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Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
Published on: June 3, 2021
Impact of Parenchymal Hemorrhage on Internal Carotid Artery Wall Shear Stress in Post-Traumatic Vasospasm: A Dynamic
Alexey O Trofimov1, Gregory N Vlasov2, Kseniia A Trofimova1
1Privolzhsky Research Medical University: Privolzskij issledovatel'skij medicinskij universitet Ministerstva zdravoohranenia Rossijskoj Federacii.
Insights
Elevated wall shear stress (WSS) in the internal carotid artery (ICA) is linked to cerebral vasospasm (CVS) after moderate-to-severe traumatic brain injury (msTBI). Parenchymal hemorrhage further increases this hemodynamic stress, indicating WSS as a potential biomarker.
Area of Science:
- Neuroscience
- Biomedical Engineering
- Trauma Surgery
Background:
- Post-traumatic cerebral vasospasm (CVS) worsens outcomes in moderate-to-severe traumatic brain injury (msTBI).
- Wall shear stress (WSS) influences endothelial function, but its role in post-traumatic CVS is unclear.
- This study investigates ICA WSS in msTBI patients with and without parenchymal hemorrhage.
Purpose of the Study:
- To assess supraclinoid internal carotid artery (ICA) wall shear stress (WSS) in patients with moderate-to-severe traumatic brain injury (msTBI).
- To compare WSS levels between msTBI patients with and without non-surgical parenchymal hemorrhage.
- To explore the relationship between WSS and clinical outcomes in msTBI.
Main Methods:
- Retrospective cohort study of 85 msTBI patients with angiographic CVS (2013-2024).
- Patients divided into groups based on Marshall CT classification (with/without parenchymal hemorrhage).
- Dynamic helical CT angiography and Doppler ultrasound used to calculate ICA WSS via a Poiseuille-based formula.
Main Results:
- ICA WSS was significantly elevated above the reference range in both msTBI groups (p<0.001).
- Patients with parenchymal hemorrhage (Group 2) showed significantly higher WSS than those without (Group 1) (p<0.0001).
- Group 2 exhibited higher ipsilateral WSS compared to contralateral and Group 1 means; a trend towards worse outcomes (GOS) was observed.
Conclusions:
- Post-traumatic CVS in msTBI is associated with markedly elevated ICA WSS.
- Parenchymal hemorrhage amplifies hemodynamic stress, potentially driving microcirculatory remodeling.
- Elevated WSS may serve as a biomarker for secondary brain injury risk, guiding individualized management.
Background:
Post-traumatic cerebral vasospasm (CVS) significantly worsens outcomes in moderate-to-severe traumatic brain injury (msTBI). While wall shear stress (WSS) modulates endothelial function, its state in post-traumatic CVS remains poorly understood. We aimed to assess supraclinoid internal carotid artery (ICA) WSS in msTBI patients with and without non-surgical parenchymal hemorrhage.
Methods:
This retrospective cohort study (2013-2024) included 85 adults with msTBI and angiographic CVS. Patients were divided into Group 1 (Marshall II-III, no hematoma; n=43) and Group 2 (Marshall IV, non-surgical parenchymal hemorrhage; n=42). Dynamic helical CT angiography (DHCTA) and Doppler ultrasound were performed 2-5 days post-injury. WSS in the ICA C7 segment was calculated using a Poiseuille-based formula incorporating mean CBFV and vessel radius.
Results:
ICA WSS significantly exceeded the reference range (0.82 ± 0.08 Pa) in both groups (p<0.001). In Group 2, WSS was significantly higher than in Group 1 (p<0.0001). Specifically, Group 2 ipsilateral WSS (64.4 ± 9.8 Pa) was significantly higher than both the contralateral side (49.3 ± 8.3 Pa; p=0.021) and the Group 1 mean (33.2 ± 7.5 Pa; p<0.0001). No significant age-WSS correlation was observed (p=0.72). Group 2 exhibited a trend toward worse clinical outcomes (GOS), though only moderate disability (GOS 4) showed a significant difference (p<0.05).
Conclusions:
Post-traumatic CVS in msTBI is associated with markedly elevated ICA WSS. The presence of parenchymal hemorrhage further amplifies this hemodynamic stress, potentially contributing to non-physiological microcirculatory remodeling. These findings suggest WSS could serve as a biomarker for secondary brain injury risk, necessitating individualized surgical and medical management.
