Stroke: Vascular and Interventional Neurology (Nov 2023)

Abstract 223: Pre‐Thrombectomy Diagnosis of Large Vessel Occlusion with Underlying Intracranial Atherosclerotic Disease

  • Mohamed A. Tarek,
  • Mateus Damiani,
  • Mahmoud H. Mohammaden,
  • Srikant Rangaraju,
  • Pedro N. Martins,
  • Jay N. Dolia,
  • Aqueel A. Pabaney,
  • Jonathan R. Grossberg,
  • Michael Nahhas,
  • Alhamza R. Nogueira,
  • Raul G. Haussen

DOI
https://doi.org/10.1161/SVIN.03.suppl_2.223
Journal volume & issue
Vol. 3, no. S2

Abstract

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Introduction Intracranial atherosclerotic disease (ICAD) is one of the leading causes of ischemic stroke. We sought to identify variables associated with ICAD underlying large vessel occlusion strokes (LVOS) to facilitate pre‐procedural diagnosis. Methods Retrospective analysis of a prospectively collected thrombectomy single comprehensive stroke center database. Inclusion criteria: anterior circulation occlusion involving the intracranial ICA, MCA‐M1/M2/M3 or ACA(A1‐A2‐A3). ICAD cases were matched for age and sex in a 1:1 ratio to non‐ICAD controls. Results A total of 348 patients were included in the analysis. Patients with ICAD more frequently presented with vascular risk factors. ICAD LVOS showed less frequent atrial fibrillation(AF)(4%vs31%,P=0.001), and lower baseline NIHSS(14vs17,P=0.002) compared to the non‐ICAD group. The ICAD group less frequently showed hyperdense vessel sign and territorial cortical infarcts, but presented more frequently borderzone, deep subcortical and bilateral infarcts on CT compared to the non‐ICAD group. ICAD strokes had higher ASPECTS, and more frequently had calcifications at the carotid siphon as well as multifocal intracranial stenosis on CTA. CTA collaterals scores were comparable between groups. The ICAD group had lower median infarct core volume (1vs12 ml;P>0.001), Tmax>4s (249vs276 ml;P>0.003), and Tmax>6s (97vs140 ml;P4:6 s ratio (2vs1;P=0.007) on CTP compared to non‐ICAD group. On multivariable analysis, absence of AF, absence of cortical infarcts, presence calcium at ipsilateral carotid siphon, cerebrovascular stroke risk factors burden (DM‐HTN‐Hyperlipidemia‐smoking), borderzone infarcts either (superficial cortical or Internal deep border zone), and multifocal intracranial stenosis were independent factors associated with ICAD. The model (table 1) by AUC for the whole model had sensitivity of 88% [P=<0.001,95%CI(0.84‐0.91)]. Conclusion In patients with anterior circulation LVO strokes, our study suggests that presence of CVS risk factors burden, calcium at carotid siphon, borderzone infract pattern, absence of territorial cortical infarct pattern, multifocal intracranial stenosis, and absence of AF were predictors for ICAD. Additional validation is warranted