ABSTRACT NUMBER: ESOC2026A1720 ENDOTHELIAL DYSFUNCTION MEDIATES INFLAMMATION–DRIVEN POOR PROGNOSIS IN SYMPTOMATIC INTRACRANIAL ATHEROSCLEROSIS STENOSIS

Abstract Background and aims Systemic inflammation predicts poor outcomes in symptomatic intracranial atherosclerotic stenosis (sICAS), but the underlying vascular pathway remains unclear. We investigated whether endothelial dysfunction, measured by urinary albumin-to-creatinine ratio (UACR), mediates the association between inflammation and prognosis. Methods We analyzed 2,267 sICAS patients from the China National Stroke Registry III. High-sensitivity C-reactive protein (hsCRP) ≥2 mg/L and UACR ≥30 mg/g were exposures, and 90-day poor outcome (modified Rankin Scale 3–6) was the endpoint. Multivariable logistic regression and mediation analysis were performed. In 277 patients from a sICAS-CFD cohort, patient-specific computational fluid dynamics was used to assess the relationship between UACR and post-stenotic perfusion. Results Both hsCRP ≥2 mg/L (adjusted odds ratio [aOR] 1.43, 95% CI 1.12–1.84) and UACR ≥30 mg/g (aOR 1.91, 95% CI 1.49–2.45) independently predicted poor outcome. UACR mediated 22.2% of the adverse effect of hsCRP (p = 0.008), with stronger mediation in patients with hypertension or diabetes. In the CFD cohort, hypoperfused patients with preserved post-stenotic mean arterial pressure (≥70 mmHg) had significantly higher UACR (p = 0.040). Conclusions Endothelial dysfunction, reflected by UACR, partially links inflammation to disability in sICAS, while distal vascular dysfunction drives perfusion failure beyond macroscopic pressure loss. Conflict of interest Wuqiong.nothing to disclose