Abstract
INTRODUCTION/PURPOSE: Cerebral vasospasm (CVS) is a major complication after aneurysmal subarachnoid hemorrhage (aSAH), causing delayed cerebral ischemia in up to 70% of cases. Wall shear stress (WSS), the tangential force of blood on vessel walls within cerebral vessels, is the “cornerstone" that ensures the stability of cerebral blood flow and microcirculation under pulsatile blood flow conditions. While elevated WSS is linked to aneurysm rupture, its role in post‐rupture CVS remains unclear. This study evaluated WSS in intracranial internal carotid artery (ICA) segments to assess cerebral arterial stiffness in aSAH patients with and without CVS, hypothesizing that CVS correlates with increased WSS, indicating localized hemodynamic stress and potential targets for reducing ischemia. MATERIALS/METHODS: This observational retrospective non‐randomized single‐center study was conducted to analyze a maintained database cohort (2013‐2024). The study protocol was approved by the University's Ethics Committee. Informed consent was waived due to the retrospective nature of the study design. A total of 102 patients with aSAH (mean age 37.5 ± 8.2 years, 53 m, 49 w) were enrolled. Group I included 51 patients without CVS, and Group II included 51 aSAH patients with CVS. The inclusion criteria were as follows: aneurysmal SAH, age 16‐70 years, serum creatinine <120 mg/L, Glasgow Coma Scale 8 ‐13, angiographic” CVS on CTASI; dynamic multiphase perfusion computed tomography (PCT) during the first 5 days after onset. The computed tomography angiography source image (CTASI) analysis enabled us to visualize the brain's main vessels and assess the state of their lumen. In all patients included in this study, the minimal intensive projection data analysis identified local luminal narrowing of the cerebral artery of more than 30% of the diameter compared to adjacent sections of the same vascular segment. Based on this, an “angiographic" CVS was diagnosed. Dynamic computed tomography angiography was performed 2‐3 days after the onset of SAH. WSS in the intracranial segment of the ICA was calculated using the Hagen‐Poiseuille equation based on viscosity (0.0035 Pa·s), flow rate from velocity, and radius from CTASI. Statistical analysis was performed using the paired t‐test to compare WSS between the CVS and contralateral hemispheres. Data are presented as Mean ± SEM, with significance set at p < 0.05. RESULTS: WSS values in both groups of SAH patients were significantly elevated compared to normative levels of 10‐20 dynes/cm(2) (p<0.05). In Group I, the mean WSS in the intracranial segment of ICA was 25.1 ± 3.6 dynes/cm(2), indicating post‐SAH stress. Group II demonstrated significantly higher WSS values, particularly on the side of CVS, with a mean of 47.2 ± 4.1 dynes/cm(2) (p < 0.01 vs. Group I and contralateral). WSS was consistently higher on the side affected by CVS, indicating localized vascular stress. CONCLUSION: In CVS patients, WSS was significantly elevated in the vasospasm basin (p < 0.01), indicating persistent regional hemodynamic alterations that may sustain ischemia. WSS could serve as a biomarker for CVS severity and guide therapies, such as vasodilators. Prospective studies should track WSS changes in relation to outcomes to improve aSAH risk assessment and treatment.