Pharmacodynamic comparison of butylphthalide and edaravone dexborneol in acute cerebral infarction – a mechanism-based subgroup analysis focusing on culprit vessel and etiology

Abstract

Introduction/Objective This study compared the pharmacodynamics of butylphthalide and sodium chloride (BSC) with those of edaravone dexborneol (ED) in middle-aged and elderly patients with acute cerebral infarction (ACI), focusing on etiology and culprit vessel stratification.

Methods A total of 138 middle-aged and elderly patients with ACI admitted to our hospital from January 2023 to June 2025 were enrolled and randomly assigned to the BSC group (n = 69) and the ED group (n = 69). Both groups received standard ACI treatment; the BSC group received BSC injection (25 mg twice daily), and the ED group received ED injection (30 mg twice daily). The main outcome measures were the National Institutes of Health Stroke Scale (NIHSS) score, modified Rankin Scale (mRS) score, and mean flow velocity (Vm) of the middle cerebral artery before and after treatment. The secondary indices included coagulation-related parameters [platelet count (PLT) and white blood cell (WBC) count] and safety evaluation. Subgroup analyses were based on culprit vessel type (large-vessel / small-vessel disease) and etiologic category (atherosclerotic infarction / cardioembolism).

Results Findings revealed that, compared with the ED group, the BSC group had a significantly lower NIHSS score (p < 0.05) and a significantly higher Vm in the middle cerebral artery, especially in the large-vessel disease subgroup (p < 0.05). Coagulation profiles showed that after seven days of treatment, platelet counts were lower in the BSC group compared with the ED group (p < 0.05). In the atherosclerotic infarction subgroup, BSC resulted in lower PLT counts than in the ED group (p < 0.05). Safety assessments indicated comparable adverse event rates and liver/kidney function between the groups (p > 0.05), with no cases of serious bleeding or organ damage.

Conclusion BSC exerts a pathology type-dependent therapeutic effect via its multi-target mechanism (vascular endothelial growth factor-mediated collateral augmentation and platelet-activating factor-dependent platelet inhibition), demonstrating significant etiology-specific efficacy and supporting its prioritization in large-vessel or atherosclerotic ACI subtypes.

Keywords: butylphthalide; edaravone dexborneol; acute cerebral infarction; middle-aged and elderly adults; neuroprotection; hemodynamics