Epilepsy & behavior : E&B · 2026
Association between admission D-dimer levels and post-stroke epilepsy risk: a retrospective cohort study.
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Cai Zhongran, Wang Xiaohua, Xu Xiaowei
Аннотация
BACKGROUND: Post-stroke epilepsy (PSE) is a severe complication following acute ischemic stroke (AIS), yet early identification of patients at high risk remains challenging. This study evaluated the association between baseline D-dimer levels and incident PSE within one year after AIS.
METHODS: In this secondary analysis of a multicenter retrospective cohort, 21,459 patients with first-ever AIS were included. D-dimer was modeled as a log2-transformed continuous variable. Multivariable logistic regression with progressive adjustment, restricted cubic spline analysis, and sensitivity analyses were performed. Internal validation was conducted using bootstrap resampling.
RESULTS: The median baseline D-dimer level was 0.92 mg/L (IQR 0.65-1.49). PSE occurred in 936 patients (4.36%). After full adjustment, each doubling of D-dimer was associated with a 3.3-fold increase in PSE odds (OR 3.33, 95% CI 2.94-3.78). The association remained consistent in sensitivity analyses excluding patients with deep vein thrombosis (OR 3.86, 95% CI 3.37-4.43), atrial fibrillation (OR 3.50, 95% CI 3.04-4.04), or extreme D-dimer values (OR 3.41, 95% CI 2.99-3.91). A non-linear relationship was observed, with PSE risk rising more steeply at higher D-dimer levels. The C-statistic for the fully adjusted model was 0.968.
CONCLUSION: Elevated baseline D-dimer levels were independently associated with an increased risk of PSE within one year after AIS. As a routinely available biomarker, D-dimer may inform risk assessment in acute stroke units; however, external validation in independent cohorts with prospective PSE ascertainment is required before clinical implementation.
METHODS: In this secondary analysis of a multicenter retrospective cohort, 21,459 patients with first-ever AIS were included. D-dimer was modeled as a log2-transformed continuous variable. Multivariable logistic regression with progressive adjustment, restricted cubic spline analysis, and sensitivity analyses were performed. Internal validation was conducted using bootstrap resampling.
RESULTS: The median baseline D-dimer level was 0.92 mg/L (IQR 0.65-1.49). PSE occurred in 936 patients (4.36%). After full adjustment, each doubling of D-dimer was associated with a 3.3-fold increase in PSE odds (OR 3.33, 95% CI 2.94-3.78). The association remained consistent in sensitivity analyses excluding patients with deep vein thrombosis (OR 3.86, 95% CI 3.37-4.43), atrial fibrillation (OR 3.50, 95% CI 3.04-4.04), or extreme D-dimer values (OR 3.41, 95% CI 2.99-3.91). A non-linear relationship was observed, with PSE risk rising more steeply at higher D-dimer levels. The C-statistic for the fully adjusted model was 0.968.
CONCLUSION: Elevated baseline D-dimer levels were independently associated with an increased risk of PSE within one year after AIS. As a routinely available biomarker, D-dimer may inform risk assessment in acute stroke units; however, external validation in independent cohorts with prospective PSE ascertainment is required before clinical implementation.