Related Experiment Video
Updated: Apr 3, 2026

Pre-Chiasmatic, Single Injection of Autologous Blood to Induce Experimental Subarachnoid Hemorrhage in a Rat Model
Published on: June 18, 2021
Association between nimodipine use and 28-day mortality in non-traumatic subarachnoid hemorrhage: Insights from
Xuhui Liu1, Xujie Wang2, Rongfei Xie2
1Department of Neurology, The Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, China.
Background:
The precise relationship between nimodipine use, specifically its dose-response effect, and 28-day mortality in non-traumatic subarachnoid hemorrhage (SAH) remains unclear. This study aimed to evaluate the exact impact of nimodipine use and its dosage on 28-day mortality in these patients.
Methods:
We conducted a retrospective cohort study using data from the Medical Information Mart for Intensive Care IV (MIMIC-IV) database. A total of 785 eligible ICU patients with non-traumatic SAH were included. Nimodipine exposure was specifically defined as the total cumulative dose administered within the first 24 h of ICU admission. Propensity score matching (PSM) was employed to balance baseline covariates between nimodipine and non-nimodipine groups, resulting in 185 matched pairs. Four Cox regression models were used to evaluate the association between nimodipine use and mortality: Model 1 (unadjusted), Model 2 (adjusted for demographic factors), Model 3 (adjusted for comorbidities and clinical severity), and Model 4 (fully adjusted for key covariates, including treatment and clinical status). Dose-response relationships were explored with Kaplan-Meier curves and restricted cubic spline analysis. Subgroup analyses were conducted to test the robustness of the effect across different patient characteristics.
Results:
Baseline characteristics between nimodipine and non-nimodipine groups were well-balanced after PSM, with no significant differences in key covariates, including age, GCS score, and comorbidities. Before matching, nimodipine use was associated with a significant reduction in mortality (HR = 0.39, p < 0.001) in all models, with a 61% reduction in risk in the unadjusted model (Model 1). After PSM, the hazard ratio improved to 0.20 (p < 0.001), indicating an 80% reduction in mortality in Model 4. Higher nimodipine doses (60-150 mg and ≥150 mg) showed a dose-dependent protective effect, with the highest dose group (≥150 mg) exhibiting the most significant reduction in mortality (HR = 0.09, p < 0.001). These findings remained consistent across various clinical subgroups, including age, ventilation status, and Glasgow Coma Scale (GCS) score. Kaplan-Meier survival curves and subgroup analyses demonstrated that nimodipine use was associated with significantly lower 28-day mortality across both unmatched and matched cohorts. The dose-response relationship was confirmed through restricted cubic spline analysis.
Conclusion:
Nimodipine use is significantly associated with reduced 28-day mortality in non-traumatic SAH patients, with a dose-dependent effect. The results emphasize the importance of early intervention and appropriate dosing. Future research should focus on optimizing nimodipine dosing and timing to enhance survival outcomes in this patient population.

