, Lisboa, Portugal
  3. 3Radiology and Imaging Sciences, Emory University School of Medicine, Atlanta, Georgia, USA
  4. 4Neurology, Emory University School of Medicine, Atlanta, Georgia, USA
  5. 5Department of Neurology, Hospital Vall d'Hebron, Barcelona, Spain
  1. Correspondence to Dr Diogo C Haussen, Neurology, Marcus Stroke and Neuroscience Center, Grady Memorial Hospital. Emory University School of Medicine, Atlanta, Georgia, USA; diogo.haussen{at}emory.edu

Abstract

Background Carotid webs (CaW) are now recognized as a cause of ischemic stroke in young patients. The thromboembolic potential appears related to the CaW’s morphology and consequent impact on local flow dynamics. We aim to evaluate the reliability of different measurement methods for the quantification of CaW and their relationship to symptomatic status, presence of large vessel occlusion stroke (LVOS), clot burden and final infarct volume.

Methods This was a retrospective analysis of the local comprehensive stroke center CaW database (September 2014–July 2019). CT angiograms (CTAs) were reviewed independently by two raters, blinded to the clinical information and laterality of the stroke/transient ischemic attack. CaW were quantified with 1-D (length), 2-D (area) and 3-D (volume) measurements via Osirix software. Final infarct volume was calculated on MRI. Patients with superimposed CaW thrombus and no repeat imaging were excluded.

Results Forty-eight CaW (37 symptomatic and 11 contralateral/asymptomatic) in 38 patients were included. Mean age (±SD) was 48.7 (±8.5) years, 78.9% were women and 77.1% were black. Inter-rater agreement was 0.921 (p<0.001) for 1-D, 0.930 (p<0.001) for 2-D, and 0.937 (p<0.001) for 3-D CaW measurements. When comparing symptomatic with asymptomatic CaW, mean web length was 3.2 mm versus 2.5 mm (p<0.02), median area was 5.8 versus 5.0 mm2 (p=0.35) and median volume was 15.0 versus 10.6 mm3 (p<0.04), respectively. CaW with a thinner profile (longer intraluminal projection compared with the base) were more likely to be symptomatic (0.67±0.17 vs 0.88±0.37; p=0.01). Average CaW 1-D and final infarct volume had a weak but positive association (Κ=0.230, p<0.05), while no association among web measurements and the presence of LVOS or clot burden was observed.

Conclusion CaW dimension quantification (1-D, 2-D and 3-D) is highly reproducible. Linear and volumetric measurements were more strongly associated with symptoms. The impact of CaW size on the presence of LVOS, clot burden and final infarct volume is unclear.

  • stroke
  • CT angiography
  • vessel wall
  • artery

Data availability statement

No data are available. Not applicable.

https://doi.org/10.1136/neurintsurg-2021-018192

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    Data availability statement

    No data are available. Not applicable.

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    Footnotes

    • Twitter @PerrydaCamaraMD, @pisanileonardo, @diogohaussen

    • Contributors CPC: study conception, design of the work, acquisition of data, statistical analysis, interpretation of data, drafting of the manuscript. RGN, ARA, LP, MM, JWA, FN, MOG, MRF: data acquisition, critical revision of manuscript. DCH: study conception, design of the work, acquisition of data, interpretation of data, critical revision of manuscript. DH is the guarantor.

    • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

    • Competing interests CPC, ARA, LP, MM, JWA, FN, MOG, MRF: none. RGN: principal Investigator, Stryker Neurovascular (DAWN trial, no compensation; Trevo 2 trial), Cerenovus/Neuravi (ENDOLOW trial, no compensation); consultant to Stryker Neurovascular; steering committee member, Stryker Neurovascular (no compensation), Medtronic (SWIFT trial, SWIFT Prime trial, no compensation), Cerenovus/Neuravi (ARISE 2 trial, no compensation); angiographic core lab, Medtronic (STAR trial); executive committee member, Penumbra (no compensation); physician advisory board, Cerenovus/Neuravi, Phenox, Anaconda, Genentech, Biogen, Prolong Pharmaceuticals, Allm (no compensation), Viz-AI; stock options, Viz-AI. DCH: consultant for Stryker, Cerenovus, Vesalio; Viz-AI; stock options.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.