Apolipoprotein E Genotype and Outcome in Aneurysmal Subarachnoid Hemorrhage

Leung, Constant; Poon, Wai-sang; Yu, Ly-Mee; Wong, George Kwok Chu; Ng, Ho Keung

doi:10.1161/hs0202.102326

Cited by 68 publications

(51 citation statements)

References 35 publications

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“…Our data supported their results. The relation between ApoE genotype and outcome after subarachnoid hemorrhage was also reported (27). In our mouse model, we did not study the rupture rate due to the lack of appropriate methods for evaluating subarachnoid hemorrhage such as CT scan and outcome after subarachnoid hemorrhage.…”

Section: Discussionmentioning

confidence: 80%

“…In preclinical models of focal and global ischemia, the absence of endogenous ApoE has been associated with a worsening of both histological and functional outcomes (14,16,17). There are likely multiple mechanisms by which endogenous ApoE plays a protective role in the injured central nervous system, as suggested by prior in vitro data demonstrating its isoformspecific antioxidant (27) and neurotrophic effects (29). In addition, ApoE polymorphisms were reported to be independent risk factors for ischemic stroke.…”

Section: Discussionmentioning

confidence: 99%

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The efficacy of apolipoprotein E deficiency in cerebral aneurysm formation

Aoki

Moriwaki²,

Takagi³

et al. 2008

Int J Mol Med

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Abstract. Subarachnoid hemorrhage due to the rupture of a cerebral aneurysm is a life-threatening disease. Despite this, the detailed mechanisms underlying the initiation and progression of cerebral aneurysm are unclear. The relation of hypercholesterolemia and apolipoprotein E (ApoE) to cerebral aneurysm formation, has been unclear until now. We used, in the present study, a previously established cerebral aneurysm model of rats and mice whose histological features were closely similar to human cerebral aneurysms. ApoE protein was expressed mainly in the endothelial cells of arterial walls both in control arteries and cerebral aneurysms. The expression of ApoE was reduced during aneurysm formation in the immunohistochemistry. The mRNA expression of ApoE in arterial walls was not different between the controls and cerebral aneurysms. Owing to the deficiency of ApoE, mice presented marked hypercholesterolemia, but there was no difference in cerebral aneurysm formation. In the present study, we clarified that ApoE was not responsible for cerebral aneurysm formation.

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Section: Discussionmentioning

confidence: 80%

Section: Discussionmentioning

confidence: 99%

The efficacy of apolipoprotein E deficiency in cerebral aneurysm formation

Aoki

Moriwaki²,

Takagi³

et al. 2008

Int J Mol Med

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“…The molecular mechanisms and genetic factors that govern the capacity for recovery following SAH are the subject of several current investigations. 16,23,35 Interestingly, no difference in the incidence of delayed recovery was seen in the patients who underwent microsurgical clipping versus endovascular coiling. In the BRAT study, 19,37 the difference in outcomes between the 2 treatment groups that was present at 6 months and 1 year disappeared at the 3-year time point.…”

Section: Figmentioning

confidence: 95%

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

Wilson¹,

Nakaji²,

Albuquerque³

et al. 2013

JNS

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Object Data regarding the time course of recovery after poor-grade subarachnoid hemorrhage (SAH) is lacking. Most SAH studies assess outcome at a single time point, often as early as 3 or 6 months following SAH. The authors hypothesized that recovery following poor-grade SAH is a dynamic process and that early outcomes may not always approximate long-term outcomes. To test this hypothesis, they analyzed long-term outcome data from a cohort of patients with poor-grade aneurysmal SAH to determine the incidence and predictors of early and delayed neurological improvement. Methods The authors reviewed outcome data from 88 poor-grade SAH patients enrolled in a prospective SAH treatment trial (the Barrow Ruptured Aneurysm Trial). They assessed modified Rankin Scale (mRS) scores at discharge, 6 months, 12 months, and 36 months after treatment to determine the incidence and predictors of neurological improvement during each interval. Results The mean aggregate mRS scores at 6 months (3.31 ± 2.1), 12 months (3.28 ± 2.2), and 36 months (3.17 ± 2.3) improved significantly compared with the mean score at hospital discharge (4.33 ± 1.3, p < 0.001), but they did not differ significantly among themselves. Between discharge and 6 months, 61% of patients improved on the mRS. The incidence of improvement between 6–12 months and 12–36 months was 18% and 19%, respectively. Hunt and Hess Grade IV versus V (OR 6.20, 95% CI 2.11–18.25, p < 0.001) and the absence of large (> 4 cm) (OR 2.76, 95% CI 1.02–7.55, p = 0.05) or eloquent (OR 5.17, 95% CI 1.89–14.10, p < 0.01) stroke were associated with improvement up to 6 months. Age ≤ 65 years (OR 5.56, 95% CI 1.17–26.42, p = 0.02), Hunt and Hess Grade IV versus V (OR 4.17, 95% CI 1.10–15.85, p = 0.03), and absence of a large (OR 8.97, 95% CI 2.65–30.40, p < 0.001) or eloquent (OR 4.54, 95% CI 1.46–14.08, p = 0.01) stroke were associated with improvement beyond 6 months. Improvement beyond 1 year was most strongly predicted by the absence of a large stroke (OR 7.62, 95% CI 1.55–37.30, p < 0.01). Conclusions A substantial minority of poor-grade SAH patients will experience delayed recovery beyond the point at which most studies assess outcome. Younger patients, those presenting in better clinical condition, and those without CT evidence of large or eloquent stroke demonstrated the highest capacity for delayed recovery.

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“…We have further examined the effect of arundic acid on astrocytic activation and delayed infarct expansion after permanent focal ischemia in apolipoprotein E knock-in mice, because the apolipoprotein E4 isoform is a salient risk factor for not only AD but also for stroke (Sorbi et al, 1995;Leung et al, 2002). The apolipoprotein E4 knock-in mice exhibited significant aggravation of astrocytic activation and delayed infarct expansion after permanent focal ischemia relative to apolipoprotein E2 or apolipoprotein E3 knock-in mice (Mori et al, 2004).…”

mentioning

confidence: 99%