Delayed Cerebral Ischemia after Aneurysmal Subarachnoid Hemorrhage: The Results of Induced Hypertension Only after the IMCVS Trial—A Prospective Cohort Study

Abstract

Delayed cerebral ischemia (DCI) is a predictor of poor outcome after aneurysmal subarachnoid hemorrhage (SAH). Treatment strategies vary and include induced hypertension and invasive endovascular treatment. After the IMCVS trial (NCT01400360), which failed to demonstrate a benefit of endovascular treatment for cerebral vasospasm (CVS) and resulted in a significantly worse outcome, we changed our treatment policy in patients with diagnosed CVS to induced hypertension only, and we present our prospective results in the subgroup of SAH patients meeting inclusion criteria of the IMCVS trial. All patients underwent screening for DIND when conscious and for CVS using CT-A/-P at day 6–8 after SAH. In the case of CVS, arterial hypertension was induced and continued until re-assessment. In total, 149 of 303 patients developed CVS. DCI developed in 35 patients (23.5%). In multivariate analyses, CVS was a predictor for the development of new infarctions. Poor admission status, re-bleeding before treatment, and DCI predicted poor outcome. The omittance of invasive endovascular rescue therapies in SAH patients with CVS, additional to induced hypertension, does not lead to a higher rate of DCI. Potential benefits of additional endovascular treatment for CVS need to be addressed in further studies searching for a subgroup of patients who may benefit.

Invasive Diagnostic and Therapeutic Management of Cerebral VasoSpasm after Aneurysmal Subarachnoid Hemorrhage (IMCVS)—A Phase 2 Randomized Controlled Trial

“…We therefore changed our treatment policy in patients with diagnosed CVS to induced hypertension only and published our prospective results in the subgroup of SAH patients meeting inclusion criteria of the IMCVS trial recently [ 21 ].…”

Subarachnoid hemorrhage: New insights on pathogenesis

“…It has been suggested that commensal gut microbiota protects against ischemic stroke pathology and that their depletion leads to increased mortality and poor outcome, including worse neurological function (Singh et al, 2016;Winek et al, 2016). These findings become relevant given that SAH is a type of hemorrhagic stroke and has also been shown to cause delayed ischemic stroke (Martin and Rymer, 2011;Guresir et al, 2022). Compared to ischemic stroke not secondary to SAH, less is known about the association between SAH and the gut microbiome.…”

Molecular mechanisms of neuronal death in brain injury after subarachnoid hemorrhage

“…Cerebral ischemia is a common complication after SAH, with >30% of patients experiencing delayed cerebral ischemia ( Stienen et al, 2014 ). Decreased cerebral hypoperfusion leads to cerebral ischemia and cerebral infarction, ultimately inducing severe neurological dysfunction, brain injury and even death ( Güresir et al, 2022 ; Hostettler et al, 2022 ). Cerebral ischemia is caused by various factors, including cerebral vasospasm, micro thrombosis, blood-brain barrier destruction, inflammatory reactions and cerebral vascular self-regulation dysfunction ( Macdonald, 2014 ).…”