Factors associated with short-term recurrent ischemic stroke: culprit plaque, collateral circulation, and pathological mechanisms.

Purpose: The purpose of the study was to investigate the predictive value of baseline plaque characteristics, perfusion injury, and pathological mechanisms for new ischemic cerebral lesions (NICLs) in medically treated patients with acute ischemic stroke (AIS) due to intracranial atherosclerotic stenosis (sICAS). Methods: This was a retrospective analysis of AIS patients with 50-99% middle cerebral artery M1 segment (MCA-M1) stenosis undergoing high-resolution vessel wall magnetic resonance imaging (HR-VWI) and computed tomography perfusion (CTP) within 1 week of admission to evaluate plaque characteristics and collateral status (CS). sICAS pathogenesis was classified into three subtypes: artery-to-artery embolism (A-A), border zone infarction (BZI), and penetrating artery occlusion, primarily based on infarct topography. Baseline clinical/imaging features and pathogenic mechanisms were compared between patients with and without NICLs during 1-year follow-up. A Cox proportional hazards regression model was used to identify independent risk factors associated with stroke recurrence. Results: Among the 78 eligible patients, 25 developed NICLs, showing significantly higher adverse CS (60.0% vs. 24.5%, p = 0.005) and a larger mismatch area (p = 0.043) than the non-NICL group, with no plaque feature differences. NICL's incidence varied significantly among pathogenesis subtypes (p = 0.003), with baseline BZI demonstrating higher recurrence rates than A-A (56% vs. 28%, p = 0.001). Multivariable Cox regression analysis found that BZI [adjusted hazard ratio, 3.28 (95% CI, 1.49-7.36); p = 0.004] and unfavorable CS [adjusted hazard ratio, 2.87 (95% CI, 1.16-7.09); p = 0.011] were independently associated with the NICLs. Conclusion: In the risk stratification for short-term recurrence for medically managed AIS, baseline CT perfusion deficits are prioritized over plaque imaging. Moreover, unfavorable CS and the pathogenic mechanism of BZI indicate compromised hemodynamics and serve as the pivotal and independent predictors of early relapse.