The role of oxidative stress as a risk factor for rupture of posterior inferior cerebellar artery aneurysms

Abstract

Cerebral aneurysm affects 2-5% of the population and posterior inferior cerebellar artery (PICA) aneurysms account for 1-3% of all intracranial aneurysms. Oxidative stress is known to contribute to the progression of cerebrovascular disease and it may be increased by inflammation, a key contributor to cerebral aneurysm development and rupture. The aim of this study was to examine the role of overall oxidative stress as a risk factor for rupture of PICA aneurysms. This study included 29 patients with PICA aneurysms: 18 ruptured and 11 unruptured. We determined catalase, malondialdehyde, myeloperoxidase and carbonyl groups in homogenates of excised aneurysm tissue after surgery and plasma levels of C reactive protein and fibrinogen. The patient's age and sex, size of aneurysms, multiplicity, history of previous subarachnoidal hemorrhage (SAH) and risk factors for oxidative stress such as hypertension and smoking were compared between unruptured and ruptured aneurysms. Maximal diameter and SAH history were independent predictors for aneurysm rupture. Activity of catalase was decreased while activity of myeloperoxidase, levels of malondialdehyde, carbonyl groups in aneurismal tissue and plasma levels of C reactive protein and fibrinogen were increased in patients with ruptured aneurysms. Plasma levels of C reactive protein and fibrinogen showed positive correlation with myeloperoxidase, malondialdehyde, carbonyl groups and PHASES score and negative correlation with catalase. These findings suggest that oxidative stress may contribute importantly to rupture of PICA aneurysms and plasma levels of C reactive protein and fibrinogen correlate with oxidative stress markers in tissue.

Pharmacological Inhibition of Epidermal Growth Factor Receptor Prevents Intracranial Aneurysm Rupture by Reducing Endoplasmic Reticulum Stress

“…19 These are in agreement with our current findings. Therefore, as a known risk factor, [59][60][61][62] oxidative stress might compound with overall EGFR activation and ER-stress induction on the aneurysm site, eventually contributing to the rupture of aneurysms.…”

Clinical efficacy of early microsurgical clipping of tumor neck in the treatment of cerebral aneurysm rupture and bleeding and its impact on oxidative stress response and prognosis of patients

“…After CA rupture and bleeding, body is in a hypercoagulable state, and brain tissue presents hypoxia, which is prone to oxidative stress response, producing a large amount of oxygen free radicals and consuming a large amount of antioxidant substances; in oxidative reaction, lipid peroxidation substance MDA receives production; if without treatment in a timely manner and inhibiting oxidative stress response, risk of secondary bleeding in patients exhibits elevation, and mortality rate increases accordingly [25]. Herein, serum sVCAM-1, sICAM-1 and MDA levels in EG two weeks after the operation exhibited depletion relative to those before the operation, and EG exhibited depletion relative to CG, suggesting that early surgery can attenuate oxidative stress response of patients with CA rupture and bleeding, which was consistent with previous studies [26].…”

Efficacy of Acetylcysteine and Selenium in Aneurysmal Subarachnoid Hemorrhage Patients: A Prospective, Multicenter, Single Blind Randomized Controlled Trial

“…Numerous studies implicating OS in the pathophysiology of SAH support to role of antioxidants in these patients. 6 7 ‘A multicenter prospective study involving traumatic brain injury showed that the low serum vitamin E level was associated with unfavorable outcome at 1 and 6 months after the injury. 59 They emphasized that vitamin E is a potent antioxidant that administration of this drug resulted in a significant reduction in mortality and improved function outcome.…”

“…Increasing evidence supports the role for systemic OS in SAH patients. 6 7 When a brain hemorrhage begins, edema develops and surrounds the hematoma. 8 During this process, hemorrhagic clots releases toxic substances like thrombin and iron causing the development of perihematomal edema (PHE) via the oxidation process.…”

“…1 ). 6 10 11 12 13 14 15 16 17 Given the supporting data regarding OS biomarkers in SAH, numerous preclinical and clinical studies evaluated its pathophysiology in SAH and assessed the efficacy of targeted antioxidant treatment. Nevertheless, conflicting results were obtained as some studies yielded beneficial effects of antioxidants, 11 18 whereas other studies failed to confirm such an effect.…”