Related Experiment Video
Updated: May 13, 2026

Analysis of Cerebral Vasospasm in a Murine Model of Subarachnoid Hemorrhage with High Frequency Transcranial Duplex Ultrasound
Published on: June 3, 2021
Haptoglobin phenotype predicts cerebral vasospasm and clinical deterioration after aneurysmal subarachnoid hemorrhage
Hiroyuki Ohnishi1, Koji Iihara, Yasuyuki Kaku
1Department of Neurosurgery, National Cerebral and Cardiovascular Center, Osaka, Japan.
Vasospasm (VS) and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) are thought to greatly affect prognosis. Haptoglobin (Hp) is a hemoglobin-binding protein expressed by a genetic polymorphism (1-1, 2-1, and 2-2). Our objects were to investigate whether the Hp phenotype could predict the incidence of cerebral infarction, favorable outcome, clinical deterioration by DCI, and angiographical VS after aneurysmal SAH. Ninety-five consecutive patients who underwent clipping or coil embolization were studied. Favorable functional outcome was defined as a modified Rankin Scale score of 0-2 at 3 months. Angiographical VS was diagnosed based on cerebral angiography findings performed between days 7 and 10 after SAH. The Hp 2-2 group had a significantly greater risk of angiographical VS than that of Hp 2-1 and 1-1 groups combined on univariate (odds ratio [OR]: 3.60, confidence interval [CI]: 1.49-8.67, P = .003) and multivariate logistic regression analyses after being adjusted for age, sex, Fisher groups, and other risk factors (OR: 3.75, CI: 1.54-9.16, P = .004). The Hp 2-2 group also showed the tendency of a greater risk of clinical deterioration by DCI with marginal significance on univariate and age- and sex-adjusted analyses (univariate OR: 2.46, CI: .90-6.74, P = .080; age- and sex-adjusted OR: 2.46, CI: .89-6.82, P = .080) but not after being adjusted for other multiple risk factors. The Hp 2-2 group was not associated with the favorable 3-month outcome and cerebral infarction (univariate: P = .867, P = .209; multivariate: P = .905, P = .292). The Hp phenotype seems to be associated with a higher rate of angiographical VS and clinical deterioration by DCI but does not affect the incidence of cerebral infarction and favorable outcome.
Vasospasm (VS) and delayed cerebral ischemia (DCI) after subarachnoid hemorrhage (SAH) are thought to greatly affect prognosis. Haptoglobin (Hp) is a hemoglobin-binding protein expressed by a genetic polymorphism (1-1, 2-1, and 2-2). Our objects were to investigate whether the Hp phenotype could predict the incidence of cerebral infarction, favorable outcome, clinical deterioration by DCI, and angiographical VS after aneurysmal SAH. Ninety-five consecutive patients who underwent clipping or coil embolization were studied. Favorable functional outcome was defined as a modified Rankin Scale score of 0-2 at 3 months. Angiographical VS was diagnosed based on cerebral angiography findings performed between days 7 and 10 after SAH. The Hp 2-2 group had a significantly greater risk of angiographical VS than that of Hp 2-1 and 1-1 groups combined on univariate (odds ratio [OR]: 3.60, confidence interval [CI]: 1.49-8.67, P = .003) and multivariate logistic regression analyses after being adjusted for age, sex, Fisher groups, and other risk factors (OR: 3.75, CI: 1.54-9.16, P = .004). The Hp 2-2 group also showed the tendency of a greater risk of clinical deterioration by DCI with marginal significance on univariate and age- and sex-adjusted analyses (univariate OR: 2.46, CI: .90-6.74, P = .080; age- and sex-adjusted OR: 2.46, CI: .89-6.82, P = .080) but not after being adjusted for other multiple risk factors. The Hp 2-2 group was not associated with the favorable 3-month outcome and cerebral infarction (univariate: P = .867, P = .209; multivariate: P = .905, P = .292). The Hp phenotype seems to be associated with a higher rate of angiographical VS and clinical deterioration by DCI but does not affect the incidence of cerebral infarction and favorable outcome.
More Related Videos
Related Concept Videos
Hemorrhagic Stroke ll: Pathophysiology
Hemorrhagic Stroke l: Introduction
Cerebral Edema ll: Pathophysiology
Hepatic Encephalopathy
Aneurysm II: Clinical Manifestations and Diagnostic Studies
Huntington Disease l: Introduction

