Cerebral ischemia complicating intracranial aneurysm: a warning sign of imminent rupture?
Ontology highlight
ABSTRACT: Background and purpose
Patients harboring nongiant cerebral aneurysms may rarely present with an ischemic infarct distal to the aneurysm. The aim of this case series was to report clinical and radiologic characteristics of these patients, their management, and outcome.Materials and methods
We undertook a single-center retrospective analysis of consecutive patients admitted during an 8-year period with an acute ischemic stroke revealing an unruptured nongiant (<25 mm) sacciform intracranial aneurysm. Clinical, radiologic, therapeutic, and follow-up data were analyzed.Results
Nine patients were included. The mean size of aneurysms was 9.6 ± 6 mm, and 5 were partially or totally thrombosed. Two patients had a fatal SAH within 3 days after stroke-symptom onset, whereas asymptomatic meningeal bleeding was diagnosed or suspected in 2 others. Most of the patients with unthrombosed aneurysms were successfully treated by endovascular coiling in the acute phase. Thrombosed aneurysms were usually treated with antithrombotics, and most recanalized secondarily, requiring endovascular treatment or surgical obliteration. No recurrence of an ischemic event or SAH was observed during the 31 ± 12 months of follow-up (from 4 to 53 months).Conclusions
In this single-center series, the frequency of early SAH in patients with ischemic stroke distal to an unruptured intracranial aneurysm was high. Acute management should be undertaken with care regarding antithrombotic use, and early endovascular coiling should be considered.
SUBMITTER: Guillon B
PROVIDER: S-EPMC7965994 | biostudies-literature |
REPOSITORIES: biostudies-literature
Similar Datasets
Project description:Clinical observations suggest that postmenopausal women have a higher incidence of aneurysmal rupture than premenopausal women. We hypothesize that a relative deficiency in estrogen may increase the risks of aneurysmal growth and subarachnoid hemorrhage in postmenopausal women. We assessed the effects of estrogen and selective estrogen receptor subtype agonists on the development of aneurysmal rupture in ovariectomized female mice. We used an intracranial aneurysm mouse model that recapitulates the key features of human intracranial aneurysms, including spontaneous rupture. Ten- to 12-week-old ovariectomized female mice received treatment with estrogen, nonselective estrogen receptor antagonist, estrogen receptor-? agonist, or estrogen receptor-? agonist starting 6 days after aneurysm induction so that the treatments affected the development of aneurysmal rupture without affecting aneurysmal formation. Estrogen significantly reduced the incidence of ruptured aneurysms and rupture rates in ovariectomized mice. Nonselective estrogen receptor antagonist abolished the protective effect of estrogen. Although estrogen receptor-? agonist did not affect the incidence of ruptured aneurysms or rupture rates, estrogen receptor-? agonist prevented aneurysmal rupture without affecting the formation of aneurysms. The protective role of estrogen receptor-? agonist was abolished by the inhibition of nitric oxide synthase. We showed that estrogen prevented aneurysmal rupture in ovariectomized female mice. The protective effect of estrogen seemed to occur through the activation of estrogen receptor-?, a predominant subtype of estrogen receptor in human intracranial aneurysms and cerebral arteries.
| S-EPMC4034536 | biostudies-literature
Project description:Background and purposeInflammation has emerged as a key component of the pathophysiology of intracranial aneurysms. Mast cells have been detected in human intracranial aneurysm tissues, and their presence was associated with intramural microhemorrhage and wall degeneration. We hypothesized that mast cells play a critical role in the development of aneurysmal rupture, and that mast cells can be used as a therapeutic target for the prevention of aneurysm rupture.MethodsIntracranial aneurysms were induced in adult mice using a combination of induced systemic hypertension and a single injection of elastase into the cerebrospinal fluid. Aneurysm formation and rupture were assessed over 3 weeks. Roles of mast cells were assessed using a mast cell stabilizer (cromolyn), a mast cell activator (C48/80), and mice that are genetically lacking mature mast cells (KitW-sh/W-sh mice).ResultsPharmacological stabilization of mast cells with cromolyn markedly decreased the rupture rate of aneurysms (80% versus 19%, n=10 versus n =16) without affecting the aneurysm formation. The activation of mast cells with C48/80 significantly increased the rupture rate of aneurysms (25% versus 100%, n=4 versus n=5) without affecting the overall rate of aneurysm formation. Furthermore, the genetic deficiency of mast cells significantly prevented aneurysm rupture (80% versus 25%, n=10 versus n=8, wild-type versus KitW-sh/W-sh mice).ConclusionsThese results suggest that mast cells play a key role in promoting aneurysm rupture but not formation. Stabilizers of mast cells may have a potential therapeutic value in preventing intracranial aneurysm rupture in patients.
| S-EPMC7606717 | biostudies-literature
Project description:To investigate the role of smoking in the rupture of intracranial aneurysms (IA), plasma miRNA profiles of smoking IA patients, non-smoking IA patients, and healthy volunteers were analyzed.
2023-11-15 | GSE231922 | GEO
Project description:Background and Purpose- Tobacco cigarette smoking is considered to be a strong risk factor for intracranial aneurysmal rupture. Nicotine is a major biologically active constituent of tobacco products. Nicotine's interactions with vascular cell nicotinic acetylcholine receptors containing ?7 subunits (?7*-nAChR) are thought to promote local inflammation and sustained angiogenesis. In this study, using a mouse intracranial aneurysm model, we assessed potential contributions of nicotine exposure and activation of ?7*-nAChR to the development of aneurysmal rupture. Methods- Intracranial aneurysms were induced by a combination of deoxycorticosterone-salt induced hypertension and a single-dose elastase injection into cerebrospinal fluid in mice. Results- Exposure to nicotine or an ?7*-nAChR-selective agonist significantly increased aneurysm rupture rate. Coexposure to an ?7*-nAChR antagonist abolished nicotine's deleterious effect. In addition, nicotine's promotion of aneurysm rupture was absent in smooth muscle cell-specific ?7*-nAChR subunit knockout mice but not in mice lacking ?7*-nAChR on endothelial cells or macrophages. Nicotine treatment increased the mRNA levels of vascular endothelial growth factor, platelet-derived growth factor-B, and inflammatory cytokines. ?7*-nAChR antagonist reversed nicotine-induced upregulation of these growth factors and cytokines. Conclusions- Our findings indicate that nicotine exposure promotes aneurysmal rupture through actions on vascular smooth muscle cell ?7*-nAChR.
| S-EPMC6214667 | biostudies-literature
Project description:Background: Intracranial aneurysm rupture is a devastating medical event with a high morbidity and mortality rate. Thus, timely detection and management are critical. The present study aimed to identify the aneurysm radiomics features associated with rupture and to build and evaluate a radiomics classification model of aneurysm rupture. Methods: Radiomics analysis was applied to CT angiography (CTA) images of 393 patients [152 (38.7%) with ruptured aneurysms]. Patients were divided at a ratio of 7:3 into retrospective training (n = 274) and prospective test (n = 119) cohorts. A total of 1,229 radiomics features were automatically calculated from each aneurysm. The feature number was systematically reduced, and the most important classifying features were selected. A logistic regression model was constructed using the selected features and evaluated on training and test cohorts. Radiomics score (Rad-score) was calculated for each patient and compared between ruptured and unruptured aneurysms. Results: Nine radiomics features were selected from the CTA images and used to build the logistic regression model. The radiomics model has shown good performance in the classification of the aneurysm rupture on training and test cohorts [area under the receiver operating characteristic curve: 0.92 [95% confidence interval CI: 0.89-0.95] and 0.86 [95% CI: 0.80-0.93], respectively, p < 0.001]. Rad-score showed statistically significant differences between ruptured and unruptured aneurysms (median, 2.50 vs. -1.60 and 2.35 vs. -1.01 on training and test cohorts, respectively, p < 0.001). Conclusion: The results indicated the potential of aneurysm radiomics features for automatic classification of aneurysm rupture on CTA images.
| S-EPMC7937935 | biostudies-literature
Project description:Highlights • In our department of neurosurgery, we noticed a higher rate of patients with ruptured aneurysm who had a deteriorated neurological presentation on admission during COVID-19 pandemic (2020 group, n?=?26).• A group control included 28 consecutive patients managed at the same institution for the same disease in 2019, during the same time frame (2019 group).• Rates of poor neurological presentation and severe radiological presentation on hospital admission were higher during COVID-19 pandemic (p?=?0.01 and p?=?0.02, respectively).• During COVID-19 pandemic (2020 group), the delayed hospital admission was longer (p?=?0.005). Therefore, vasospasm’s rate on presentation was also higher (p?=?0.04).• In 2020, patients with only sudden headache may have feared immediate hospital admission because of potential COVID-19 contamination.• In case of recurrent COVID-19 pandemic, educating the population concerning specific symptoms such as sudden headache, neurological deficit or even sudden chest pain should be emphasized. Background/objectives The present study aimed at evaluating the impact on the early outcome of patients with ruptured intracranial aneurysms. Methods Our study prospectively included 26 consecutive patients with ruptured intracranial aneurysm managed at our institution in context of COVID-19 pandemic between March 1st, 2020 and April, 26th, 2020 (2020 group). A group control included other 28 consecutive patients managed at the same institution for the same disease in 2019, during the same time frame (2019 group). On admission, poor neurological status was defined as WFNS score >3. Severe radiological status was defined by the presence of intracerebral hematoma, or/and acute hydrocephalus requiring further EVD or/and the presence of vasospasm on presentation. Statistical analysis was performed to compare the 2 distinct groups. Results Rates of poor neurological presentation and severe radiological presentation on hospital admission were higher in the 2020 group (p?=?0.01 and p?=?0.02, respectively). The delayed hospital admission was 2.7 days in 2020 group and 0.75 days in 2019 group (p?=?0.005). Therefore, vasospasm’s rate on presentation was also higher in the 2020 group (p?=?0.04). Conclusion To our knowledge, this is one of the first studies demonstrating influence of the COVID-19 pandemic on patients with urgent and severe intracranial aneurysmal disease. In case of recurrent COVID-19 pandemic, educating the population concerning specific symptoms such as sudden headache, neurological deficit or even sudden chest pain should be emphasized.
| S-EPMC7723459 | biostudies-literature
Project description:ObjectiveAlthough smoking is a known risk factor for intracranial aneurysm (IA) rupture, the exact relationship between IA rupture and smoking intensity and duration, as well as duration of smoking cessation, remains unknown.MethodsIn this case-control study, we analyzed 4,701 patients with 6,411 IAs diagnosed at the Brigham and Women's Hospital and Massachusetts General Hospital between 1990 and 2016. We divided individuals into patients with ruptured aneurysms and controls with unruptured aneurysms. We performed univariable and multivariable logistic regression analyses to determine the association between smoking status and ruptured IAs at presentation. In a subgroup analysis among former and current smokers, we assessed the association between ruptured aneurysms and number of packs per day, duration of smoking, and duration since smoking cessation.ResultsIn multivariable analysis, current (odds ratio [OR] 2.21, 95% confidence interval [CI] 1.89-2.59) and former smoking status (OR 1.56, 95% CI 1.31-1.86) were associated with rupture status at presentation compared with never smokers. In a subgroup analysis among current and former smokers, years smoked (OR 1.02, 95% CI 1.01-1.03) and packs per day (OR 1.46, 95% CI 1.25-1.70) were significantly associated with ruptured aneurysms at presentation, whereas duration since cessation among former smokers was not significant (OR 1.00, 95% CI 0.99-1.02).ConclusionsCurrent cigarette smoking, smoking intensity, and smoking duration are significantly associated with ruptured IAs at presentation. However, the significantly increased risk persists after smoking cessation, and smoking cessation does not confer a reduced risk of aneurysmal subarachnoid hemorrhage beyond that of reducing the cumulative dose.
| S-EPMC5649762 | biostudies-literature
Project description:Inflammation is emerging as a critical factor in the pathophysiology of intracranial aneurysm. TLR4 (toll-like receptor 4) contributes not only to the innate immune responses but also to the inflammatory processes associated with vascular disease. Therefore, we examined the contribution of the TLR4 pathway to the development of the rupture of intracranial aneurysm. We used a mouse model of intracranial aneurysm. TLR4 inhibition significantly reduced the development of aneurysmal rupture. In addition, the rupture rate and levels of proinflammatory cytokines were lower in TLR4 knockout mice than the control littermates. Macrophage/monocyte-specific TLR4 knockout mice had a lower rupture rate than the control littermate mice. Moreover, the deficiency of MyD88 (myeloid differentiation primary-response protein 88), a key mediator of TLR4, reduced the rupture rate. These findings suggest that the TLR4 pathway promotes the development of intracranial aneurysmal rupture by accelerating inflammation in aneurysmal walls. Inhibition of the TLR4 pathway in inflammatory cells may be a promising approach for the prevention of aneurysmal rupture and subsequent subarachnoid hemorrhage.
| S-EPMC7377296 | biostudies-literature
Project description:BackgroundAcetylsalicylic acid (ASA) and statins have been identified as potentially reducing the risk of intracranial aneurysms (IA) rupture. We aim to determine the effect of this drugs on the risk of rupture of IA.Patients and methodsWe performed a retrospective cohort study from a prospective database of patients with IA treated in our institution between January 2013 and December 2018. Demographics, previous oral treatments, presence of multiple aneurysms, size of aneurysm, lobulation, location and morphology of the aneurysms were recorded. Patients were dichotomized as ruptured and unruptured IA.ResultsA total of 408 IA were treated, of which 283 (68.6%) were in women. The median age was 53, 194 (47.5%) were ruptured IA. 38 patients (9.3%) were receiving ASA and 84 (20.6%) were receiving statins at the moment of the IA diagnosis. In the multivariable regression analysis, ASA plus statin use and multiple aneurysms were independently associated with unruptured IA (OR 5.01, 95% CI, 1.37-18.33, P = 0.015 and OR 2.72, 95% CI 1.68-4.27, P<0.001, respectively). Whereas, lobulated wall aneurysm and PComA/AComA location were inversely and independently associated with unruptured IA condition (OR 0.34, 95% CI 0.21-0.55, P<0.001 and OR 0.37, 95% CI 0.23-0.60, P<0.001, respectively). However, ASA and statins in monotherapy were not independently associated with unruptured IA condition.ConclusionsIn our study population ASA plus statins treatment is independently associated with unruptured IA. Larger and prospective studies are required to explore this potential protective effect against IA rupture.
| S-EPMC7891751 | biostudies-literature
Project description:Objective: Recently, abundant number of studies have revealed many functions of circular RNAs in multiple diseases, however, the role of circular RNA in the rupture of human intracranial aneurysm is still unknown. This study aims to explore the potential functions of circular RNA in the rupture of human intracranial aneurysms. Methods: The differentially expressed circular RNAs between un-ruptured intracranial aneurysms (n = 5) and ruptured intracranial aneurysms (n = 5) were analyzed with the Arraystar human circRNAs microarray. Quantitative real-time PCR (qPCR) was used to verify the results of the circRNA microarray. The role of circular RNA in intracranial aneurysm rupture was assessed in vitro. MTT assay, CCK-8 assay, Caspase3/7 assay, assay of cell apoptosis and Celigo wound healing was conducted to evaluate the relationship between circular RNA and the rupture of human intracranial aneurysms. Results: A total of 13,175 circRNA genes were detected. Among them 63 circRNAs upregulated and 54 circRNAs downregulated significantly in ruptured intracranial aneurysms compared with un-ruptured intracranial aneurysms (p < 0.05 Fold Change > 1.5). Five upregulated circRNAs were selected for further study (hsa_circ_0001947, hsa_circ_0043001, hsa_circ_0064557, hsa_circ_0058514, hsa_circ_0005505). The results of qPCR showed only hsa_circ_0005505 significantly upregulated (p < 0.05). The expression of hsa_circ_0005505 was higher in ruptured intracranial aneurysm tissues. And our in vitro data showed that hsa_circRNA_005505 promotes the proliferation, migration and suppresses the apoptosis of vascular smooth muscle cell. Conclusion: This study revealed an important role of hsa_circ_0005505 in the proliferation, migration and apoptosis of vascular smooth muscle cell, and indicated that hsa_circ_0005505 may associate with the pathological process of intracranial aneurysms.
| S-EPMC8316638 | biostudies-literature