Intracranial Aneurysm Wall Research Articles

Circulating collagen breakdown products as a biomarker for presence and instability of human intracranial aneurysms.

There is an unmet need for improved detection of intracranial aneurysms (IAs) and distinction between stable and unstable (high rupture risk) IAs. Within the IA wall, synthesis and degradation of type I collagen as the main molecular constituent balance each other to maintain IA stability. We hypothesized that collagen breakdown products could serve as molecular markers for IA presence and instability. This prospective, cross-sectional, single-center study included patients with unstable (growing/symptomatic/ruptured) and stable IAs and controls. We determined C-telopeptide (CTx) and c-terminal telopeptide (ICTP) as breakdown products of type I collagen in arterial and venous blood. We included 107 participants with IAs (52 stable/44 unstable) and 41 controls. The correlation between intra-aneurysmal and venous levels was r = 0.63 (p < 0.001) for ICTP, r = 0.55 (p = 0.001) for CTx. The odds of harboring an IA were five times higher for participants with high compared to low venous levels of collagen breakdown products (ICTP: odds ratio (OR) 4.9 (95% CI 1.1-22.7); CTx: OR 5.3 (95% CI 1.4-20.0)). The OR for having an unstable IA was 9.3 (95% CI 2.1-41.5) for patients with high compared to low venous ICTP levels. The area under the curve for ICTP levels as a marker for IA instability was 0.75. Increased levels of venous collagen breakdown products, especially ICTP levels, could serve as a biomarker for IA presence and instability and complement current data for management of unruptured IAs on an individual patient level. Future studies with longitudinal data are needed to validate ICTP as a biomarker for high risk IAs.

Integrated metagenomic and metabolomic analysis reveals distinctive stage-specific gut-microbiome-derived metabolites in intracranial aneurysms

ObjectiveOur study aimed to explore the influence of gut microbiota and their metabolites on intracranial aneurysms (IA) progression and pinpoint-related metabolic biomarkers derived from the gut microbiome.DesignWe recruited 358 patients...

Does it stable? Intracranial aneurysm wall enhancement might be the warning signals: a meta-analysis of observational studies.

Magnetic resonance vessel wall imaging (MR-VWI) is an emerging imaging technology used to assess the progressive risk of unruptured intracranial aneurysms (UIAs). Unlike the standard evaluation model, MR-VWI is still debatable. This study aims to further define the potential relationship between aneurysm wall enhancement (AWE) and aneurysm stability. Using "intracranial aneurysm", "magnetic resonance", and "enhancement" as keywords, relevant studies were systematically searched in PubMed, Embase, and Cochrane, and the qualified studies were enrolled for further analysis. There were 13 case-control studies, 4 cohort studies, and 2,678 cases of intracranial aneurysms included in the meta-analysis. It was shown that AWE was correlated with intracranial aneurysm rupture (OR = 35.90, 95% CI: 15.58 to 82.75, p < 0.001), growth (OR = 6.69, 95% CI: 2.69 to 16.63, p < 0.001), and presence of symptoms (OR = 14.46, 95% CI: 9.07 to 23.05, p < 0.001). This finding had a high diagnostic value, but the correlation was probably not independent of aneurysm size. The pooled relative risks of the follow-up studies revealed that the risk of UIA progression was approximately 3.33 times higher with AWE than without AWE (RR = 3.33, 95% CI: 2.33 to 4.78, p < 0.001). In addition, the pooled results demonstrated that quantitative indices of VWI enhancement were equally linked with aneurysm stability (OR = 19.61, 95% CI: 10.63 to 36.17, p < 0.001). AWE is an effective imaging method to assess the stability of UIAs, and it can be a marker for the prophylactic treatment of small unruptured intracranial aneurysms in the future, which remains to be validated by prospective studies with large samples.

Temporal Changes on Postgadolinium MR Vessel Wall Imaging Captures Enhancement Kinetics of Intracranial Atherosclerotic Plaques and Aneurysms.

Analysis of vessel wall contrast kinetics (ie, wash-in/washout) is a promising method for the diagnosis and risk-stratification of intracranial atherosclerotic disease plaque (ICAD-P) and the intracranial aneurysm walls (IA-W). We used black-blood MR imaging or MR vessel wall imaging to evaluate the temporal relationship of gadolinium contrast uptake kinetics in ICAD-Ps and IA-Ws compared with normal anatomic reference structures. Patients with ICAD-Ps or IAs who underwent MR vessel wall imaging with precontrast, early postcontrast (5-15 minutes), and delayed postcontrast (20-30 minutes) 3D T1-weighted TSE sequences were retrospectively studied. ROIs of a standardized diameter (2 mm) were used to measure the signal intensities of the cavernous sinus, pituitary infundibulum, temporalis muscle, and choroid plexus. Point ROIs were used for ICAD-Ps and IA-Ws. All ROI signal intensities were normalized to white matter signal intensity obtained using ROIs of 10-mm diameter. Measurements were acquired on precontrast, early postcontrast, and delayed postcontrast 3D T1 TSE sequences for each patient.ajnr;45/9/1206/T1T1T1Table 1:MR-VWI parameters for ICAD-Ps and IAsParameterValueSequence3D TSEScan planeAxialFOV (mm)160TR/TE (ms)800/28-32BW (Hx/pixel)370θ120Acceleration2ETL42Matrix acquisition0.5 mm ×0.5 mmMatrix recon0.5 mm ×0.5 mmNo. of slices/thick120/0.5Note:-FOV indicates field of view; TR, the repetition time; TE, the echo time; BW, bandwidth; ETL, echo train length; Matrix recon, matrix reconstruction. Ten patients with 17 symptomatic ICAD-Ps and 30 patients with 34 IA-Ws were included and demonstrated persisting contrast uptake (P < .001) of 7.21% and 10.54% beyond the early phase (5-15 minutes postcontrast) and in the delayed phase (20-30 minutes postcontrast) on postcontrast MR vessel wall imaging. However, normal anatomic reference structures including the pituitary infundibulum and cavernous sinus demonstrated a paradoxical contrast washout in the delayed phase. In both ICAD-Ps and IA-Ws, the greatest percentage of quantitative enhancement (>70%-90%) occurred in the early phase of postcontrast imaging, consistent with the rapid contrast uptake kinetics of neurovascular pathology. Using standard MR vessel wall imaging techniques, our results demonstrate the effects of gadolinium contrast uptake kinetics in ICAD-Ps and IA-Ws with extended accumulating enhancement into the delayed phase (> 15 minutes) as opposed to normal anatomic reference structures that conversely exhibit decreasing enhancement. Because these relative differences are used to assess qualitative patterns of ICAD-P and IA-W enhancement, our findings highlight the importance of standardizing acquisition time points and MR vessel wall imaging protocols to interpret pathologic enhancement for the risk stratification of cerebrovascular pathologies.

Description of the local hemodynamic environment in intracranial aneurysm wall subdivisions.

Intracranial aneurysms (IAs) pose severe health risks influenced by hemodynamics. This study focuses on the intricate characterization of hemodynamic conditions within the IA walls and their influence on bleb development, aiming to enhance understanding of aneurysm stability and the risk of rupture. The methods emphasized utilizing a comprehensive dataset of 359 IAs and 213 IA blebs from 268 patients to reconstruct patient-specific vascular models, analyzing blood flow using finite element methods to solve the unsteady Navier-Stokes equations, the segmentation of aneurysm wall subregions and the hemodynamic metrics wall shear stress (WSS), its metrics, and the critical points in WSS fields were computed and analyzed across different aneurysm subregions defined by saccular, streamwise, and topographical divisions. The results revealed significant variations in these metrics, correlating distinct hemodynamic environments with wall features on the aneurysm walls, such as bleb formation. Critical findings indicated that regions with low WSS and high OSI, particularly in the body and central regions of aneurysms, are prone to conditions that promote bleb formation. Conversely, areas exposed to high WSS and positive divergence, like the aneurysm neck, inflow, and outflow regions, exhibited a different but substantial risk profile for bleb development, influenced by flow impingements and convergences. These insights highlight the complexity of aneurysm behavior, suggesting that both high and low-shear environments can contribute to aneurysm pathology through distinct mechanisms.

AnXplore: a comprehensive fluid-structure interaction study of 101 intracranial aneurysms.

Advances in computational fluid dynamics continuously extend the comprehension of aneurysm growth and rupture, intending to assist physicians in devising effective treatment strategies. While most studies have first modelled intracranial aneurysm walls as fully rigid with a focus on understanding blood flow characteristics, some researchers further introduced Fluid-Structure Interaction (FSI) and reported notable haemodynamic alterations for a few aneurysm cases when considering wall compliance. In this work, we explore further this research direction by studying 101 intracranial sidewall aneurysms, emphasizing the differences between rigid and deformable-wall simulations. The proposed dataset along with simulation parameters are shared for the sake of reproducibility. A wide range of haemodynamic patterns has been statistically analyzed with a particular focus on the impact of the wall modelling choice. Notable deviations in flow characteristics and commonly employed risk indicators are reported, particularly with near-dome blood recirculations being significantly impacted by the pulsating dynamics of the walls. This leads to substantial fluctuations in the sac-averaged oscillatory shear index, ranging from -36% to +674% of the standard rigid-wall value. Going a step further, haemodynamics obtained when simulating a flow-diverter stent modelled in conjunction with FSI are showcased for the first time, revealing a 73% increase in systolic sac-average velocity for the compliant-wall setting compared to its rigid counterpart. This last finding demonstrates the decisive impact that FSI modelling can have in predicting treatment outcomes.

Optimizing timing for quantification of intracranial aneurysm enhancement: a multi-phase contrast-enhanced vessel wall MRI study.

Aneurysm wall enhancement (AWE) on high-resolution contrast-enhanced vessel wall MRI (VWMRI) is an emerging biomarker for intracranial aneurysms (IAs) stability. Quantification methods of AWE in the literature, however, are variable. We aimed to determine the optimal post-contrast timing to quantify AWE in both saccular and fusiform IAs. Consecutive patients with unruptured IAs were prospectively recruited. VWMRI was acquired on 1 pre-contrast and 4 consecutive post-contrast phases (each phase was 9 min). Signal intensity values of cerebrospinal fluid (CSF) and aneurysm wall on pre- and 4 post-contrast phases were measured to determine the aneurysm wall enhancement index (WEI). AWE was also qualitatively analyzed on post-contrast images using previous grading criteria. The dynamic changes of AWE grade and WEI were analyzed for both saccular and fusiform IAs. Thirty-four patients with 42 IAs (27 saccular IAs and 15 fusiform IAs) were included. The changes in AWE grade occurred in 8 (30%) saccular IAs and 6 (40%) in fusiform IAs during the 4 post-contrast phases. The WEI of fusiform IAs decreased 22.0% over time after contrast enhancement (p = 0.009), while the WEI of saccular IAs kept constant during the 4 post-contrast phases (p > 0.05). When performing quantitative analysis of AWE, acquiring post-contrast VWMRI immediately after contrast injection achieves the strongest AWE for fusiform IAs. While the AWE degree is stable for 36 min after contrast injection for saccular IAs. The standardization of imaging protocols and analysis methods for AWE will be helpful for imaging surveillance and further treatment decisions of patients with unruptured IAs. Imaging protocols and measurements of intracranial aneurysm wall enhancement are reported heterogeneously. Aneurysm wall enhancement for fusiform intracranial aneurysms (IAs) is strongest immediately post-contrast, and stable for 36 min for saccular IAs. Future multi-center studies should investigate aneurysm wall enhancement as an emerging marker of aneurysm growth and rupture.

Distribution of rupture sites and blebs on intracranial aneurysm walls suggests distinct rupture patterns in ACom and MCA aneurysms.

The mechanisms behind intracranial aneurysm formation and rupture are not fully understood, with factors such as location, patient demographics, and hemodynamics playing a role. Additionally, the significance of anatomical features like blebs in ruptures is debated. This highlights the necessity for comprehensive research that combines patient-specific risk factors with a detailed analysis of local hemodynamic characteristics at bleb and rupture sites. Our study analyzed 359 intracranial aneurysms from 268 patients, reconstructing patient-specific models for hemodynamic simulations based on 3D rotational angiographic images and intraoperative videos. We identified aneurysm subregions and delineated rupture sites, characterizing blebs and their regional overlap, employing statistical comparisons across demographics, and other risk factors. This work identifies patterns in aneurysm rupture sites, predominantly at the dome, with variations across patient demographics. Hypertensive and anterior communicating artery (ACom) aneurysms showed specific rupture patterns and bleb associations, indicating two pathways: high-flow in ACom with thin blebs at impingement sites and low-flow, oscillatory conditions in middle cerebral artery (MCA) aneurysms fostering thick blebs. Bleb characteristics varied with gender, age, and smoking, linking rupture risks to hemodynamic factors and patient profiles. These insights enhance understanding of the hemodynamic mechanisms leading to rupture events. This analysis elucidates the role of localized hemodynamics in intracranial aneurysm rupture, challenging the emphasis on location by revealing how flow variations influence stability and risk. We identify two pathways to wall failure-high-flow and low-flow conditions-highlighting the complexity of aneurysm behavior. Additionally, this research advances our knowledge of how inherent patient-specific characteristics impact these processes, which need further investigation.

Intracranial arterial calcification in patients with unruptured and ruptured intracranial aneurysms.

Arterial calcification is thought to protect against rupture of intracranial aneurysms, but studies in a representative population of intracranial aneurysm patients have not yet been performed. The aim was to compare the prevalence of aneurysm wall calcification and intracranial carotid artery calcification (ICAC) between patients with an unruptured intracranial aneurysm (UIA) and a ruptured intracranial aneurysm (RIA). We matched 150 consecutive UIA patients to 150 RIA patients on age and sex. Aneurysm wall calcification and ICAC were quantified on non-contrast enhanced computed tomography images with the modified Agatston score. We compared the prevalence of aneurysm wall calcification, ICAC, and severe ICAC (defined as a modified Agatston score in the fourth quartile) between UIA and RIA patients using univariate and multivariate conditional logistic regression models adjusted for aneurysm characteristics and cardiovascular risk factors. Aneurysm wall calcification was more prevalent in UIA compared to RIA patients (OR 5.2, 95% CI: 2.0-13.8), which persisted after adjustment (OR 5.9, 95% CI: 1.7-20.2). ICAC prevalence did not differ between the two groups (crude OR 0.9, 95% CI: 0.5-1.8). Severe ICAC was more prevalent in UIA patients (OR 2.0, 95% CI: 1.1-3.6), but not after adjustment (OR 1.0, 95% CI: 0.5-2.3). Aneurysm wall calcification but not ICAC was more prevalent in UIAs than in RIAs, which corresponds to the hypothesis that calcification may protect against aneurysmal rupture. Aneurysm wall calcification should be further assessed as a predictor of aneurysm stability in prospective cohort studies. Calcification of the intracranial aneurysm wall was more prevalent in unruptured than ruptured intracranial aneurysms after adjustment for cardiovascular risk factors. Calcification may therefore protect the aneurysm against rupture, and aneurysm wall calcification is a candidate predictor of aneurysm stability. Aneurysm wall calcification was more prevalent in patients with unruptured than ruptured aneurysms, while internal carotid artery calcification was similar. Aneurysm wall calcification but not internal carotid artery calcification is a candidate predictor of aneurysm stability. Cohort studies are needed to assess the predictive value of aneurysm wall calcification for aneurysm stability.

Decoding the Cell Atlas and Inflammatory Features of Human Intracranial Aneurysm Wall by Single-Cell RNA Sequencing.

Intracranial aneurysm (IA) is common and occasionally results in life-threatening hemorrhagic strokes. However, the cell architecture and inflammation in the IA dome remain less understood. Single-cell RNA sequencing was performed on ruptured and unruptured human IA domes for delineating the cell atlas, gene expression perturbations, and inflammation features. Two external bulk mRNA sequencing-based data sets and serological results of 126 patients were collected for validation. As a result, a total of 21 332 qualified cells were captured. Vascular cells, including endothelial cells, smooth muscle cells, fibroblasts, and pericytes, were assigned in extremely sparse numbers (4.84%), and were confirmed by immunofluorescence staining. Pericytes, characterized by ABCC9 and HIGD1B, were identified in the IA dome for the first time. Abundant immune cells were identified, with the proportion of monocytes/macrophages and neutrophils being remarkably higher in ruptured IA. The lymphocyte compartment was also thoroughly categorized. By leveraging external data sets and machine learning algorithms, macrophages were robustly associated with IA rupture, irrespective of their polarization status. The single nucleotide polymorphism rs2280543, which is identified in East Asian populations, was associated with macrophage metabolic reprogramming through regulating TALDO1 expression. This study provides insights into the cellular architecture and inflammatory features in the IA dome and may enlighten novel therapeutics for unruptured IA.

Intracranial aneurysm wall displacement depicted by amplified Flow predicts growth

BackgroundAbnormal intracranial aneurysm (IA) wall motion has been associated with IA growth and rupture. Recently, a new image processing algorithm called amplified Flow (aFlow) has been used to successfully track...

Decoding the biology and clinical implication of neutrophils in intracranial aneurysm.

Abundant neutrophils have been identified in both ruptured and unruptured intracranial aneurysm (IA) domes, with their function and clinical implication being poorly characterized. We employed single-cell RNA sequencing (scRNA-Seq) datasets of both human and murine model, and external bulk mRNA sequencing datasets to thoroughly explore the features and functional heterogeneous of neutrophils infiltrating the IA dome. We found that both unruptured and ruptured IA dome contain a substantial population of neutrophils, characterized by FCGR3B, G0S2, CSF3R, and CXCR2. These cells exhibited heterogeneity in terms of function and differentiation. Despite similar transcriptional activation, neutrophils in IA dome expressed a repertoire of gene programs that mimicked transcriptomic alterations observed from bone marrow to peripheral blood, showing self-similarity. In addition, the recruitment of neutrophils in unruptured IA was primarily mediated by monocytes/macrophages, and once ruptured, both neutrophils, and a specific subset of inflammatory smooth muscle cells (SMCs) were involved in the process. The receiver operator characteristic curve (ROC) analysis indicated that distinct neutrophil subclusters were associated with IA formation and rupture, respectively. By reviewing current studies, we found that neutrophils play a detrimental role to IA wall integrity through secreting specific ligands, ferroptosis driven by ALOX5AP and PTGS2, and the formation of neutrophil extracellular traps (NETs) mediated by PADI4. This study delineated the biology and potential clinical implications of neutrophils in IA dome and provided a reliable basis for future researches.

Association between intracranial aneurysm wall enhancement and intracranial atherosclerotic plaque: a cross-sectional study using high-resolution vessel wall imaging.

Intracranial aneurysms and intracranial atherosclerosis are prevalent cerebrovascular diseases, and individuals with atherosclerosis have a higher incidence of aneurysms than those without atherosclerosis. However, few studies have conducted combined analyses to investigate the potential association between intracranial aneurysms and intracranial atherosclerosis. This retrospective cross-sectional study aimed to investigate the association between the characteristics of the aneurysm wall and intracranial large arterial plaque using high-resolution vessel wall imaging (HR-VWI). Hospitalized patients diagnosed with anterior circulation unruptured intracranial aneurysms (UIAs), who were diagnosed at Huashan Hospital of Fudan University in Shanghai, China, between March 2016 to February 2018, were consecutively recruited for this study. The patients' pre-treatment HR-VWI images and 3D time-of-flight magnetic resonance angiography (3D-TOF-MRA) images were collected. The patients and UIAs were divided into two groups according to the presence or absence of plaque in the M1 segment of the middle cerebral artery (MCA). Clinical information and aneurysm characteristics were compared between the two groups. Aneurysm wall enhancement (AWE) and M1 plaque were graded on scales of 0 to 2 on HR-VWI. Based on the gradings, the correlation between AWE and the M1 plaques was analyzed. A total of 109 patients with 128 saccular UIAs in the anterior circulation were enrolled in the study. Of the patients, there were 56 patients (with 65 UIAs) in the group with M1 plaque and 53 patients (with 63 UIAs) in the group without plaque. There were significant differences between the two groups in terms of both their clinical information (age and hypertension) and aneurysm characteristics (AWE pattern and AWE degree). The grades of the AWE patterns and the AWE degrees of the UIAs were higher in the group with M1 plaque than in the group without plaque. In the M1 plaque group, the grade of M1 plaque was positively correlated with the grade of AWE pattern (correlation coefficient R=0.41, P=0.001) and the grade of AWE degree (correlation coefficient R=0.50, P<0.001). MCA atherosclerosis plaque was associated with the AWE of saccular aneurysms. When evaluating UIAs, attention should also be paid to the large arterial wall, which may assist in assessing the stability of the aneurysm and enable better decision making.

Wall permeability on magnetic resonance imaging is associated with intracranial aneurysm symptoms and wall enhancement.

Wall remodeling and inflammation accompany symptomatic unruptured intracranial aneurysms (UIAs). The volume transfer constant (Ktrans) of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) reflects UIA wall permeability. Aneurysmal wall enhancement (AWE) on vessel wall MRI (VWI) is associated with inflammation. We hypothesized that Ktrans is related to symptomatic UIAs and AWE. Consecutive patients with UIAs were prospectively recruited for 3-T DCE-MRI and VWI from January 2018 to March 2023. UIAs were classified as asymptomatic and symptomatic if associated with sentinel headache or oculomotor nerve palsy. Ktrans and AWE were assessed on DCE-MRI and VWI, respectively. AWE was evaluated using the AWE pattern and wall enhancement index (WEI). Spearman's correlation coefficient and univariate and multivariate analyses were used to assess correlations between parameters. We enrolled 82 patients with 100 UIAs (28 symptomatic and 72 asymptomatic). The median Ktrans (2.1 versus 0.4min-1; p < 0.001) and WEI (1.5 versus 0.4; p < 0.001) were higher for symptomatic aneurysms than for asymptomatic aneurysms. Ktrans (odds ratio [OR]: 1.60, 95% confidence interval [95% CI]: 1.01-2.52; p = 0.04) and WEI (OR: 3.31, 95% CI: 1.05-10.42; p = 0.04) were independent risk factors for symptomatic aneurysms. Ktrans was positively correlated with WEI (Spearman's coefficient of rank correlation (rs) = 0.41, p < 0.001). The combination of Ktrans and WEI achieved an area under the curve of 0.81 for differentiating symptomatic from asymptomatic aneurysms. Ktrans may be correlated with symptomatic aneurysms and AWE. Ktrans and WEI may provide an additional value than the PHASES score for risk stratification of UIAs. The volume transfer constant (Ktrans) from DCE-MRI perfusion is associated with symptomatic aneurysms and provides additional value above the clinical PHASES score for risk stratification of intracranial aneurysms. • The volume transfer constant is correlated with intracranial aneurysm symptoms and aneurysmal wall enhancement. • Dynamic contrast-enhanced and vessel wall MRI facilitates understanding of the pathophysiological characteristics of intracranial aneurysm walls. • The volume transfer constant and wall enhancement index perform better than the traditional PHASES score in differentiating symptomatic aneurysms.

Image-based hemodynamic simulations for intracranial aneurysms: the impact of complex vasculature

PurposeHemodynamics play an important role in the assessment of intracranial aneurysm (IA) development and rupture risk. The purpose of this study was to examine the impact of complex vasculatures onto the intra-vessel and intra-aneurysmal blood flow.MethodsComplex segmentation of a subject-specific, 60-outlet and 3-inlet circle of Willis model captured with 7T magnetic resonance imaging was performed. This model was trimmed to a 10-outlet model version. Two patient-specific IAs were added onto both models yielding two pathological versions, and image-based blood flow simulations of the four resulting cases were carried out. To capture the differences between complex and trimmed model, time-averaged and centerline velocities were compared. The assessment of intra-saccular blood flow within the IAs involved the evaluation of wall shear stresses (WSS) at the IA wall and neck inflow rates (NIR).ResultsLower flow values are observed in the majority of the complex model. However, at specific locations (left middle cerebral artery 0.5 m/s, left posterior cerebral artery 0.25 m/s), higher flow rates were visible when compared to the trimmed counterpart. Furthermore, at the centerlines the total velocity values reveal differences up to 0.15 m/s. In the IAs, the reduction in the neck inflow rate and WSS in the complex model was observed for the first IA (IA-A δNIRmean = − 0.07ml/s, PCA.l δWSSmean = − 0.05 Pa). The second IA featured an increase in the neck inflow rate and WSS (IA-B δNIRmean = 0.04 ml/s, PCA.l δWSSmean = 0.07 Pa).ConclusionBoth the magnitude and shape of the flow distribution vary depending on the model’s complexity. The magnitude is primarily influenced by the global vessel model, while the shape is determined by the local structure. Furthermore, intra-aneurysmal flow strongly depends on the location in the vessel tree, emphasizing the need for complex model geometries for realistic hemodynamic assessment and rupture risk analysis.

Time-of-flight and black-blood MRI to study intracranial arteries in rats

Intracranial aneurysms (IAs) are usually incidentally discovered by magnetic resonance imaging (MRI). Once discovered, the risk associated with their treatment must be balanced with the risk of an unexpected rupture. Although clinical observations suggest that the detection of contrast agent in the aneurysm wall using a double-inversion recovery black-blood (BB) sequence may point to IA wall instability, the exact meaning of this observation is not understood. Validation of reliable diagnostic markers of IA (in)stability is of utmost importance to deciding whether to treat or not an IA. To longitudinally investigate IA progression and enhance our understanding of this devastating disease, animal models are of great help. The aim of our study was to improve a three-dimensional (3D)-time-of-flight (TOF) sequence and to develop a BB sequence on a standard preclinical 3-T MRI unit to investigate intracranial arterial diseases in rats. We showed that our 3D-TOF sequence allows reliable measurements of intracranial artery diameters, inter-artery distances, and angles between arteries and that our BB sequence enables us to visualize intracranial arteries. We report the first BB-MRI sequence to visualize intracranial arteries in rats using a preclinical 3-T MRI unit. This sequence could be useful for a large community of researchers working on intracranial arterial diseases.Relevance statement We developed a black-blood MRI sequence to study vessel wall enhancement in rats with possible application to understanding IAs instability and finding reliable markers for clinical decision-making.Key points• Reliable markers of aneurysm stability are needed for clinical decision.• Detection of contrast enhancement in the aneurysm wall may be associated with instability.• We developed a black-blood MRI sequence in rats to be used to study vessel wall enhancement of IAs.Graphical

Analysis of intracranial saccular aneurysm wall: neuroimaging and histopathological correlates

Contrast enhancement of intracranial aneurysm wall during MRI with targeted visualization of vascular wall correlates with previous aneurysm rupture and, according to some data, may be a predictor of further rupture of unruptured aneurysms. To analyze possible causes of aneurysm contrast enhancement considering morphological data of aneurysm walls. The study included 44 patients with intracranial aneurysms who underwent preoperative MRI between November 2020 and September 2022. Each aneurysm was assessed regarding contrast enhancement pattern. Microsurgical treatment of aneurysm was accompanied by resection of its wall for subsequent histological and immunohistochemical analysis regarding thrombosis, inflammation and neovascularization. Specimens were subjected to histological and immunochemical analysis. Immunohistochemical analysis was valuable to estimate inflammatory markers CD68 and CD3, as well as neurovascularization marker SD31. Aneurysms with contrast-enhanced walls were characterized by higher number of CD3+, CD68+, CD31+ cells and parietal clots. Intensity of contrast enhancement correlated with aneurysm wall abnormalities. Contrast enhancement of aneurysm wall can characterize various morphological abnormalities.

Lymphocyte-mediated Inflammation in the Human Saccular Intracranial Aneurysm Wall

Lymphocyte-mediated Inflammation in the Human Saccular Intracranial Aneurysm Wall

Gadolinium-enhanced intracranial aneurysm wall imaging and risk of aneurysm growth and rupture: a multicentre longitudinal cohort study

ObjectivesIn patients with an unruptured intracranial aneurysm, gadolinium enhancement of the aneurysm wall is associated with growth and rupture. However, most previous studies did not have a longitudinal design and did not adjust for aneurysm size, which is the main predictor of aneurysm instability and the most important determinant of wall enhancement. We investigated whether aneurysm wall enhancement predicts aneurysm growth and rupture during follow-up and whether the predictive value was independent of aneurysm size.Materials and methodsIn this multicentre longitudinal cohort study, individual patient data were obtained from twelve international cohorts. Inclusion criteria were as follows: 18 years or older with ≥ 1 untreated unruptured intracranial aneurysm < 15 mm; gadolinium-enhanced aneurysm wall imaging and MRA at baseline; and MRA or rupture during follow-up. Patients were included between November 2012 and November 2019. We calculated crude hazard ratios with 95%CI of aneurysm wall enhancement for growth (≥ 1 mm increase) or rupture and adjusted for aneurysm size.ResultsIn 455 patients (mean age (SD), 60 (13) years; 323 (71%) women) with 559 aneurysms, growth or rupture occurred in 13/194 (6.7%) aneurysms with wall enhancement and in 9/365 (2.5%) aneurysms without enhancement (crude hazard ratio 3.1 [95%CI: 1.3–7.4], adjusted hazard ratio 1.4 [95%CI: 0.5–3.7]) with a median follow-up duration of 1.2 years.ConclusionsGadolinium enhancement of the aneurysm wall predicts aneurysm growth or rupture during short-term follow-up, but not independent of aneurysm size.Clinical relevance statementGadolinium-enhanced aneurysm wall imaging is not recommended for short-term prediction of growth and rupture, since it appears to have no additional value to conventional predictors.Graphical abstractKey Points• Although aneurysm wall enhancement is associated with aneurysm instability in cross-sectional studies, it remains unknown whether it predicts risk of aneurysm growth or rupture in longitudinal studies.• Gadolinium enhancement of the aneurysm wall predicts aneurysm growth or rupture during short-term follow-up, but not when adjusting for aneurysm size.• While gadolinium-enhanced aneurysm wall imaging is not recommended for short-term prediction of growth and rupture, it may hold potential for aneurysms smaller than 7 mm.

Unveiling Bacterial Autophagosomes in Human Intracranial Aneurysm Wall Tissue: A Rare Insight.

Unveiling Bacterial Autophagosomes in Human Intracranial Aneurysm Wall Tissue: A Rare Insight.