Predicting Long-Term Outcomes After Poor-Grade Aneurysmal Subarachnoid Hemorrhage Using Decision Tree Modeling

Neurosurgery ◽  
2020 ◽  
Vol 87 (3) ◽  
pp. 523-529 ◽  
Author(s):  
Jinjin Liu ◽  
Ye Xiong ◽  
Ming Zhong ◽  
Yunjun Yang ◽  
Xianzhong Guo ◽  
...  

Abstract BACKGROUND Despite advances in the treatment of poor-grade aneurysmal subarachnoid hemorrhage (aSAH), predicting the long-term outcome of aSAH remains challenging, although essential. OBJECTIVE To predict long-term outcomes after poor-grade aSAH using decision tree modeling. METHODS This was a retrospective analysis of a prospective multicenter observational registry of patients with poor-grade aSAH with a World Federation of Neurosurgical Societies (WFNS) grade IV or V. Outcome was assessed by the modified Rankin Scale (mRS) at 12 mo, and an unfavorable outcome was defined as an mRS of 4 or 5 or death. Long-term prognostic models were developed using multivariate logistic regression and decision tree algorithms. An additional independent testing dataset was collected for external validation. Overall accuracy, sensitivity, specificity, and area under receiver operating characteristic curves (AUC) were used to assess model performance. RESULTS Of the 266 patients, 139 (52.3%) had an unfavorable outcome. Older age, absence of pupillary reactivity, lower Glasgow coma score (GCS), and higher modified Fisher grade were independent predictors of unfavorable outcome. Modified Fisher grade, pupillary reactivity, GCS, and age were used in the decision tree model, which achieved an overall accuracy of 0.833, sensitivity of 0.821, specificity of 0.846, and AUC of 0.88 in the internal test. There was similar predictive performance between the logistic regression and decision tree models. Both models achieved a high overall accuracy of 0.895 in the external test. CONCLUSION Decision tree model is a simple tool for predicting long-term outcomes after poor-grade aSAH and may be considered for treatment decision-making.

Neurosurgery ◽  
2021 ◽  
Vol 89 (Supplement_2) ◽  
pp. S7-S7
Author(s):  
Jinjin Liu ◽  
Ye Xiong ◽  
Ming Zhong ◽  
Yunjun Yang ◽  
Xianzhong Guo ◽  
...  

2007 ◽  
Vol 8 (3) ◽  
pp. 374-379 ◽  
Author(s):  
William J. Mack ◽  
Zachary L. Hickman ◽  
Andrew F. Ducruet ◽  
James T. Kalyvas ◽  
Matthew C. Garrett ◽  
...  

2020 ◽  
Vol 144 ◽  
pp. e743-e749
Author(s):  
Shinichiro Yoshikawa ◽  
Tomoya Kamide ◽  
Yuichiro Kikkawa ◽  
Kaima Suzuki ◽  
Toshiki Ikeda ◽  
...  

2014 ◽  
Vol 35 (2) ◽  
pp. 267-276 ◽  
Author(s):  
Mark K Donnelly ◽  
Yvette P Conley ◽  
Elizabeth A Crago ◽  
Dianxu Ren ◽  
Paula R Sherwood ◽  
...  

Preclinical studies show that epoxyeicosatrienoic acids (EETs) regulate cerebrovascular tone and protect against cerebral ischemia. We investigated the relationship between polymorphic genes involved in EET biosynthesis/metabolism, cytochrome P450 (CYP) eicosanoid levels, and outcomes in 363 patients with aneurysmal subarachnoid hemorrhage (aSAH). Epoxyeicosatrienoic acids and dihydroxyeicosatetraenoic acid (DHET) cerebrospinal fluid (CSF) levels, as well as acute outcomes defined by delayed cerebral ischemia (DCI) or clinical neurologic deterioration (CND), were assessed over 14 days. Long-term outcomes were defined by Modified Rankin Scale (MRS) at 3 and 12 months. CYP2C8∗4 allele carriers had 44% and 36% lower mean EET and DHET CSF levels ( P=0.003 and P=0.007) and were 2.2- and 2.5-fold more likely to develop DCI and CND ( P=0.039 and P=0.041), respectively. EPHX2 55Arg, CYP2J2∗7, CYP2C8∗1B, and CYP2C8 g.36785A allele carriers had lower EET and DHET CSF levels. CYP2C8 g.25369T and CYP2C8 g.36755A allele carriers had higher EET levels. Patients with CYP2C8∗2C and EPHX2 404del variants had worse long-term outcomes while those with EPHX2 287Gln, CYP2J2∗7, and CYP2C9 g.816G variants had favorable outcomes. Epoxyeicosatrienoic acid levels were associated with Fisher grade and unfavorable 3-month outcomes. Dihydroxyeicosatetraenoic acids were not associated with outcomes. No associations passed Bonferroni multiple testing correction. These are the first clinical data demonstrating the association between the EET biosynthesis/metabolic pathway and the pathophysiology of aSAH.


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