Angiographic Vasospasm Is Strongly Correlated With Cerebral Infarction After Subarachnoid Hemorrhage

Abstract

Background and Purpose-The long-standing concept that delayed cerebral infarction after aneurysmal subarachnoid hemorrhage results exclusively from large artery vasospasm recently has been challenged. We used data from the CONSCIOUS-1 trial to determine the relationship between angiographic vasospasm and cerebral infarction after subarachnoid hemorrhage. Methods-We performed a post hoc exploratory analysis of the CONSCIOUS-1 data. All patients underwent catheter angiography before treatment and 9Ϯ2 days after subarachnoid hemorrhage. CT was performed before and after aneurysm treatment, and 6 weeks after subarachnoid hemorrhage. Angiograms and CT scans were assessed by centralized blinded review. Angiographic vasospasm was classified as none/mild (0%-33% decrease in arterial diameter), moderate (34%-66%), or severe (Ն67%

Cortical Spreading Ischemia in the Absence of Proximal Vasospasm after Aneurysmal Subarachnoid Hemorrhage: Evidence for a Dual Mechanism of Delayed Cerebral Ischemia

“…The natural logic would be for DCI to develop as a consequence of the cerebral blood flow reduction from proximal vasospasm. This is consistent with the clinical experience of generations of neurosurgeons (Crowley et al, 2011) and more recently of neurointerventionalists (Kimball et al, 2011). However, inconsistencies in this 'a priori' concept emerged, for example, from the findings (1) that nimodipine improves outcome without influencing proximal angiographic vasospasm (Dorhout Mees et al, 2007), (2) that the predictive value of angiographic vasospasm for DCI is < 50% in some series (Dankbaar et al, 2009)-arguably worse than from tossing a coin, and (3) from meta-analyses of SAH clinical trials suggesting that pharmacological prevention of angiographic vasospasm is not associated with improved clinical outcome ); yet, cerebral infarction is highly correlated with poor outcome (Fergusen and Macdonald, 2007;Vergouwen et al, 2011).…”

“…However, inconsistencies in this 'a priori' concept emerged, for example, from the findings (1) that nimodipine improves outcome without influencing proximal angiographic vasospasm (Dorhout Mees et al, 2007), (2) that the predictive value of angiographic vasospasm for DCI is < 50% in some series (Dankbaar et al, 2009)-arguably worse than from tossing a coin, and (3) from meta-analyses of SAH clinical trials suggesting that pharmacological prevention of angiographic vasospasm is not associated with improved clinical outcome ); yet, cerebral infarction is highly correlated with poor outcome (Fergusen and Macdonald, 2007;Vergouwen et al, 2011). However, other series show a high correlation between angiographic vasospasm and DCI (Crowley et al, 2011). This paradox of prevention of vasospasm without improvement in outcome in combination yet a high correlation of vasospasm with poor outcome led to the hypothesis that DCI contributes to poor outcome by a 'double hit' process including some mixture of large artery vasospasm and constriction in the cerebral microcirculation (that would not be evident on angiography-save perhaps as a delay in dye transit).…”

Pharmacologic Reduction of Angiographic Vasospasm in Experimental Subarachnoid Hemorrhage: Systematic Review and Meta-Analysis

“…Most of these studies tested drugs directed at reducing angiographic vasospasm. This was based on the hypothesis that since angiographic vasospasm is strongly correlated with cerebral infarction (Crowley et al, 2011) and cerebral infarction is correlated with unfavorable clinical outcome on the Glasgow outcome scale (Fergusen and Macdonald, 2007) then reducing vasospasm should improve clinical outcome.…”

A Phase I proof-of-concept and safety trial of sildenafil to treat cerebral vasospasm following subarachnoid hemorrhage

“…4,82 A significant predictor of developing DCI is angiographic CVS of intracranial vessels. 6,7,47 Approximately abbreviatioNs cGMP = cyclic guanosine monophosphate; CVS = cerebrovascular vasospasm; DCI = delayed cerebral ischemia; DSA = digital subtraction angiography; DSMB = Data Safety Monitoring Board; eNOS = endothelial nitric oxide synthase; ICA = internal carotid artery; ICP = intracranial pressure; MAP = mean arterial pressure; MCA = middle cerebral artery; NNICU = Neurology/Neurosurgery ICU; NO = nitric oxide; PDE-V = phosphodiesterase-V; SAH = subarachnoid hemorrhage. obJective Studies show that phosphodiesterase-V (PDE-V) inhibition reduces cerebral vasospasm (CVS) and improves outcomes after experimental subarachnoid hemorrhage (SAH).…”