Statins, which improve the bioavailability of endogenous nitric oxide and upregulate endothelial nitric oxide synthase, have been used to prevent cerebral vasospasm after aneurysmal subarachnoid hemorrhage. The objective of this study was to determine whether statin therapy diminished vasospasm-induced ischemia as assessed using daily measurements of serum S100B, a biomarker for cerebral ischemia, and computed tomography measurement of ischemic lesion volume.Single-center study of cases and historical controls.Neurointensive care unit in a university hospital.Consecutive patients with aneurysmal subarachnoid hemorrhage treated with clipping or coiling within 96 hrs of symptom onset (n = 278) were included from April 2004 to October 2007.Oral atorvastatin, 40 mg/day for 21 days, was used routinely starting on December 1, 2005, in 142 patients, who were compared with the 136 patients managed earlier.Ischemic lesion size was measured using computed tomography on the last available scan and serum S100B was assayed daily for 15 days after admission. Angiographic narrowing was semiquantitatively assessed in patients with vasospasm. In the overall population, cerebral vasospasm was significantly less common in the statin-treated group. Severity of vasospasm, as assessed on the most severe angiogram, was lowered with statin. Statins significantly reduced volume of ischemia in patients with vasospasm and an uncomplicated coiling procedure. S100B levels were significantly lower in statin-treated patients, and the decrease was greatest among high-grade patients (World Federation of Neurological Surgeons 3-5). No differences were found between statin-treated and untreated groups regarding rescue therapy intensity or 1-yr clinical outcomes.Atorvastatin reduces the incidence, the severity and the ischemic consequences of vasospasm as assessed on computed tomography. In high-grade World Federation of Neurological Surgeons patients, atorvastatin decreases serum levels of S100B, a biomarker of brain ischemia. Despite these positive effects on biomarkers, no improvement of outcome was seen in the overall population, although there was a tendency for a better clinical outcome in high-grade patients.
Objectives: Studies of new neuroprotective approaches in patients with subarachnoid aneurysmal hemorrhage and better family information would benefit from the development of laboratory markers of brain ischemia. The goal of this study was to evaluate mean 15-day S100B for predicting outcomes after subarachnoid aneurysmal hemorrhage. Design: Single center prospective cohort with consecutive inclusions. Setting: Anesthesiology and Critical Care Neurosurgical Unit of a university hospital. Patients: One hundred nine patients admitted within 48 hrs after subarachnoid aneurysmal hemorrhage onset and treated by surgical clipping or coiling within 48 hrs following admission. Interventions: We recorded initial World Federation of Neurologic Surgeons and Fisher grades; comorbidities; initial severity; aneurysm location; presence of acute hydrocephalus; presence of intraventricular hemorrhage; initial seizures and neurogenic lung edema; initial troponin values; treatment of aneurysm; and occurrence of vasospasm. Measurements and Main Results: S100B was assayed daily over the first 15 days. Glasgow Outcome Scores were recorded at intensive care unit discharge and after 6 and 12 months. The main outcome criterion was the 12-month Glasgow Outcome Scale score dichotomized as poor (Glasgow Outcome Scale 1–3) or good (Glasgow Outcome Scale 4–5). Seventy percent of patients had good 12-month outcome. Poor outcome was associated with higher initial World Federation of Neurologic Surgeons and Fisher scores, neurogenic lung edema, high mean 15-day S100B but not initial, troponin initial value, intraventricular hemorrhage, angiographically documented vasospasm, all in an univariate manner. After multivariate analysis, only mean 15-day S100B value significantly predicted outcome (p < 0.0005). The best cutoff for the mean 15-day S100B value was 0.23 μg/L (specificity 0.90, 95% confidence interval [CI] 0.81–0.95; sensitivity 0.91, 95% CI 0.75–0.98; area under the curve 0.98, 95% CI 0.87−0.99). Conclusion: S100B elevation over the first 15 days after subarachnoid aneurysmal hemorrhage is associated with poor outcome after subarachnoid aneurysmal hemorrhage. This result supports the use of S100B as a surrogate marker for brain ischemia in patients with subarachnoid aneurysmal hemorrhage.
S100B has been described as a biologic marker of neuronal damage. The purpose of this study was to assess its prognostic value in patients with subarachnoid aneurysmal hemorrhage.Seventy-four patients (32 men and 42 women; age, 48 +/- 11 yr) admitted within 48 h after subarachnoid hemorrhage onset and treated by surgical clipping or coiling within 2 days after admission were included. World Federation of Neurological Surgeons, Fisher, and Glasgow outcome scores at intensive care unit discharge and at 6 months were evaluated. Blood concentrations of S100B were determined at admission and daily up to day 8.The time course of S100B was increased in patients with high World Federation of Neurological Surgeons and Fisher scores. Patients who underwent surgical clipping had an S100B time course longer than that of those who underwent coiling. This difference remained true after stratification for World Federation of Neurological Surgeons and Fisher scores. The threshold of mean daily value of S100B predicting a poor outcome at 6 months was 0.4 microg/l (sensitivity = 0.50 [95% confidence interval (CI), 0.29-0.71], specificity = 0.87[corrected] [95% CI, 0.76-0.95]). In multivariate analysis, high World Federation of Neurological Surgeons score (odds ratio = 9.5 [95% CI, 3.1-29.4]), mean daily S100B value above 0.4 microg/l (odds ratio = 7.3 [95% CI, 2.3-23.6]), and age (odds ratio = 1.08 per year [95% CI, 1.01-1.15]) were independent predictors of a poor 6-month outcome (Glasgow outcome score 1-3).Mean daily value of S100B assessed during the first 8 days is a prognostic tool complementary to initial clinical evaluation in subarachnoid hemorrhage patients.
An increasing number of elderly patients are treated for aneurysmal subarachnoid hemorrhage. Given that elderly age is associated with both poor outcome and an increased risk of hydrocephalus, we sought to investigate the interaction between age and hydrocephalus in outcome prediction.We enrolled 933 consecutive patients treated for subarachnoid hemorrhage between 2002 and 2010 and followed them for 1 yr after intensive care unit discharge. We first performed stepwise analyses to determine the relationship among neurologic events, elderly age (60 or more yr old), and 1-yr poor outcome (defined as Rankin 4-6). Within the most parsimonious model, we then tested for interaction between admission hydrocephalus and elderly age. Finally, we tested the association between age as a stratified variable and 1-yr poor outcome for each subgroup of patients with neurologic events.24.1% (n=225) of subarachnoid hemorrhage patients were 60 yr old or more and 19.3% (n=180) had 1-yr poor outcomes. In the most parsimonious model (area under the receiver operating characteristic curve, 0.84; 95% CI: 0.82 to 0.88; P<0.001), elderly age and admission hydrocephalus were two independent predictors for 1-yr outcome (P<0.001 and P=0.004, respectively). Including the significant interaction between age and hydrocephalus (P=0.04) improved the model's outcome prediction (P=0.03), but elderly age was no longer a significant predictor. Finally, stratified age was associated with 1-yr poor outcome for hydrocephalus patients (P=0.007), but not for patients without hydrocephalus (P=0.87).In this observational study, elderly age and admission hydrocephalus predicted poor outcome, but elderly age without hydrocephalus did not. An external validation, however, will be needed to generalize this finding.
Background Coiling of ruptured intracranial aneurysms in elderly patients remains debatable in terms of technical feasibility and clinical outcome. Aims In this observational cohort study we aimed to assess the technical feasibility, complication profile and clinical outcomes of elderly patients with subarachnoid hemorrhage (SAH) treated with endovascular therapy. Methods The study included 59 consecutive patients (47 women) aged ≥70 years (mean age 76 years, range 71–84) admitted to our institution with SAH from January 2002 to July 2011. The patients were treated for 66 aneurysms (regular coiling: n=62 (94%), balloon-assisted technique: n=2 (3%), stent and coil technique: n=2 (3%)). World Federation of Neurosurgery (WFNS) grade at admission was 1 in 13 patients, 2 in 23 patients, 3 in 8 patients, 4 in 11 patients and 5 in 4 patients. We analysed data by univariate and multivariate statistical analyses with an emphasis on the initial clinical situation, complications and clinical outcome. Results The technical success rate was 98% with a procedure-related deficit rate of 10% and procedure-related death rate of 5%. The Glasgow Outcome Scale score at 6 months was 1 in 15 patients (25.4%), 2 in 8 patients (13.6%), 3 in 14 patients (23.7%), 4 in 11 patients (18.6%) and 5 in 11 patients (18.6%). Patients admitted with a high initial WFNS grade did not differ statistically in terms of clinical outcome. The final clinical outcome was not significantly correlated with age, initial Fisher score or procedure-related complications. Conclusions Endovascular treatment of elderly patients with ruptured cerebral aneurysms is feasible, safe and beneficial regardless of the presenting WFNS score.
