Endothelial cell activation seems to be an important process in the multifactorial pathophysiology of delayed cerebral ischemia (DCI) and subsequent poor clinical outcome after aneurysmal subarachnoid hemorrhage (aSAH).

To assess the association between biomarker levels of endothelial activation and the occurrence of DCI and poor clinical outcome six months after aSAH.

Between October 2018 and November 2020, 75 aSAH patients were included. Blood samples were taken on admission, days 3–5 and days 9–11 after aSAH. Ten patients with unruptured intracranial aneurysms served as controls. Poor outcome was assessed at six months, defined by a modified Rankin Scale score of 4–6. The cohort was dichotomized into patients with and without DCI and good and poor outcomes. Biomarker levels of von Willebrand factor (vWF), E-selectin, thrombomodulin, syndecan-1 and matrix metalloproteinase (MMP-9) were analyzed and compared between groups by a T-test or Mann–Whitney U test, depending on the normality of the data.

Twelve (16.0%) patients developed DCI, and 39 (41.9%) patients had poor outcomes at six months post-aSAH. None of the biomarkers showed significant differences between patients with and without DCI. vWF and syndecan-1 were elevated on admission and on days 9–11 in patients with poor outcomes (p < 0.05 and p = 0.02, respectively).

Levels of vWF, E-selectin, thrombomodulin, syndecan-1 and MMP-9 were not associated with the occurrence of DCI, although higher levels of vWF and syndecan-1 were associated with poor outcome at six months. Further research is needed to establish the role of these biomarkers in aSAH patients.

Mean cerebral blood flow velocity (mean-CBFV) obtained from Transcranial Doppler (TCD) poorly predicts cerebral vasospasm in patients with aneurysmal subarachnoid hemorrhage (aSAH). Variability descriptors of mean-CBFV obtained during extended TCD recordings may improve this prediction. We assessed the feasibility of generating reliable linear and non-linear descriptors of mean-CBFV variability using extended recordings in aSAH patients and in healthy controls. We also explored which of those metrics might have the ability to discriminate between aSAH patients and healthy controls, and among patients who would go on to develop vasospasm and those who would not.

Bilateral mean-CBFV, blood pressure, and heart rate were continuously recorded for 40 minutes in aSAH patients (n = 8) within the first 5 days after ictus, in age-matched healthy controls (n = 8) and in additional young controls (n = 8). We obtained linear [standard deviation, coefficient of variations, and the very-low (0.003–0.040 Hz), low (0.040–0.150 Hz), and high-frequency (0.15–0.4 Hz) power spectra] and non-linear (Fractality, deterministic Chaos analyses) variability metrics.

We successfully obtained TCD recordings from patients and healthy controls and calculated the desired metrics of mean-CBFV variability. Differences were appreciable between aSAH patients and healthy controls, as well as between aSAH patients who later developed vasospasm and those who did not.

A 40-minute TCD recording provides reliable variability metrics in aSAH patients and healthy controls. Future studies are required to determine if mean-CBFV variability metrics remain stable over time, and whether they may serve to identify patients who are at greatest risk of developing cerebral vasospasm after aSAH.