Background Carotid web (CaW) constitutes a possible cause of ischemic stroke, particularly large vessel occlusion syndromes. We aim to evaluate misdiagnosis rates and diagnosis trends for CaW.
Methods Based on CT angiography (CTA), we prospectively identified a cohort of patients with symptomatic CaW treated at two comprehensive stroke centers (CSC) from 2014 to 2020 to assess misdiagnosis. Official CTA reports from the CSCs and referring hospitals were then reviewed for mention of CaW. For diagnosis trends, we retrospectively analyzed a CSC electronic medical record, identifying patients with CaW mentioned in an official CTA report from 2011 to 2020.
Results For misdiagnosis, 56 patients with symptomatic CaW were identified in the CSCs; 16 (28%) had bilateral CaW, totaling 72 CaWs. Only one CaW (5.5%) was reported at referring facilities, from 14 patients/18 CaWs imaged with CTA. Conversely, 43 (69%) CaWs were reported from 49 patients/62 CaWs at the CSC (p<0.01). For diagnosis trends, from 2011 to 2020, 242 patients at a CSC accounted for 266 CTA reports mentioning CaW. The majority of these reports (n=206, 77%) were associated with stroke/transient ischemic attack (TIA) ICD-9/ICD-10 codes. The rate of CaW diagnosis adjusted per 1000 patients with stroke/TIA increased over time, 2015 being the most significant point of change ('joinpoint'; p=0.01). The analysis of CaW mentions normalized per 1000 CTA reports also showed increasing rates of diagnosis over time (joinpoint:2014; p<0.02).
Conclusion CaW was predominantly identified in patients with strokes/TIAs rather than asymptomatic patients. CaW was commonly overlooked in facilities with lower levels of cerebrovascular certification. Recognition of CaW at a CSC has significantly increased over time, independent of overall imaging and stroke patient volume.
- vessel wall
- CT angiography
Data availability statement
The data that supports the findings of this study are available from the corresponding author upon reasonable request.
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Contributors EMO, RGN, and DCH conceived and planned the study. EMO, SK, ARA-B, BL, FN, CPC, and CCP contributed to data acquisition. EMO and DCH performed statistical calculations. EMO, DCH, BL, and JWA contributed to interpretation of the results. EMO and DCH took lead in writing the paper, with all other authors providing critical feedback that helped shape the final manuscript.
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 The declared interests below are associations with commercial entities that could be viewed as having an interest in the general area of the submitted manuscript. None of these entities provided direct funding or sponsorship in support of this paper. DCH: Consultant for Stryker and Vesalio, Viz-AI (stock options). 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 Inc (no compensation), Viz-AI (stock options).
Provenance and peer review Not commissioned; externally peer reviewed.
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