Rupture Of Unruptured Intracranial Aneurysms Research Articles

An In vivo Pilot Study to Estimate the Swelling of the Aneurysm Wall Rabbit Model Generated with Pulsed Fluid Against the Aneurysm Wall.

This study addresses the critical issue of evaluating the risk of rupture of unruptured intracranial aneurysms (UIAs) through the assessment of the mechanical properties of the aneurysm wall. To achieve this, an original approach based on the development of an in vivo deformation device prototype (DDP) of the vascular wall is proposed. The DDP operates by pulsing a physiological fluid onto the vascular wall and measuring the resulting deformation using spectral photon counting computed tomography (SPCCT) imaging. In this preliminary study conducted on a rabbit animal model, an aneurysm was induced on the carotid artery, followed by deformation of the aneurysm sac wall using the DDP. The change in luminal volume of the aneurysm sac induced by the deformation of the vascular wall was then quantified. The initial experimental results demonstrated an increase in the luminal volume of the aneurysm sac in relation to the increased flow rate of the fluid pulsed by the DDP onto the arterial wall. Measurement of the pressure generated by the DDP in relation to the different flow rate values imposed by the pulsation system revealed experimental values of the same order of magnitude as dynamic blood pressure. Furthermore, theoretical pressure values on the deformed area, calculated using Euler's theorem, appeared to be correlated with experimental pressure measurements. This equivalence between theory and experiment is a key element in the use of the DDP for estimating the mechanical properties of the vascular wall, particularly for the use of finite element models to characterise the stress state of the deformed vascular wall. This preliminary work thus presents a novel, innovative, and promising approach for the evaluation and management of the risk of rupture of unruptured intracranial aneurysms.

Peri-Aneurysmal Contact as a Risk Factor for Aneurysmal Rupture in Unruptured Intracranial Aneurysms: An Overview

The occurrence and growth of unruptured intracranial aneurysms are believed to be influenced by intraluminal factors of blood flow dynamics and pathological factors of the aneurysm wall. In addition to these, the deformation and rupture of aneurysms require consideration of physical extra-luminal factors due to contact between the aneurysm and surrounding structures including brain parenchyma, cranial nerves, arteries, veins, cranial base bone and dura mater. The extra-luminal factors of aneurysms were evaluated based on the presence of peri-aneurysmal contact. Peri-aneurysmal contact, depending on the type, location, and size of aneurysms, influenced the growth pattern of the aneurysm. Recently, with the imaging of magnetic resonance cisternography, it had become possible to non-invasively assess the anatomical relationship between the outer wall of aneurysms and the surrounding structures. Fusion images overlaying 3D magnetic resonance cisternography with 3D computed tomography angiography or 3D magnetic resonance angiography detailed the anatomical relationship of peri-aneurysmal contact, position of contact sites, and depth. We depicted the anatomical construction of peri-aneurysmal contact and bleb in unruptured intracranial aneurysms using fusion images and studied the intraluminal blood flow dynamics using computational fluid dynamics. As a result, peri-aneurysmal contact was observed to be involved as an independent variable in the process of bleb formation. It was suggested that factors extra-luminal to the aneurysm, such as peri-aneurysmal contact, might have a greater impact on bleb formation than intraluminal factors like blood flow dynamics. Peri-aneurysmal contact emerged as a noteworthy extra-luminal factor, particularly associated with bleb formation, presenting a substantial risk of rupture in unruptured intracranial aneurysms. These findings underscore the importance of considering the presence and extent of peri-aneurysmal contact alongside intraluminal and wall-related factors in future evaluations. The implications of this overview extend to the development of risk assessment protocols, providing valuable insights for guiding early intervention strategies and ultimately contributing to improved patient outcomes.

Statins may Decrease Aneurysm wall Enhancement of Unruptured Fusiform Intracranial Aneurysms: A high-resolution 3T MRI Study.

Inflammation plays an integral role in the formation, growth, and progression to rupture of unruptured intracranial aneurysms. Aneurysm wall enhancement (AWE) in high-resolution magnetic resonance imaging (HR-MRI) has emerged as a surrogate biomarker of vessel wall inflammation and unruptured intracranial aneurysm instability. We investigated the correlation between anti-inflammatory drug use and three-dimensional AWE of fusiform intracranial aneurysms (FIAs). We retrospectively analyzed consecutive patients with FIAs in our database who underwent 3T HR-MRI at three Chinese centers. FIAs were classified as fusiform-type, dolichoectatic-type, or transitional-type. AWE was objectively defined using the aneurysm-to-pituitary stalk contrast ratio in three-dimensional space by determining the contrast ratio of the average signal intensity in the aneurysmal wall and pituitary stalk on post-contrast T1-weighted images. Data on aneurysm size, morphology, and location, as well as patient demographics and comorbidities, were collected. Univariate and multivariate logistic regression analyses were performed to determine factors independently associated with AWE of FIAs on HR-MRI. In total, 127 FIAs were included. In multivariate analysis, statin use (β = -0.236, P = 0.007) was the only independent factor significantly associated with decreased AWE. In the analysis of three FIA subtypes, the fusiform and transitional types were significantly associated with statin use (rs = -0.230, P = 0.035; and rs = -0.551, P = 0.010; respectively). It establishes an incidental correlation between the use of statins daily for ≥ 6 months and decreased AWE of FIAs. The findings also indicate that the pathophysiology may differ among the three FIA subtypes.

Unruptured untreated intracranial aneurysms: a retrospective analysis of outcomes of 445 aneurysms managed conservatively

Background Factors predicting the growth or rupture of unruptured intracranial aneurysms (UIAs) remain under debate. Increased availability of neuro-imaging has led to increasing incidental findings, therefore understanding the natural history is vital to make appropriate management and follow-up decisions. We analysed a large dataset of UIAs to better identify patients at increased risk, therefore requiring enhanced monitoring and/or prophylactic intervention. Methods Electronic patient records were reviewed from consecutive patients regarding the following data: baseline demographics; past medical and smoking history; indication for imaging detecting the UIA(s); size, location and morphology of UIA(s), duration of imaging follow-up, detection of growth and rupture. Logistic regression was used to identify risk factors for UIA growth or rupture. Subgroup analysis was performed for ‘small’ aneurysms (<7mm). Results 445 UIAs in 274 patients were analysed. Total imaging follow-up was 2268 aneurysm-years (median 3.8 years/UIA). 27 UIAs grew (1.2% annually), and 15 ruptured (0.46%). 70.1% of UIAs were detected incidentally. Mean aneurysm diameter was 4.1mm. Logistic regression identified age < 50, autosomal dominant polycystic kidney disease (ADPKD), hypertension and diameter > 7mm as significant risk factors for growth/rupture. Additionally, previous smoking compared to current smoking was a protective factor against growth or rupture, but no significant difference was seen when comparing current- with non-smokers. Small aneurysm subgroup analysis identified diameter > 5mm, age < 50, ADPKD, and ongoing smoking as risk factors. No significant difference was observed in risk between those with and without previous SAH. Conclusions This study underlines the need for imaging surveillance of even small UIAs. Smoking is a modifiable risk factor for growth/rupture of pre-existing aneurysms, while ADPKD is a particularly strong risk factor.

Mondor disease of the breast.

<h3>Background and purpose</h3> Despite several landmark studies, the natural history of unruptured intracranial aneurysms (UIA) remains uncertain. Our aim was to identify or confirm factors predictive of rupture of UIA being observed conservatively with serial CT angiography (CTA) in a North American patient population. <h3>Methods</h3> We performed a retrospective review of patients with UIA being followed with serial CTA studies from 1999 to 2010. The following features for each aneurysm were cataloged from the official radiologic reports and CTA images: maximum diameter, growth between follow-up studies, location, multiplicity, wall calcification, intraluminal thrombus and morphology. Univariate logistic regression analysis of the potential independent risk factors for aneurysm rupture was performed. Statistically significant risk factors from the univariate analysis were then entered into a multivariate logistic regression analysis. <h3>Results</h3> 152 patients with a total of 180 UIA had at least two CTA studies. Six aneurysms in six different patients ruptured during the CTA follow-up period for an overall rupture rate of 3.3% and an annual rupture rate of 0.97%. All ruptured aneurysms were ≥9 mm. In the univariate analysis, the statistically significant predictors of aneurysm rupture were aneurysm size (p=0.003), aneurysm growth (p&lt;0.0001) and aneurysm multilobulation (p=0.001). The risk factors that remained significant following the multivariate analysis were growth (OR 55.9; 95% CI 4.47 to 700.08; p=0.002) and multilobulation (OR 17.4; 95% CI 1.52 to 198.4; p=0.022). <h3>Conclusions</h3> Aneurysm morphology and interval growth are characteristics predictive of a higher risk of subsequent rupture during conservative CTA follow-up.

Characteristics of Unruptured Intracranial Aneurysms with Delayed Rupture Following Coil Embolization: Case Series and Review of the Literature.

Long-term clinical outcomes including delayed rupture of unruptured intracranial aneurysms (UIAs) after coil embolization (CE) remain unclear. The purpose of this study was to evaluate the precise timing of re-treatment for recanalized UIAs before rupture. From February 2012 to June 2020, a total of 197 patients with 207 UIAs underwent CE in our institution and were followed up for more than 6 months. The follow-up period, as well as morphological changes from treatment to recanalization, regrowth, and rupture, was retrospectively analyzed. Delayed rupture was defined as a rupture that occurred more than 1 month after CE. The average length of follow-up was 48.7 months. Three of 207 UIAs (1.45%) ruptured after CE. The aneurysm locations were the middle cerebral artery (MCA), anterior communicating artery (AcomA), and internal carotid artery-posterior communicating artery (ICA-Pcomm). The annual rupture rate after CE was 0.36%. Immediately after the first CE, treated aneurysms were graded according to the Modified Raymond-Roy Classification with class II for MCA aneurysms and class IIIb for AcomA and ICA-Pcomm aneurysms. The ICA-Pcomm aneurysm was treated with two additional CEs and was finally graded as class I. In all cases, DSA or MRA before aneurysm rupture showed recanalization and regrowth of aneurysms. The average periods from final embolization to regrowth and from regrowth to rupture were 54.3 months (±16.8) and 2.3 months (±0.9), respectively. UIAs with recanalization and regrowth after CE should undergo re-treatment as early as possible.

Difference in Rupture Risk Between Familial and Sporadic Intracranial Aneurysms: An Individual Patient Data Meta-analysis.

We combined individual patient data (IPD) from prospective cohorts of patients with unruptured intracranial aneurysms (UIAs) to assess to what extent patients with familial UIA have a higher rupture risk than those with sporadic UIA. For this IPD meta-analysis, we performed an Embase and PubMed search for studies published up to December 1, 2020. We included studies that (1) had a prospective study design; (2) included 50 or more patients with UIA; (3) studied the natural course of UIA and risk factors for aneurysm rupture including family history for aneurysmal subarachnoid haemorrhage and UIA; and (4) had aneurysm rupture as an outcome. Cohorts with available IPD were included. All studies included patients with newly diagnosed UIA visiting one of the study centers. The primary outcome was aneurysmal rupture. Patients with polycystic kidney disease and moyamoya disease were excluded. We compared rupture rates of familial vs sporadic UIA using a Cox proportional hazard regression model adjusted for PHASES score and smoking. We performed 2 analyses: (1) only studies defining first-degree relatives as parents, children, and siblings and (2) all studies, including those in which first-degree relatives are defined as only parents and children, but not siblings. We pooled IPD from 8 cohorts with a low and moderate risk of bias. First-degree relatives were defined as parents, siblings, and children in 6 cohorts (29% Dutch, 55% Finnish, 15% Japanese), totaling 2,297 patients (17% familial, 399 patients) with 3,089 UIAs and 7,301 person-years follow-up. Rupture occurred in 10 familial cases (rupture rate: 0.89%/person-year; 95% confidence interval [CI] 0.45-1.59) and 41 sporadic cases (0.66%/person-year; 95% CI 0.48-0.89); adjusted hazard ratio (HR) for familial cases 2.56 (95% CI 1.18-5.56). After adding the 2 cohorts excluding siblings as first-degree relatives, resulting in 9,511 patients, the adjusted HR was 1.44 (95% CI 0.86-2.40). The risk of rupture of UIA is 2.5 times higher, with a range from a 1.2 to 5 times higher risk, in familial than in sporadic UIA. When assessing the risk of rupture in UIA, family history should be taken into account.

Risk of Aneurysm Rupture After Thrombolysis in Patients With Acute Ischemic Stroke and Unruptured Intracranial Aneurysms.

Unruptured intracranial aneurysms (UIAs) are considered to be a relative contraindication for IV thrombolysis (IVT) in acute ischemic stroke (AIS). Currently, however, data are limited on the risk of UIA rupture after IVT. Our objective was to assess whether IVT for AIS can lead to a UIA rupture and intracranial hemorrhages (ICHs) in patients with unruptured UIAs. This was a prospective cohort study of consecutive patients treated in a comprehensive stroke center between 2005 and 2019. We assessed radiology reports and records at the Finnish Care Register for Health Care to identify patients with UIAs among all patients with AIS treated with IVT at the center. We analyzed patient angiograms for aneurysm characteristics and other brain imaging studies for ICHs after IVT. The main outcome was in-hospital ICHs attributable to a UIA rupture after IVT. Secondary outcomes were in-hospital symptomatic ICHs (European-Australian Cooperative Acute Stroke Study [ECASS-2] criteria, i.e., NIH Stroke Scale score increase ≥4 points) and any in-hospital ICHs. A total of 3,953 patients were treated with IVT during the 15-year study period. One hundred thirty-two (3.3%) of the 3,953 patients with AIS had a total of 155 UIAs (141 saccular and 14 fusiform). The mean diameter of UIAs was 4.7 ± 3.8 mm, with 18.7% being ≥7 mm and 9.7% ≥10 mm in diameter. None of the 141 saccular UIAs ruptured after IVT. Three patients (2.3%, 95% confidence interval [CI] 0.6%-5.8%) with large fusiform basilar artery UIAs had a fatal rupture at 27 hours, 43 hours, and 19 days after IVT. All 3 were administered anticoagulation treatments after IVT, and anticoagulation took effect during the UIA rupture. Any ICHs and symptomatic ICHs were detected in 18.9% (95% CI 12.9%-26.2%) and 8.3% (95% CI 4.4%-13.8%) of all patients with AIS, respectively. IVT appears to be safe in patients with AIS with saccular UIAs, including larges UIAs (≥10 mm). Anticoagulation after AIS in patients with large fusiform posterior circulation UIAs may increase the risk of aneurysm rupture.

Outcome of Patients with Multiple Intracranial Aneurysms after Subarachnoid Hemorrhage and Future Risk of Rupture of Unruptured Aneurysm.

The purpose was to study the risk of rupture of unruptured intracranial aneurysms (UIAs) of patients with multiple intracranial aneurysms after subarachnoid hemorrhage (SAH), in a long-term follow-up study, from variables known at baseline. Future rupture risk was compared in relation to outcome after SAH. The series consists of 131 patients with 166 UIAs and 2854 person-years of follow-up between diagnosis of UIA and its rupture, death or the last follow-up contact. These were diagnosed before 1979, when UIAs were not treated in our country. Those patients with a moderate or severe disability after SAH, according to the Glasgow Outcome Scale, had lower rupture rates of UIA than those with a good recovery or minimal disability (4/37 or 11%, annual UIA rupture rate of 0.5% (95% confidence interval (CI) 0.1–1.3%) during 769 follow-up years vs. 27/94 or 29%, 1.3% (95% CI 0.9–1.9%) during 2085 years). Those with a moderate or severe disability differed from others by their older age. Those with a moderate or severe disability tended to have a decreased cumulative rate of aneurysm rupture (log rank test, p = 0.066) and lower relative risk of UIA rupture (hazard ratio 0.39, 95% CI 0.14–1.11, p = 0.077). Multivariable hazard ratios showed at least similar results, suggesting that confounding factors did not have a significant effect on the results. The results of this study without treatment selection of UIAs suggest that patients with a moderate or severe disability after SAH have a relatively low risk of rupture of UIAs. Their lower treatment indication may also be supported by their known higher treatment risks.

Integrated Transcriptional Profiling Analysis and Immune-Related Risk Model Construction for Intracranial Aneurysm Rupture.

Intracranial aneurysms (IAs) may cause lethal subarachnoid hemorrhage upon rupture, but the molecular mechanisms are poorly understood. The aims of this study were to analyze the transcriptional profiles to explore the functions and regulatory networks of differentially expressed genes (DEGs) in IA rupture by bioinformatics methods and to identify the underlying mechanisms. In this study, 1,471 DEGs were obtained, of which 619 were upregulated and 852 were downregulated. Gene enrichment analysis showed that the DEGs were mainly enriched in the inflammatory response, immune response, neutrophil chemotaxis, and macrophage differentiation. Related pathways include the regulation of actin cytoskeleton, leukocyte transendothelial migration, nuclear factor κB signaling pathway, Toll-like receptor signaling pathway, tumor necrosis factor signaling pathway, and chemokine signaling pathway. The enrichment analysis of 20 hub genes, subnetworks, and significant enrichment modules of weighted gene coexpression network analysis showed that the inflammatory response and immune response had a causal relationship with the rupture of unruptured IAs (UIAs). Next, the CIBERSORT method was used to analyze immune cell infiltration into ruptured IAs (RIAs) and UIAs. Macrophage infiltration into RIAs increased significantly compared with that into UIAs. The result of principal component analysis revealed that there was a difference between RIAs and UIAs in immune cell infiltration. A 4-gene immune-related risk model for IA rupture (IRMIR), containing CXCR4, CXCL3, CX3CL1, and CXCL16, was established using the glmnet package in R software. The receiver operating characteristic value revealed that the model represented an excellent clinical situation for potential application. Enzyme-linked immunosorbent assay was performed and showed that the concentrations of CXCR4 and CXCL3 in serum from RIA patients were significantly higher than those in serum from UIA patients. Finally, a competing endogenous RNA network was constructed to provide a potential explanation for the mechanism of immune cell infiltration into IAs. Our findings highlighted the importance of immune cell infiltration into RIAs, providing a direction for further research.

Candidate drugs for preventive treatment of unruptured intracranial aneurysms: A cross-sectional study.

Background and purposeEstablishment of drug therapy to prevent rupture of unruptured intracranial aneurysms (IAs) is needed. Previous human and animal studies have gradually clarified candidate drugs for preventive treatment of IA rupture. However, because most of these candidates belong to classes of drugs frequently co-administered to prevent cardiovascular diseases, epidemiological studies evaluating these drugs simultaneously should be performed. Furthermore, because drugs included in the same class may have different effects in terms of disease prevention, drug-by-drug assessments are important for planning intervention trials.Materials and methodsWe performed a cross-sectional study enrolling patients diagnosed with IAs between July 2011 and June 2019 at our institution. Patients were divided into ruptured or unruptured groups. The drugs investigated were selected according to evidence suggested by either human or animal studies. Univariate and multivariate logistic regression analyses were performed to assess the association of drug treatment with rupture status. We also performed drug-by-drug assessments of the association, including dose-response relationships, with rupture status.ResultsIn total, 310 patients with ruptured and 887 patients with unruptured IAs were included. Multivariate analysis revealed an inverse association of statins (odds ratio (OR), 0.54; 95% confidence interval (CI) 0.38–0.77), calcium channel blockers (OR, 0.41; 95% CI 0.30–0.58), and angiotensin II receptor blockers (ARBs) (OR, 0.67; 95% CI 0.48–0.93) with ruptured IAs. Moreover, inverse dose-response relationships with rupture status were observed for pitavastatin and rosuvastatin among statins, benidipine, cilnidipine, and amlodipine among calcium channel blockers, and valsartan, azilsartan, candesartan, and olmesartan among ARBs. Only non-aspirin non-steroidal anti-inflammatory drugs were positively associated with ruptured IAs (OR, 3.24; 95% CI 1.71–6.13).ConclusionsThe present analysis suggests that several types of statins, calcium channel blockers, and ARBs are candidate drugs for preventive treatment of unruptured IAs.

Atorvastatin and growth, rupture of small unruptured intracranial aneurysm: results of a prospective cohort study

Background and aims:The role of statins in unruptured intracranial aneurysm (UIA) growth and rupture remains ambiguous. This study sought to determine whether atorvastatin is associated with aneurysm growth and rupture in patients harboring UIA <7 mm.Methods:This prospective, multicenter cohort study consecutively enrolled patients with concurrent UIA <7 mm and ischemic cerebrovascular disease from four hospitals between 2016 and 2019. Baseline and follow-up patient information was recorded. Because of the strong anti-inflammatory effect of aspirin, patients using aspirin were excluded. Patients taking atorvastatin 20 mg daily were atorvastatin users. The primary and exploratory endpoints were aneurysm rupture and growth, respectively.Results:Among the 1087 enrolled patients, 489 (45.0%) took atorvastatin, and 598 (55%) took no atorvastatin. After a mean follow-up duration of 33.0 ± 12.5 months, six (1.2%) and five (0.8%) aneurysms ruptured in atorvastatin and non-atorvastatin groups, respectively. In the adjusted multivariate Cox analysis, UIA sized 5 to <7 mm, current smoker, and uncontrolled hypertension were associated with aneurysm rupture, whereas atorvastatin [adjusted hazard ratio (HR) 1.495, 95% confidence interval (CI) 0.417–5.356, p = 0.537] was not. Of 159 patients who had follow-up imaging, 34 (21.4%) took atorvastatin and 125 (78.6%) took no atorvastatin. Aneurysm growth occurred in five (14.7%) and 21 (16.8%) patients in atorvastatin and non-atorvastatin groups (mean follow-up: 20.2 ± 12.9 months), respectively. In the adjusted multivariate Cox analysis, UIAs sized 5 to <7 mm and uncontrolled hypertension were associated with a high growth rate; atorvastatin (adjusted HR 0.151, 95% CI 0.031–0.729, p = 0.019) was associated with a reduced growth rate.Conclusions:We conclude atorvastatin use is associated with a reduced risk of UIA growth, whereas atorvastatin is not associated with UIA rupture.The trial registry name:The Clinic Benefit and Risk of Oral Aspirin for Unruptured Intracranial Aneurysm Combined With Cerebral IschemiaClinical Trial Registration-URL: http://www.clinicaltrials.gov Unique identifier:NCT02846259

Three-Month Outcome of Carotid Artery Stenting in Patients with/without Coexistent Unruptured Intracranial Aneurysms

Introduction: Safety of carotid artery stenting (CAS) in patients having carotid stenosis with coexistent unruptured intracranial aneurysms (UIAs) is rarely reported. Thus, we studied the 3-month outcome of CAS in the presence of coexistent UIAs in our institution. Methods: A retrospective analysis of patients receiving CAS at our institution from September 2011 to December 2019 was carried out. Patients were stratified into 2 groups: group of CAS with UIAs (CAS-UIA) and group of CAS without UIAs (CAS). The main complications within 3 months after stenting were TIA, ischemic stroke, symptomatic intracranial hemorrhage (sICH), rupture of UIAs, and death. The baseline characteristics and complications of the 2 groups were compared. Results: Five hundred fifty-six patients (CAS, n = 468; CAS-UIA, n = 88) were included and 604 stenting procedures were performed. More patients had hypertension in the CAS-UIA group (87.5 vs. 73.7%, p = 0.006). There was no significant difference in TIAs, ischemic stroke, sICH, and death within 3 months after stenting between the CAS and CAS-UIA groups. None of the 113 coexistent UIAs detected in 88 patients had aneurysm rupture within 3 months after CAS. Conclusions: In our large cohort of CAS patients, coexistent UIAs are not uncommon. Stenting of a carotid artery in the presence of coexistent UIAs could be conducted safely. Together with 3-month dual antiplatelet therapy, CAS did not increase the rupture risk of the coexistent UIAs within 3 months.

Role of Morphological and Hemodynamic Factors in Predicting Intracranial Aneurysm Rupture: A Review.

Intracranial aneurysms (IAs) carry the risk of rupture, which will lead to subarachnoid hemorrhage, which has a high mortality and morbidity risk. However, the treatment of IA's carries mortality and morbidity risks too. There are well-known risk factors for the rupture of IAs like age, size, and site. However, choosing patients with unruptured IAs for treatment is still a big challenge. This review article aimed to find out the relationship between morphological and hemodynamic characters of IAs with their rupture and incorporate these factors with well-known factors to yield an accurate module for predicting the rupture of IAs and decision-making in the treatment of unruptured IAs.We searched in PubMed and Medline databases by using the following keywords: IAs, subarachnoid hemorrhage, and risk of rupture, morphology, and hemodynamic “mesh.” A total of 19 studies with 7269 patients and 9167 IAs, of which 1701 had ruptured, were reviewed thoroughly. Some modules like population, hypertension, age, size, earlier subarachnoid hemorrhage, and site (PHASES) score that involve well-known risk factors can be used to assess the risk of rupture of IAs. However, decision making for treating unruptured IA needs more detailed and more accurate modules. Studying morphological and hemodynamic factors and incorporation of them with well-known risk factors to yield a more comprehensive module will be very helpful in treating unruptured IA. Among morphological factors, aspect ratio (AR), size ratio (SR), aneurysm height, and bottle-neck factor showed significant effects on the growth and rupture of IA. Besides, wall shear stress (WSS), oscillatory shear index (OSI), and low wall shear stress area (LSA) as hemodynamic factors could have a substantial impact on the formation, shape, growth, and rupture of unruptured IA.

Hemodynamic Features of Microsurgically Identified, Thin-Walled Regions of Unruptured Middle Cerebral Artery Aneurysms Characterized Using Computational Fluid Dynamics.

Thin-walled regions (TWRs) of aneurysm surfaces observed in microscopic surgery are thought to be vulnerable areas for growth and rupture of unruptured intracranial aneurysms (UIAs). To identify hemodynamic features of TWRs of aneurysms by using computational fluid dynamics (CFD) analyses of unruptured middle cerebral artery bifurcation (MCAB) aneurysms. Nine patients with 11 MCAB aneurysms were enrolled, and their TWRs were identified. CFD analysis was performed using 3 parameters: pressure, wall shear stress (WSS), and WSS divergence (WSSD). Each parameter was evaluated for its correspondence with TWR. Among 11 aneurysms, 15 TWRs were identified. Corresponding matches with CFD parameters (pressure, WSS, and WSSD) were 73.33, 46.67, and 86.67%, respectively. WSSD, a hemodynamic parameter that accounts for both magnitude and directionality of WSS, showed the highest correspondence. High WSSD might correspond with TWR of intracranial aneurysms, which are likely high-risk areas for rupture.

Decreased contrast enhancement on high-resolution vessel wall imaging of unruptured intracranial aneurysms in patients taking aspirin.

Inflammation plays an integral role in the formation, growth, and progression to rupture of unruptured intracranial aneurysms (UIAs). Animal and human studies have suggested that, due to its antiinflammatory effect, aspirin (ASA) may decrease the risks of growth and rupture of UIAs. High-resolution vessel wall imaging (HR-VWI) has emerged as a noninvasive method to assess vessel wall inflammation and UIA instability. To the authors' knowledge, to date no studies have found a significant correlation between patient use of ASA and contrast enhancement of UIAs on HR-VWI. The University of Iowa HR-VWI Project database was analyzed. This database is a compilation of data on patients with UIAs who prospectively underwent HR-VWI on a 3T Siemens MRI scanner. The presence of aneurysmal wall enhancement was objectively defined using the aneurysm-to-pituitary stalk contrast ratio (CRstalk). This ratio was calculated by measuring the maximal signal intensity in the aneurysmal wall and the pituitary stalk on postcontrast T1-weighted images. Data on aneurysm size, morphology, and location and patient demographics and comorbidities were collected. Use of ASA was defined as daily intake of ≥ 81 mg during the previous 6 months or longer. Univariate and multivariate logistic regression analyses were performed to determine factors independently associated with increased contrast enhancement of UIAs on HR-VWI. In total, 74 patients harboring 96 UIAs were included in the study. The mean patient age was 64.7 ± 12.4 years, and 60 patients (81%) were women. Multivariate analysis showed that age (OR 1.12, 95% CI 1.05-1.19), aneurysm size ≥ 7 mm (OR 21.3, 95% CI 4.88-92.8), and location in the anterior communicating, posterior communicating, and basilar arteries (OR 10.7, 95% CI 2.45-46.5) were significantly associated with increased wall enhancement on HR-VWI. On the other hand, use of ASA was significantly associated with decreased aneurysmal wall enhancement on HR-VWI (OR 0.22, 95% CI 0.06-0.83, p = 0.026). The study results establish a correlation between use of ASA daily for ≥ 6 months and significant decreases in wall enhancement of UIAs on HR-VWI. The findings also demonstrate that detection of wall enhancement using HR-MRI may be a valuable noninvasive method for assessing aneurysmal wall inflammation and UIA instability.

Observed rupture of unruptured intracranial aneurysms

Aim: To study the aneurysms where pre and post-rupture imaging was available to determine the impact of rupture on morphology and size of the aneurysm.Methods: A retrospective case series where all cases of ruptured aneurysms over a 5-year period were evaluated and cases identified where pre and post rupture imaging was available. These were then studied in detail.Results: The actual change in the volume of the aneurysm pre and post rupture was quite small and the underlying shape/morphology did not change at all.Conclusion: Post-rupture morphology of aneurysms can be used as representative of pre-rupture morphology. Further larger studies in collaboration with other neurosurgical centres to corroborate this view would be helpful.

Hemodynamic Analysis of Postoperative Rupture of Unruptured Intracranial Aneurysms after Placement of Flow-Diverting Stents: A Matched Case-Control Study.

Postoperative rupture of intracranial aneurysm has been reported as a fatal complication after flow-diverter placement. We assessed several hemodynamic variables to explore risk factors in the postoperative rupture process. We enrolled 10 patients with intracranial aneurysms, treated with flow diverters between September 2014 and December 2018, who experienced postoperative aneurysm rupture (postoperative aneurysm rupture group). We matched these subjects 1:2 with 20 patients with postoperative unruptured (postoperative unruptured group) intracranial aneurysms based on clinical and morphologic factors. Using computational fluid dynamics, we assessed hemodynamic changes pre- and posttreatment between the 2 groups on a number of qualitative and quantitative parameters. In the postoperative aneurysm rupture group, the proportion of patients with aneurysms with an unstable flow pattern increased to 60.0% after treatment, while the proportion in the postoperative unruptured group decreased to 20.0%, a significant difference between the 2 groups (P = .028). Energy loss in the postoperative unruptured group decreased after treatment but increased in the postoperative aneurysm rupture group. The reduction ratio of energy loss showed a significant difference between the 2 groups (22.73% ± 53.59% for postoperative unruptured versus -158.81% ± 183.95% for postoperative aneurysm rupture, P = .02). Other parameters and changes of pre- and posttreatment hemodynamic parameters showed no significant difference between 2 groups. Compared with pretreatment, unstable flow pattern and higher energy loss after Pipeline Embolization Device placement for intracranial aneurysm may be the important hemodynamic risk factors related to delayed aneurysm rupture.

Growth and rupture of unruptured intracranial aneurysms.

Risk factors for growth of unruptured intracranial aneurysms (UIAs) during a lifelong follow-up in relation to subsequent rupture are unknown. The author's aim in this study was to investigate whether risk factors for UIA growth are different for those that lead to rupture than for those that do not. The series consists of 87 patients with 111 UIAs diagnosed before 1979, when UIAs were not treated. A total follow-up time of the patients was 2648 person-years for all-cause death and 2182 years when patients were monitored until the first rupture, death due to unrelated causes, or the last contact (annual incidence of aneurysm rupture, 1.2%). The follow-up time between aneurysm measurements was 1669 person-years. Risk factors for UIA growth were analyzed in relation to subsequent rupture. The median follow-up time between aneurysm measurements was 21.7 years (range 1.2-51.0 years). In 40 of the 87 patients (46%), the UIAs increased in size ≥ 1 mm, and in 31 patients (36%) ≥ 3 mm. All ruptured aneurysms in 27 patients grew during the follow-up of 324 person-years (mean growth rates 6.1 mm, 0.92 mm/year, and 37%/year), while growth without rupture occurred in 13 patients during 302 follow-up years (3.9 mm, 0.18 mm/year, and 4%/year) and no growth occurred in 47 patients during 1043 follow-up years. None of the 60 patients without aneurysm rupture experienced one during the subsequent 639 follow-up years after the last aneurysm measurement. Independent risk factors for UIA growth (≥ 1 mm) in all patients were female sex (adjusted OR 3.08, 95% CI 1.04-9.13) and smoking throughout the follow-up time (adjusted OR 3.16, 95% CI 1.10-9.10), while only smoking (adjusted OR 4.36, 95% CI 1.27-14.99) was associated with growth resulting in aneurysm rupture. Smoking was the only independent risk factor for UIA growth ≥ 3 mm resulting in aneurysm rupture (adjusted OR 4.03, 95% CI 1.08-15.07). Cigarette smoking at baseline predicted subsequent UIA growth, while smoking at the end of the follow-up was associated with growth resulting in aneurysm rupture. Cigarette smoking is an important risk factor for UIA growth, particularly for growth resulting in rupture. Cessation of smoking may reduce the risk of devastating aneurysm growth.

Treatment Scoring of Unruptured Intracranial Aneurysms.

Background and Purpose- The purpose was to obtain a reliable treatment score for unruptured intracranial aneurysms (UIAs) from variables known at baseline. Methods- The series included 142 patients with UIAs diagnosed between 1956 and 1978 when UIAs were not treated and were followed up until the first aneurysm rupture, death, or the last contact. Previously published UIA treatment score was recorded, and finally, a new treatment score was constructed. Results- The median follow-up time was 21.0 years (interquartile range, 10.4-31.8 years). A total of 34 patients had an aneurysm rupture during 3064 person-years of follow-up. The UIA treatment score differed slightly between those with and without an aneurysm rupture (9.4±2.8 versus 8.3±3.1, P=0.082). The receiver operating characteristics curve of the UIA treatment score for predicting rupture showed a modest area under the curve (AUC; 0.618, 95% CI, 0.502-0.733; P=0.059). The best new treatment score consisted of 4 variables: age <40 years (2 points), current smoking (2 points), UIA size ≥7 mm (3 points), and location (anterior communicating artery, 5 points; internal carotid bifurcation, 4 points; and posterior communicating artery, 2 points). Scores of 5 to 12 points were associated with high cumulative UIA rupture rates (16%-60% at 10 years and 49%-80% at 30 years), favoring UIA treatment. Scores of 1 to 4 points (3% at 10 years and 18% at 30 years) favored conservative treatment and needed additional indications for treatment. Patients with a score of 0 points should not be treated (no ruptures during 513 follow-up years). The area under the curve for this scoring was 0.755 (95% CI, 0.657-0.853; P<0.001) and was better than that of the UIA treatment score (P=0.02). Conclusions- This new simple and rapid scoring system is reliable for evaluating treatment indications with regard to the lifelong prevention of aneurysm rupture.