scholarly journals Relationship between Postmenopausal Estrogen Deficiency and Aneurysmal Subarachnoid Hemorrhage

2015 ◽  
Vol 2015 ◽  
pp. 1-6 ◽  
Author(s):  
Sadaharu Tabuchi
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Aneurysm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Experimental Studies ◽  
Reproductive Factors ◽  
Estrogen Deficiency ◽  
Therapeutic Implications ◽  
Vascular Physiology ◽  
Postmenopausal Estrogen ◽  
Molecular Pathophysiology

Aneurysmal subarachnoid hemorrhage (SAH) is one of the most severe forms of stroke, which results from the rupture of a cerebral aneurysm. SAH is the only type of stroke with a female predominance, suggesting that reproductive factors may play a significant role in the etiology. Estrogen has important effects on vascular physiology and pathophysiology of cerebral aneurysm and SAH and, thus, potential therapeutic implications. There have been growing bodies of epidemiological and experimental studies which support the hypothesis of a significant relationship between estrogen deficiency and cerebral aneurysm formation with subsequent SAH. This hypothesis is the focus of this review as well as possible pathology-based therapeutics with regard to aspects of molecular pathophysiology, especially related to women’s health.

scholarly journals Cigarette smoking and outcomes after aneurysmal subarachnoid hemorrhage: a nationwide analysis

2017 ◽  
Vol 129 (2) ◽  
pp. 446-457 ◽  
Author(s):  
Hormuzdiyar H. Dasenbrock ◽  
Robert F. Rudy ◽  
Pui Man Rosalind Lai ◽  
Timothy R. Smith ◽  
Kai U. Frerichs ◽  
...  
Keyword(s):  
Sensitivity Analysis ◽  
Subarachnoid Hemorrhage ◽  
Cigarette Smoking ◽  
Cerebral Aneurysm ◽  
Scale Score ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Institutional Care ◽  
Care Facility ◽  
Severity Scale ◽  
The Impact

OBJECTIVEAlthough cigarette smoking is one of the strongest risk factors for cerebral aneurysm development and rupture, there are limited data evaluating the impact of smoking on outcomes after aneurysmal subarachnoid hemorrhage (SAH). Additionally, two recent studies suggested that nicotine replacement therapy was associated with improved neurological outcomes among smokers who had sustained an SAH compared with smokers who did not receive nicotine.METHODSPatients who underwent endovascular or microsurgical repair of a ruptured cerebral aneurysm were extracted from the Nationwide Inpatient Sample (NIS, 2009–2011) and stratified by cigarette smoking. Multivariable logistic regression analyzed in-hospital mortality, complications, tracheostomy or gastrostomy placement, and discharge to institutional care (a nursing or an extended care facility). Additionally, the composite NIS-SAH outcome measure (based on mortality, tracheostomy or gastrostomy, and discharge disposition) was evaluated, which has been shown to have excellent agreement with a modified Rankin Scale score greater than 3. Covariates included in regression constructs were patient age, sex, race/ethnicity, insurance status, socioeconomic status, comorbidities (including hypertension, drug and alcohol abuse), the NIS-SAH severity scale (previously validated against the Hunt and Hess grade), treatment modality used for aneurysm repair, and hospital characteristics. A sensitivity analysis was performed matching smokers to nonsmokers on age, sex, number of comorbidities, and NIS-SAH severity scale score.RESULTSAmong the 5784 admissions evaluated, 37.1% (n = 2148) had a diagnosis of tobacco use, of which 31.1% (n = 1800) were current and 6.0% (n = 348) prior tobacco users. Smokers were significantly younger (mean age 51.4 vs 56.2 years) and had more comorbidities compared with nonsmokers (p < 0.001). There were no significant differences in mortality, total complications, or neurological complications by smoking status. However, compared with nonsmokers, smokers had significantly decreased adjusted odds of tracheostomy or gastrostomy placement (11.9% vs 22.7%, odds ratio [OR] 0.63, 95% confidence interval [CI] 0.51–0.78, p < 0.001), discharge to institutional care (OR 0.71, 95% CI 0.57–0.89, p = 0.002), and a poor outcome (OR 0.65, 95% CI 0.55–0.77, p < 0.001). Similar statistical associations were noted in the matched-pairs sensitivity analysis and in a subgroup of poor-grade patients (the upper quartile of the NIS-SAH severity scale).CONCLUSIONSIn this nationwide study, smokers experienced SAH at a younger age and had a greater number of comorbidities compared with nonsmokers, highlighting the negative ramifications of cigarette smoking among patients with cerebral aneurysms. However, smoking was also associated with paradoxical superior outcomes on some measures, and future research to confirm and further understand the basis of this relationship is needed.

Association of renin-angiotensin system genetic polymorphisms and aneurysmal subarachnoid hemorrhage

2018 ◽  
Vol 128 (1) ◽  
pp. 86-93 ◽  
Author(s):  
Christoph J. Griessenauer ◽  
R. Shane Tubbs ◽  
Paul M. Foreman ◽  
Michelle H. Chua ◽  
Nilesh A. Vyas ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Aneurysm ◽  
Genetic Polymorphisms ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Renin Angiotensin System ◽  
The United States ◽  
Dominant Effect ◽  
Potential Implication ◽  
Angiotensin System ◽  
Renin Angiotensin

OBJECTIVERenin-angiotensin system (RAS) genetic polymorphisms are thought to play a role in cerebral aneurysm formation and rupture. The Cerebral Aneurysm Renin-Angiotensin System (CARAS) study prospectively evaluated common RAS polymorphisms and their relation to aneurysmal subarachnoid hemorrhage (aSAH).METHODSThe CARAS study prospectively enrolled aSAH patients and controls at 2 academic centers in the United States. A blood sample was obtained from all patients for genetic evaluation and measurement of plasma angiotensin-converting enzyme (ACE) concentration. Common RAS polymorphisms were detected using 5′ exonuclease (TaqMan) genotyping assays and restriction fragment length polymorphism analysis.RESULTSTwo hundred forty-eight patients were screened, and 149 aSAH patients and 50 controls were available for analysis. There was a recessive effect of the C allele of the angiotensinogen (AGT) C/T single-nucleotide polymorphism (SNP) (OR 1.94, 95% CI 0.912–4.12, p = 0.0853) and a dominant effect of the G allele of the angiotensin II receptor Type 2 (AT2) G/A SNP (OR 2.11, 95% CI 0.972–4.57, p = 0.0590) on aSAH that did not reach statistical significance after adjustment for potential confounders. The ACE level was significantly lower in aSAH patients with the II genotype (17.6 ± 8.0 U/L) as compared with the ID (22.5 ± 12.1 U/L) and DD genotypes (26.6 ± 14.2 U/L) (p = 0.0195).CONCLUSIONSThe AGT C/T and AT2 G/A polymorphisms were not significantly associated with aSAH after controlling for potential confounders. However, a strong trend was identified for a dominant effect of the G allele of the AT2 G/A SNP. Downregulation of the local RAS may contribute to the formation of cerebral aneurysms and subsequent presentation with aSAH. Further studies are required to elucidate the relevant pathophysiology and its potential implication in treatment of patients with aSAH.

scholarly journals Statins Improve Clinical Outcome After Non-aneurysmal Subarachnoid Hemorrhage: A Translational Insight From a Systematic Review of Experimental Studies

2021 ◽  
Vol 12 ◽  
Author(s):  
Sepide Kashefiolasl ◽  
Marlies Wagner ◽  
Nina Brawanski ◽  
Volker Seifert ◽  
Stefan Wanderer ◽  
...  
Keyword(s):  
Systematic Review ◽  
Subarachnoid Hemorrhage ◽  
Clinical Outcome ◽  
Lower Risk ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Experimental Studies ◽  
Delayed Cerebral Ischemia ◽  
Statin Treatment ◽  
Favorable Outcome ◽  
Simvastatin Treatment

The efficacy of statin-treatment in aneurysmal subarachnoid hemorrhage (SAH) remains controversial. We aimed to investigate the effects of statin-treatment in non-aneurysmal (na)SAH in accordance with animal research data illustrating the pathophysiology of naSAH. We systematically searched PubMed using PRISMA-guidelines and selected experimental studies assessing the statin-effect on SAH. Detecting the accordance of the applied experimental models with the pathophysiology of naSAH, we analyzed our institutional database of naSAH patients between 1999 and 2018, regarding the effect of statin treatment in these patients and creating a translational concept. Patient characteristics such as statin-treatment (simvastatin 40 mg/d), the occurrence of cerebral vasospasm (CVS), delayed infarction (DI), delayed cerebral ischemia (DCI), and clinical outcome were recorded. In our systematic review of experimental studies, we found 13 studies among 18 titles using blood-injection-animal-models to assess the statin-effect in accordance with the pathophysiology of naSAH. All selected studies differ on study-setting concerning drug-administration, evaluation methods, and neurological tests. Patients from the Back to Bedside project, including 293 naSAH-patients and 51 patients with simvastatin-treatment, were recruited for this analysis. Patients under treatment were affected by a significantly lower risk of CVS (p &lt; 0.01; OR 3.7), DI (p &lt; 0.05; OR 2.6), and DCI (p &lt; 0.05; OR 3). Furthermore, there was a significant association between simvastatin-treatment and favorable-outcome (p &lt; 0.05; OR 3). However, dividing patients with statin-treatment in pre-SAH (n = 31) and post-SAH (n = 20) treatment groups, we only detected a tenuously significant higher chance for a favorable outcome (p &lt; 0.05; OR 0.05) in the small group of 20 patients with statin post-SAH treatment. Using a multivariate-analysis, we detected female gender (55%; p &lt; 0.001; OR 4.9), Hunt&amp;Hess ≤III at admission (p &lt; 0.002; OR 4), no anticoagulant-therapy (p &lt; 0.0001; OR 0.16), and statin-treatment (p &lt; 0.0001; OR 24.2) as the main factors improving the clinical outcome. In conclusion, we detected a significantly lower risk for CVS, DCI, and DI in naSAH patients under statin treatment. Additionally, a significant association between statin treatment and favorable outcome 6 months after naSAH onset could be confirmed. Nevertheless, unified animal experiments should be considered to create the basis for developing new therapeutic schemes.

scholarly journals The Role of the Microcirculation in Delayed Cerebral Ischemia and Chronic Degenerative Changes after Subarachnoid Hemorrhage

2013 ◽  
Vol 33 (12) ◽  
pp. 1825-1837 ◽  
Author(s):  
Leif Østergaard ◽  
Rasmus Aamand ◽  
Sanja Karabegovic ◽  
Anna Tietze ◽  
Jakob Udby Blicher ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Vasogenic Edema ◽  
Delayed Cerebral Ischemia ◽  
Tissue Hypoxia ◽  
Brain Oxygenation ◽  
Metabolic Derangement ◽  
Therapeutic Implications ◽  
Potential Sources

The mortality after aneurysmal subarachnoid hemorrhage (SAH) is 50%, and most survivors suffer severe functional and cognitive deficits. Half of SAH patients deteriorate 5 to 14 days after the initial bleeding, so-called delayed cerebral ischemia (DCI). Although often attributed to vasospasms, DCI may develop in the absence of angiographic vasospasms, and therapeutic reversal of angiographic vasospasms fails to improve patient outcome. The etiology of chronic neurodegenerative changes after SAH remains poorly understood. Brain oxygenation depends on both cerebral blood flow (CBF) and its microscopic distribution, the so-called capillary transit time heterogeneity (CTH). In theory, increased CTH can therefore lead to tissue hypoxia in the absence of severe CBF reductions, whereas reductions in CBF, paradoxically, improve brain oxygenation if CTH is critically elevated. We review potential sources of elevated CTH after SAH. Pericyte constrictions in relation to the initial ischemic episode and subsequent oxidative stress, nitric oxide depletion during the pericapillary clearance of oxyhemoglobin, vasogenic edema, leukocytosis, and astrocytic endfeet swelling are identified as potential sources of elevated CTH, and hence of metabolic derangement, after SAH. Irreversible changes in capillary morphology and function are predicted to contribute to long-term relative tissue hypoxia, inflammation, and neurodegeneration. We discuss diagnostic and therapeutic implications of these predictions.

P3708Prognostic significance of electrocardiographic changes after subarachnoid hemorrhage

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
T Yuba ◽  
Y Kimura ◽  
T Mukaida ◽  
T Aoyama ◽  
H Hirano ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Glasgow Coma Scale ◽  
Cerebral Aneurysm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Aneurysm Rupture ◽  
Qt Prolongation ◽  
Autonomic Nerve ◽  
World Federation ◽  
Coma Scale ◽  
Traumatic Subarachnoid Hemorrhage

Abstract Background and purpose Many reports have examined electrocardiographic (ECG) changes after subarachnoid hemorrhage from long ago; however, there are few reports on the prognosis of patients who have an ECG abnormality. Therefore, in this study, the prognoses of patients with subarachnoid hemorrhage showing abnormal ECG findings were retrospectively analyzed. Methods Over 30 months from January 2014 to June 2016, 199 patients (mean age, 61.1±17.0 years; 46.7% male) admitted with a subarachnoid hemorrhage (SAH) were enrolled. To assess the mechanism underlying abnormal ECG in the SAH, predictor variables, such as demographics (age, sex, and body surface area), hemodynamics (heart rate and systolic blood pressure), blood biochemical results, neurological assessments (Glasgow Coma Scale), and computed tomography (CT) severity classification (World Federation of Neurosurgical Societies classification) were recorded. The subarachnoid hemorrhage was classified into either the cerebral aneurysm rupture group (N=132) or traumatic subarachnoid hemorrhage group (N=67) and analyzed. Results In the cerebral aneurysm rupture group, the QT prolongation was significantly increased compared with the traumatic subarachnoid hemorrhage group (424.8±87.7 ms vs. 400.5±95.8 ms, P<0.05). There was a correlation between consciousness level (Glasgow Coma Scale) on admission and QT prolongation, and significant QT prolongation was observed in critical patients (Pearson's correlation coefficient test P=0.04). ST changes correlated with CT classification severity (WFNS classification), and the most severe group (WFNS Grade 5) showed significant ST changes. On admission, the cerebral aneurysm rupture group and 97.0% in the traumatic subarachnoid hemorrhage group. Conclusions Significantly prolonged QT and ST changes are noted in patients with severe aneurysmal subarachnoid hemorrhage. The cause of the ECG abnormality in subarachnoid hemorrhage patients is not yet understood. A small number of experimental animal models have shown that electrocardiogram abnormalities associated with subarachnoid hemorrhage develop in the brain stem, and an autonomic nerve abnormality may also be involved. A D-dimer is positively correlated with both aneurysm trauma and traumatic subarachnoid hemorrhage and may be used for auxiliary diagnosis of a subarachnoid hemorrhage.

Endothelin polymorphisms as a risk factor for cerebral aneurysm rebleeding following aneurysmal subarachnoid hemorrhage

2017 ◽  
Vol 157 ◽  
pp. 65-69 ◽  
Author(s):  
Paul M. Foreman ◽  
Robert M. Starke ◽  
Philipp Hendrix ◽  
Mark R. Harrigan ◽  
Winfield S. Fisher ◽  
...  
Keyword(s):  
Risk Factor ◽  
Subarachnoid Hemorrhage ◽  
Cerebral Aneurysm ◽  
Aneurysmal Subarachnoid Hemorrhage

Multiple ruptured cerebral aneurysms in a child with Takayasu arteritis

2008 ◽  
Vol 1 (1) ◽  
pp. 83-87 ◽  
Author(s):  
Suresh N. Magge ◽  
H. Isaac Chen ◽  
Michael F. Stiefel ◽  
Linda Ernst ◽  
Ann Marie Cahill ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Aneurysm ◽  
Takayasu Arteritis ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Cerebral Aneurysms ◽  
Artery Aneurysm ◽  
Anterior Communicating Artery ◽  
Rare Presentation ◽  
Anterior Communicating Artery Aneurysm ◽  
Clip Application

✓The authors report the case of an 18-month-old girl who presented with a ruptured anterior communicating artery aneurysm, and who was later diagnosed with Takayasu arteritis. Her initial aneurysm was successfully treated with clip application. However, over a 6-month period she had multiple ruptures from new and rapidly recurring aneurysms adjacent to the clips. These aneurysms were treated with repeated craniotomy and clip application and then with endovascular coil placement. Aneurysmal subarachnoid hemorrhage is a rare presentation of Takayasu arteritis. To the authors' knowledge, this is the youngest reported patient with Takayasu arteritis to present with a ruptured cerebral aneurysm.

scholarly journals Therapeutic Implications of Estrogen for Cerebral Vasospasm and Delayed Cerebral Ischemia Induced by Aneurysmal Subarachnoid Hemorrhage

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Dale Ding ◽  
Robert M. Starke ◽  
Aaron S. Dumont ◽  
Gary K. Owens ◽  
David M. Hasan ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Ischemia ◽  
Cerebral Vasospasm ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Delayed Cerebral Ischemia ◽  
Therapeutic Implications ◽  
Delayed Neurological Deterioration ◽  
Adenosine A2a ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide

Cerebral vasospasm (CV) remains the leading cause of delayed morbidity and mortality following aneurysmal subarachnoid hemorrhage (SAH). However, increasing evidence supports etiologies of delayed cerebral ischemia (DCI) other than CV. Estrogen, specifically 17β-estradiol (E2), has potential therapeutic implications for ameliorating the delayed neurological deterioration which follows aneurysmal SAH. We review the causes of CV and DCI and examine the evidence for E2-mediated vasodilation and neuroprotection. E2 potentiates vasodilation by activating endothelial nitric oxide synthase (eNOS), preventing increased inducible NOS (iNOS) activity caused by SAH, and decreasing endothelin-1 production. E2 provides neuroprotection by increasing thioredoxin expression, decreasing c-Jun N-terminal kinase activity, increasing neuroglobin levels, preventing SAH-induced suppression of the Akt signaling pathway, and upregulating the expression of adenosine A2a receptor. The net effect of E2 modulation of these various effectors is the promotion of neuronal survival, inhibition of apoptosis, and decreased oxidative damage and inflammation. E2 is a potentially potent therapeutic tool for improving outcomes related to post-SAH CV and DCI. However, clinical evidence supporting its benefits remains lacking. Given the promising preclinical data available, further studies utilizing E2 for the treatment of patients with ruptured intracranial aneurysms appear warranted.

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