Cerebral Infarction After Subarachnoid Hemorrhage Contributes to Poor Outcome by Vasospasm-Dependent and -Independent Effects

Abstract

Background and Purpose-The pathogenesis of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage remains incompletely understood. It is generally assumed that it is caused by angiographic vasospasm. Our aim was to clarify the relationship among angiographic vasospasm, neurological worsening, cerebral infarction, and poor outcome and to investigate whether cerebral infarction also contributes to poor outcome by vasospasm-independent effects. Methods-This exploratory analysis used data from 413 patients included in the Clazosentan to Overcome Neurological Ischemia and Infarction Occurring After Subarachnoid Hemorrhage (CONSCIOUS-1) trial. We studied the incidence of neurological worsening, cerebral infarction, and poor outcome in patients with and without angiographic vasospasm. Path analysis implemented by structural equation modeling was performed to determine direct and indirect path coefficients. Results-Of the 194 patients with moderate to severe vasospasm, 43% had neurological worsening of any cause, 20% had cerebral infarction, and 46% poor outcome. Path coefficients for direct effects on poor outcome were 0.20 for World Federation of Neurological Surgeons Grade 4 to 5, 0.13 for history of hypertension, 0.19 for angiographic vasospasm, 0.16 for neurological worsening, and 0.11 for new cerebral infarction. Cerebral infarction contributed to poor outcome by vasospasm-dependent and -independent effects. Conclusions-Our data show that the majority of patients with moderate to severe angiographic vasospasm did not have neurological worsening of any cause or cerebral infarction. Besides, cerebral infarction also has a direct effect on outcome independent of angiographic vasospasm. This suggests that other coexisting factors might be involved in the pathogenesis of delayed cerebral ischemia, which should also be an important research target to improve outcome after subarachnoid hemorrhage. (Stroke. 2011;42:924-929.)

Time course of recovery following poor-grade SAH: the incidence of delayed improvement and implications for SAH outcome study design

“…This association supports the notion that vasospasm and cerebral ischemia are significant contributors to early and late SAH-related morbidity. 18,22,26,28,29,31,42,43 It also suggests that maneuvers to avoid cerebral ischemia during hospitalization are critical in optimizing the capacity for continued long-term clinical improvement.…”

Lower incidence of cerebral infarction correlates with improved functional outcome after aneurysmal subarachnoid hemorrhage

“…The sensitivity analysis that reported on functional outcome 3 months after Cerebral infarction and outcome after SAH MDI Vergouwen et al SAH showed similar findings, though the poor outcome analysis had CIs that included 1.00. Previous studies found strong associations between vasospasm, DCI, cerebral infarction, and poor functional outcome (Fisher et al, 1977;Vergouwen et al, 2011;Rabinstein et al, 2004;Fergusen and Macdonald 2007). However, associations do not always represent causal relationships.…”

The Impact of Nonsteroidal Anti-inflammatory Drugs on Inflammatory Response After Aneurysmal Subarachnoid Hemorrhage

“…Having a direct impact on outcome, the occurrence of cerebral infarction was assessed as a confounding factor [17]. Cerebral infarction was defined as new ischemic lesions, which could not be attributed to surgery or endovascular intervention.…”

“…To investigate whether application of NSAIDs had an impact on outcome an unconditional logistic regression, unadjusted and adjusted for confounding covariates, was performed. Age, WFNS grade, occurrence of cerebral infarctions and fever were defined as confounding factors, representing generally accepted, clinically meaningful predictors in patients with SAH [17][18][19][20]. For the significant factors, odds ratios (OR) and their 95% confidence intervals (CI) were calculated.…”