Aneurysm Initiation Research Articles

Branching and nonbranching intracranial aneurysms in the presence of a persistent stapedial artery and an aberrant internal carotid artery assessed with computational hemodynamics: illustrative case.

The mechanisms underlying the initiation and progression of bifurcation versus lateral wall aneurysms are not well understood. Computational fluid dynamics (CFD) can improve the understanding of these mechanisms and can consequently help identify patients at higher risk for developing aneurysms and monitor them more closely. A 36-year-old man presented with a ruptured anterior communicating artery aneurysm, which was successfully treated with microsurgical clipping. Imaging also revealed a persistent stapedial artery with an elongated and tortuous posterior communicating artery (PComA). Fourteen years later, he was readmitted for a ruptured aneurysm on a PComA loop. CFD helped identify considerable collateral circulation due to the aberrant internal carotid artery (ICA). High flow rates trigger both types of aneurysms, but nuances exist in the hemodynamic mechanisms that drive their growth. Berry aneurysms and lateral wall aneurysms initially start due to a high flow rate, a common underlying cause. However, the formation of true sidewall aneurysms is primarily characterized by locally increased wall shear stress, while the development of berry aneurysms is mainly linked to high local blood pressure at arterial bifurcations. An aberrant ICA can lead to supraphysiological compensatory flow in the anterior and posterior circulation, increasing the risk of intracranial aneurysm formation at both branching and nonbranching sites, underscoring the need for lifelong monitoring. https://thejns.org/doi/10.3171/CASE24421.

A Review of Hemodynamic Parameters in Cerebral Aneurysm

Abstract—A cerebral aneurysm is a localized dilation that weakens the wall of a blood vessel in the brain. This condition comes in the form of abnormal widening, ballooning or in the form of a bleb. Gaining an understanding of the initiation, growth, and rupture of cerebral aneurysm has played a critical role in finding treatments that prevent the possibility of mortality and morbidity. Cerebral aneurysm develops as a result of the thinning of artery wall, and it is often difficult to diagnose prior to its rupture that leads to several fatal diseases, including brain damage, hemorrhagic stroke, behavioral inconsistency, and eye movement disturbance. A computational fluid dynamic study of cerebral aneurysm employs blood flow simulation wherein hemodynamic parameters indicate the rupture status of a vessel. These hemodynamic parameters actually trigger the biological factors of blood flow in the brain vessels with aneurysm. This paper offers a review of these hemodynamic parameters, and it elucidates the correlation of these parameters with cerebral aneurysm. Specifically, this review highlights the hemodynamic parameters that are related to the formation, growth, and morphological features, namely, size and shape, of cerebral aneurysm Keywords—Cerebral aneurysm, Hemodynamics, Wall shear stress, rupture risk, ansys

Assessing the impact of fetal-type posterior cerebral artery variations on cerebral hemodynamics

The circle of Willis (CoW) is a critical, arterial structure that ensures balanced, cerebral-blood supply. The fetal-type posterior cerebral artery (f-PCA) is a CoW variant that can significantly affect hemodynamics and elevate the risk of cerebrovascular diseases. This study used computational fluid dynamics simulations and a patient-specific, three-dimensional model to evaluate the hemodynamic effects of the f-PCA variants on cerebral-blood flow and key hemodynamic indices—such as time-averaged wall-shear stress (TAWSS), oscillatory shear index (OSI), pulsatility index, and resistive index. The fetal ratio (FR) is defined as the ratio of the diameter of the posterior communicating artery (PCoA) to that of the first segment (P1) of the PCA. Our findings indicate that as the FR increases, the contribution of the basilar artery to the second segment (P2) of PCA decreases significantly. Specifically, the flow rate through ipsilateral P1 decreased by 40.0% for FR = 1 and 70.9% for FR = 2, with the internal carotid artery (ICA) compensating for this reduction. Moreover, variations in f-PCA led to significant increases in TAWSS and OSI in key arterial segments (including the ipsilateral P1, PCoA, and the anterior communicating artery), which are associated with a higher risk of aneurysm initiation and growth. Under conditions of unilateral stenosis in the ipsilateral ICA, f-PCA models exhibit a more complex and pronounced impact on blood flow than models without f-PCA, emphasizing the need for detailed hemodynamic assessments in clinical evaluations and preoperative planning to mitigate the risks associated with CoW anatomical variations.

Molecular Mechanisms Underlying Intracranial Aneurysm Rupture

Intracranial aneurysms, a major cause of subarachnoid hemorrhage(SAH), pose a significant social burden due to their poor patient outcomes. Recent studies, including those using animal models, have shed light on a new disease concept: intracranial aneurysms as a chronic inflammatory disease. This process is triggered by abnormal hemodynamic forces and mediated by immune cells like macrophages and neutrophils. The initiation of intracranial aneurysms is a two-step process. First, high wall shear stress and mechanical stretch work together to promote macrophage infiltration into the arterial walls. This infiltration is facilitated by endothelial cells and fibroblasts, which are activated to produce chemoattractants. Once the lesions enlarge, low wall shear stress and turbulent flow take over, maintaining macrophage infiltration. As the disease progresses towards rupture, infiltration creates hypoxic conditions that exacerbate the situation. These conditions, in turn, induce the formation of neovessels at the weakest point of the aneurysm and promote specific inflammatory microenvironments rich in neutrophils. The excessive tissue destruction caused by neutrophil-mediated inflammation ultimately leads to lesion rupture. Therefore, intracranial aneurysm rupture requires not only structural changes but also qualitative alterations within the chronic inflammatory environment. This suggests that factors mediating chronic inflammation could be potential targets for predicting or preventing aneurysm rupture.

A model with multiple intracranial aneurysms: possible hemodynamic mechanisms of aneurysmal initiation, rupture and recurrence

BackgroundHemodynamic factors play an important role in aneurysm initiation, growth, rupture, and recurrence, while the mechanism of the hemodynamic characteristics is still controversial. A unique model of multiple aneurysms (initiation, growth, rupture, and recurrence) is helpful to avoids the confounders and further explore the possible hemodynamic mechanisms of aneurysm in different states.MethodsWe present a model with multiple aneurysms, and including the states of initiation, growth, rupture, and recurrence, discuss the proposed mechanisms, and describe computational fluid dynamic model that was used to evaluate the likely hemodynamic effect of different states of the aneurysms.ResultsThe hemodynamic analysis suggests that high flow impingement and high WSS distribution at normal parent artery was found before aneurysmal initiation. The WSS distribution and flow velocity were decreased in the new sac after aneurysmal growth. Low WSS was the risk hemodynamic factor for aneurysmal rupture. High flow concentration region on the neck plane after coil embolization still marked in recanalized aneurysm.ConclusionsAssociations have been identified between high flow impingement and aneurysm recanalization, while low WSS is linked to the rupture of aneurysms. High flow concentration and high WSS distribution at normal artery associated with aneurysm initiation and growth, while after growth, the high-risk hemodynamics of aneurysm rupture was occurred, which is low WSS at aneurysm dome.

Abstract 3015: Matrix Metalloproteinase Inhibition In Rat Abdominal Aortic Aneurysm

Background: Matrix metalloproteinases (MMPs) have a robust proteolytic activity and play a fundamental role in degradation of extracellular matrix proteins. This degradation is a hallmark of the initiation, progression, and rupture of abdominal aortic aneurysms (AAAs). Hypothesis: We hypothesized that broad inhibition of MMPs with a 3 rd generation MMP inhibitor (GM6001) can reduce AAA inflammation and rupture using an established rat model. Aims: Our study aimed to investigate the potential of GM6001 in reducing AAA-related inflammation using a rat model, filling a critical gap in AAA research. Methods: Male Sprague-Dawley rats underwent intraluminal infrarenal perfusion of abdominal aorta using porcine pancreatic elastase (PPE), and daily β-aminopropionitrile (BAPN) to promote AAA rupture. Starting on postoperative day 3 (POD3) rats were treated daily either with or without GM6001 via intraperitoneal injections. On POD6, treated and untreated groups, underwent PET/CT imaging using a pan-MMP radiotracer 64Cu-RYM2 and in vivo aortic diameter measurement using ultrasound. Rate of rupture of treated and untreated groups was observed until POD14 (Fig 1A). Results: Treated rats demonstrated no evidence of toxicity or weight loss. Compared to untreated rats, treated rats had lower AAA rupture rates (P<0.01; Fig 1B), smaller AAA diameters (P<0.05; Fig 1C), and lower AAA MMP radiotracer uptake (P<0.05; Fig 1D,1G). Total and active MMP-9 were significantly lower in treated rats (Fig 1E-F). In addition, IL-1B, IL-17A, IL-18, IFN-y, and RANTAS were significantly lower in treated rats, but TNF-a was higher (Fig 1H-M). VVG staining demonstrated a higher content of preserved elastin in treated rats (Fig 1N). Conclusion: Inhibition of MMPs with a 3 rd generation MMP inhibitor appears to be a promising therapeutic approach to impede the progression, inflammation, and rupture of AAAs in rats. This may represent a renewed pathway for MMP inhibition in human subjects with AAAs.

A matched-pair case control study identifying hemodynamic predictors of cerebral aneurysm growth using computational fluid dynamics.

Introduction: Initiation and progression of cerebral aneurysms is known to be driven by complex interactions between biological and hemodynamic factors, but the hemodynamic mechanism which drives aneurysm growth is unclear. We employed robust modeling and computational methods, including temporal and spatial convergence studies, to study hemodynamic characteristics of cerebral aneurysms and identify differences in these characteristics between growing and stable aneurysms. Methods: Eleven pairs of growing and non-growing cerebral aneurysms, matched in both size and location, were modeled from MRA and CTA images, then simulated using computational fluid dynamics (CFD). Key hemodynamic characteristics, including wall shear stress (WSS), oscillatory shear index (OSI), and portion of the aneurysm under low shear, were evaluated. Statistical analysis was then performed using paired Wilcoxon rank sum tests. Results: The portion of the aneurysm dome under 70% of the parent artery mean wall shear stress was higher in growing aneurysms than in stable aneurysms and had the highest significance among the tested metrics (p = 0.08). Other metrics of area under low shear had similar levels of significance. Discussion: These results align with previously observed hemodynamic trends in cerebral aneurysms, indicating a promising direction for future study of low shear area and aneurysm growth. We also found that mesh resolution significantly affected simulated WSS in cerebral aneurysms. This establishes that robust computational modeling methods are necessary for high fidelity results. Together, this work demonstrates that complex hemodynamics are at play within cerebral aneurysms, and robust modeling and simulation methods are needed to further study this topic.

Global tendencies and frontier topics in hemodynamics research of intracranial aneurysms: a bibliometric analysis from 1999 to 2022

Background: Hemodynamics plays a crucial role in the initiation, enlargement, and rupture of intracranial aneurysms (IAs). This bibliometric analysis aimed to map the knowledge network of IA hemodynamic research.Methods: Studies on hemodynamics in IAs published from 1999 to 2022 were retrieved from the Web of Science Core Collection (WoSCC). The contributions of countries, institutions, authors, and journals were identified using VOSviewer, Scimago Graphica, and Microsoft Excel. Tendencies, frontier topics, and knowledge networks were analyzed and visualized using VOSviewer and CiteSpace.Results: We identified 2,319 publications on hemodynamics in IAs. The annual number of publications exhibited an overall increasing trend. Among these, the United States, Japan, and China were the three major contributing countries. Capital Medical University, State University of New York (SUNY) Buffalo University, and George Mason University were the three most productive institutions. Meng H ranked first among authors regarding the number of articles and citations, while Cebral JR was first among co-cited authors. The American Journal of Neuroradiology was the top journal in terms of the number of publications, citations, and co-citations. In addition, the research topics can be divided into three clusters: hemodynamics itself, the relationship of hemodynamics with IA rupture, and the relationship of hemodynamics with IA treatment. The frontier directions included flow diverters, complications, morphology, prediction, recanalization, and four-dimensional flow magnetic resonance imaging (4D flow MRI).Conclusion: This study drew a knowledge map of the top countries, institutions, authors, publications, and journals on IA hemodynamics over the past 2 decades. The current and future hotspots of IA hemodynamics mainly include hemodynamics itself (4D flow MRI), its relationship with IA rupture (morphology and prediction), and its relationship with IA treatment (flow diverters, complications, and recanalization).

PB1402 NBEAL2 and the Intragranular Proteoglycan, Serglycin, Both Contribute to the Initiation and Progression of Aortic Aneurysms

PB1402 NBEAL2 and the Intragranular Proteoglycan, Serglycin, Both Contribute to the Initiation and Progression of Aortic Aneurysms

The protective effects of pirfenidone in preventing abdominal aortic aneurysm formation.

Vascular endothelial growth factor (VEGF)-mediated angiogenesis participates in the initiation and progression of abdominal aortic aneurysm (AAA). Pirfenidone is a compound that has anti-inflammatory and antioxidant properties and suppresses angiogenesis. Pirfenidone targets the extracellular matrix (ECM) and has therapeutic effects on fibrotic diseases. Therefore, we speculated that pirfenidone might have meaningful therapeutic effects in AAA, and the current study was designed to investigate this capacity. An AAA model was constructed in mice using a long-term injection of angiotensin II (Ang II), followed by a 28-day administration of 200 mg/kg/day pirfenidone. Increased maximal external diameter of the abdominal artery, promoted levels of VEGF-A and its receptor VEGF-R2, upregulated matrix metallopeptidases (MMP)-2 and MMP-9, and elevated release of pro-inflammatory cytokines were observed in AAA mice, which were extremely repressed by 200 mg/kg pirfenidone. Human aortic endothelial cells (HAECs) were stimulated with Ang II for 1 day, in the presence or absence of pirfenidone (100 nM). Elevated expression of VEGF-A and VEGF-R2, facilitated proliferation, increased tube formation ability, and upregulated MMP-2 and MMP-9 were observed in Ang II-stimulated HAECs, all of which were significantly rescued by 100 nM pirfenidone. Finally, the elevated levels of myeloid differentiation primary response 88 and phosphorylated nuclear factor-kappa-B subunit p65 observed in Ang II-stimulated HAECs were repressed by pirfenidone. Collectively, pirfenidone alleviated AAA by inhibiting ECM degradation and ameliorating endothelial dysfunction.

Fluid-structure interaction study for biomechanics and risk factors in Stanford type A aortic dissection.

Aortic dissection is a life-threatening condition with a rising prevalence in the elderly population, possibly as a consequence of the increasing population life expectancy. Untreated aortic dissection can lead to myocardial infarction, aortic branch malperfusion or occlusion, rupture, aneurysm formation and death. This study aims to assess the potential of a biomechanical model in predicting the risks of a non-dilated thoracic aorta with Stanford type A dissection. To achieve this, a fully coupled fluid-structure interaction model was developed under realistic blood flow conditions. This model of the aorta was developed by considering three-dimensional artery geometry, multiple artery layers, hyperelastic artery wall, in vivo-based physiological time-varying blood velocity profiles, and non-Newtonian blood behaviours. The results demonstrate that in a thoracic aorta with Stanford type A dissection, the wall shear stress (WSS) is significantly low in the ascending aorta and false lumen, leading to potential aortic dilation and thrombus formation. The results also reveal that the WSS is highly related to blood flow patterns. The aortic arch region near the brachiocephalic and left common carotid artery is prone to rupture, showing a good agreement with the clinical reports. The results have been translated into their potential clinical relevance by revealing the role of the stress state, WSS and flow characteristics as the main parameters affecting lesion progression, including rupture and aneurysm. The developed model can be tailored for patient-specific studies and utilised as a predictive tool to estimate aneurysm growth and initiation of wall rupture inside the human thoracic aorta.

Reduction of rupture risk in ICA aneurysms by endovascular techniques of coiling and stent: numerical study

The initiation, growth, and rupture of cerebral aneurysms are directly associated with Hemodynamic factors. This report tries to disclose effects of endovascular technique (coiling and stenting) on the quantitative intra-aneurysmal hemodynamic and the rupture of cerebral aneurysms. In this paper, Computational Fluid Dynamic are done to investigate and compare blood hemodynamic inside aneurysm under effects of deformation (due to stent) and coiling of aneurysm. The blood stream inside the sac of aneurysm as well as pressure and OSI distribution on the aneurysm wall are compared in nine cases and results of two distinctive cases are compared and reported. Obtained results specifies that the mean WSS is reduced up to 20% via coiling of the aneurysm while the deformation of the aneurysm (applying stent) could reduce the mean WSS up to 71%. In addition, comparison of the blood hemodynamic shows that the blood bifurcation occurs in the dome of aneurysm when endovascular technique for the treatment is not applied. It is found that the bifurcation occurs at ostium section when ICA aneurysm is deformed by the application of stent. The impacts of coiling are mainly limited since the blood flow entrance is not limited in this technique and WSS is not reduced substantial. However, usage of stent deforms the aneurysm angle with the orientation of parent vessel and this reduces blood velocity at entrance of the ostium and consequently, WSS is decreased when deformation of the aneurysm fully occurs. These qualitative procedures provide a preliminary idea for more profound quantitative examination intended for assigning aneurysm risk of upcoming rupture.

Abstract 278: Ccr2 Inhibition Impacts Abdominal Aortic Aneurysm Rupture In Rodents

Background: There is growing evidence that monocyte chemoattractant protein (MCP-1) / C-C chemokine receptor type 2 (CCR2) axis crucially affects the initiation and progression of abdominal aortic aneurysm (AAA). We hypothesize that inhibition of CCR2 may prevent AAA inflammation and rupture. Methods: 40 Male and 49 female Sprague-Dawley rats underwent intraluminal infrarenal abdominal aortic exposure to elastase to induce AAA. Rats received daily β-aminopropionitrile to promote AAA rupture. On post-operative day 3 (POD3), a treatment group (15 males, 17 females) received daily oral gavage of a CCR2 inhibitor (CCR2i; RS-504393), and a control group (25 males, 32 females) received no CCR2i. On POD6, both groups underwent PET/CT with a CCR2 targeting radiotracer 64 Cu-DOTA-ECL1i. In addition, AAA tissue cytokine/chemokine arrays were evaluated. Incidence of AAA rupture was evaluated in the remaining surviving rats until POD14 (Figure 1A). Results: Compared with controls, the incidence of AAA rupture was reduced in treated male AAA rats (0% vs 56%, p <0.001; and tended to decreased in treated female AAA rats (18% vs 42%, p =0.09;). PET/CT demonstrated that male and female treatment groups had significantly decreased 64 Cu-DOTA-ECL1i uptake in AAAs ( p= 0.02 for male AAAs , p <0.001 for females, Figure 1B). All cytokines, including MCP-1, RANTES, IL-17A, IL-18, IL-1B, IL-6, IL-10, except TNF-a were significantly reduced in the male treatment group compared to control group ( p <0.05; Figure 1C). Interestingly, in the female treatment group, IL-1B was significantly decreased ( p <0.05), and RANTES was significantly increased ( p <0.05). Conclusion: In rats, CCR2 appears to be a promising theranostic biomarker for AAAs. CCR2i can greatly impact AAA tissue inflammation and reduces the incidence of AAA rupture. Differences between male and female rats suggest that CCR2 signaling may be different in AAA between sexes and highlights future avenues of further investigation.

Gut Microbiota-Derived Trimethylamine N-Oxide Contributes to Abdominal Aortic Aneurysm Through Inflammatory and Apoptotic Mechanisms.

Large-scale human and mechanistic mouse studies indicate a strong relationship between the microbiome-dependent metabolite trimethylamine N-oxide (TMAO) and several cardiometabolic diseases. This study aims to investigate the role of TMAO in the pathogenesis of abdominal aortic aneurysm (AAA) and target its parent microbes as a potential pharmacological intervention. TMAO and choline metabolites were examined in plasma samples, with associated clinical data, from 2 independent patient cohorts (N=2129 total). Mice were fed a high-choline diet and underwent 2 murine AAA models, angiotensin II infusion in low-density lipoprotein receptor-deficient (Ldlr-/-) mice or topical porcine pancreatic elastase in C57BL/6J mice. Gut microbial production of TMAO was inhibited through broad-spectrum antibiotics, targeted inhibition of the gut microbial choline TMA lyase (CutC/D) with fluoromethylcholine, or the use of mice genetically deficient in flavin monooxygenase 3 (Fmo3-/-). Finally, RNA sequencing of in vitro human vascular smooth muscle cells and in vivo mouse aortas was used to investigate how TMAO affects AAA. Elevated TMAO was associated with increased AAA incidence and growth in both patient cohorts studied. Dietary choline supplementation augmented plasma TMAO and aortic diameter in both mouse models of AAA, which was suppressed with poorly absorbed oral broad-spectrum antibiotics. Treatment with fluoromethylcholine ablated TMAO production, attenuated choline-augmented aneurysm initiation, and halted progression of an established aneurysm model. In addition, Fmo3-/- mice had reduced plasma TMAO and aortic diameters and were protected from AAA rupture compared with wild-type mice. RNA sequencing and functional analyses revealed choline supplementation in mice or TMAO treatment of human vascular smooth muscle cells-augmented gene pathways associated with the endoplasmic reticulum stress response, specifically the endoplasmic reticulum stress kinase PERK. These results define a role for gut microbiota-generated TMAO in AAA formation through upregulation of endoplasmic reticulum stress-related pathways in the aortic wall. In addition, inhibition of microbiome-derived TMAO may serve as a novel therapeutic approach for AAA treatment where none currently exist.

Abstract Number ‐ 56: Investigation of Aneurysmal Initiation Factor with Experimental Animal Model by Computational Fluid Dynamics Analysis

Introduction Hemodynamics has been reported to be involved in the pathophysiology of the initiation of intracranial aneurysms. Computational fluid dynamics (CFD) simulation has been widely used to investigate what kind of hemodynamics is related to intracranial aneurysm development or rupture. However, in the case of humans, it is difficult to obtain cerebrovascular images before the aneurysm formation because most of them are detected incidentally by magnetic resonance angiography (MRA) or computed tomography angiography (CTA). Therefore, the mechanism of aneurysm initiation has not been elucidated yet. In this study, CFD analysis was conducted with experimental animal models. Furthermore, immunostainings and Elastica van Gieson (EvG) staining were also performed to investigate the relationship between hemodynamics and aneurysm initiation. Methods We selected the experimental aneurysm model of a rat proposed by Shimizu et al.[1] With this model, aneurysms can be induced with a certain probability at the artificial bifurcation site created by end‐to‐side anastomosis of bilateral common carotid arteries and induced hypertension. Among the 50 rats surgically manipulated, 5 de novo cases and 14 cases without aneurysm initiation defined as stable cases were included in this study. The other 31 cases were excluded because of death or lack of imaging quality. MRA was conducted weekly until 4 weeks after manipulation. Acquired images were processed for the CFD analysis and various kinds of hemodynamic parameters were calculated. Among them, we regarded dimensionless wall shear stress divergence (WSSD*) and pressure loss coefficient (PLc) as the hemodynamic parameters previously suggested to be related to aneurysm initiation[2]. Vessels were collected after 2 weeks of follow‐up, and we observed endothelial cells (EC), smooth muscle cells (SMC), and the internal elastic lamina (IEL) at the apex of the bifurcationby immunostaining and EvG staining. Results The CFD results showed that a high WSSD* area existed at the apex of bifurcation in both de novo cases and stable cases. The averaged WSSD* of the de novo cases was 18.2% higher than that of the stable cases (de novo: 0.577 ± 0.243, stable: 0.488 ± 0.235). Likewise, the average PLc of the de novo cases was 11.5% higher than that of the stable cases (de novo: 8.22 ± 1.76, stable: 7.37 ± 2.49). The immunostaining images demonstrated that EC and SMC were more degenerated in de novo cases than in stable cases. Furthermore, the EvG staining images showed that IEL degenerated only in the de novo cases. Therefore, because WSSD* and PLc indicate a stretching force and flow impingement on the vessel wall, respectively, the elevation of those parameters may contribute to damage of EC, SMC, and IEL known as pathological features of an intracranial aneurysm. Conclusions CFD analysis and tissue observation were conducted with the vessels of the experimental animal model (5 de novo cases and 14 stable cases). Our results indicate that high WSSD* and high PLc are the factors related to aneurysm initiation.

IMAGING OF THE ANTERIOR COMMUNICATING ARTERY: NORMAL AND ABNORMAL FINDINGS RELATED TO ANEURYSM

The anterior communicating artery (AComA) is a critical component of the Circle of Willis, serving as a vital conduit that connects the bilateral anterior cerebral arteries. This study aims to provide a comprehensive overview of the imaging characteristics of the AComA, encompassing both normal variations and abnormal findings associated with aneurysm development. Utilizing advanced imaging techniques, a thorough analysis of the AComA complex was conducted in a cohort of subjects. Normal anatomical variants were meticulously documented, highlighting variations in length, diameter, and branching patterns. Abnormal findings indicative of potential aneurysm markers was carefully assessed, encompassing variations in morphology, hemodynamic flow patterns, and wall integrity. Special attention was given to elucidate the factors contributing to aneurysm initiation within the AComA complex. The clinical significance of distinguishing between normal anatomical variations and potential pathological findings was underscored, emphasizing the critical importance of early detection and intervention to mitigate the risks associated with aneurysm rupture. The findings of this study contribute valuable insights to the field of neurovascular diagnostics and therapeutic strategies. By enhancing our understanding of the AComA and its role in aneurysm development, this research aims to empower clinicians with the knowledge needed for informed decision-making and proactive management. Ultimately, the comprehensive examination of AComA imaging, encompassing both normal and abnormal variants, holds the potential to drive advancements in cerebrovascular care and improve patient outcomes.

Verifying the Accuracy of Hemodynamic Analysis Using High Spatial Resolution 3D Phase-contrast MR Imaging on a 7T MR System: Comparison with a 3T System.

Hemodynamics is important in the initiation, growth, and rupture of intracranial aneurysms. Since intracranial aneurysms are small, a high-field MR system with high spatial resolution and high SNR is desirable for this hemodynamic analysis. The purpose of this study was to investigate whether the accuracy of MR fluid dynamic (MRFD) results based on 3D phase-contrast MR (3D PC MR, non-electrocardiogram[ECG]-gated 4D Flow MRI) data from a human cerebrovascular phantom and human healthy subjects obtained by a 7T MR system was superior to those by a 3T MR system. 3D PC MR and 3D time of flight MR angiography (3D TOF MRA) imaging were performed on a 3T MR system and a 7T MR system for a human cerebrovascular phantom and 10 healthy human subjects, and MRFD analysis was performed using these data. The MRFD results from each MR system were then compared with the following items based on the computational fluid dynamics (CFD) results: 3D velocity vector field; correlation coefficient (R), angular similarity index (ASI), and magnitude similarity index (MSI) of blood flow velocity vectors. In the MRFD results of 3D velocity vectors of the cerebrovascular phantom, noise-like vectors were observed near the vascular wall on the 3T MR system, but no noise was observed on the 7T MR system, showing results similar to those of CFD. In the MRFD results of the cerebrovascular phantom and healthy subjects, the correlation coefficients R, ASI, and MSI of the 7T MR system were higher than those of the 3T MR system, and ASI and MSI of healthy human subjects were significantly different between the two systems. The accuracy of high spatial resolution MRFD using the 7T MR system exceeded that of the 3T MR system.

Dexmedetomidine alleviates inflammatory response and oxidative stress injury of vascular smooth muscle cell via α2AR/GSK-3β/MKP-1/NRF2 axis in intracranial aneurysm

Vascular smooth muscle cell (VSMC) phenotypic modulation regulates the initiation and progression of intracranial aneurysm (IA). Dexmedetomidine (DEX) is suggested to play neuroprotective roles in patients with craniocerebral injury. Therefore, we investigated the biological functions of DEX and its mechanisms against IA formation and progression in the current study. The rat primary VSMCs were isolated from Sprague–Dawley rats. IA and superficial temporal artery (STA) tissue samples were obtained from patients with IA. Flow cytometry was conducted to identify the characteristics of isolated VSMCs. Hydrogen peroxide (H2O2) was used to mimic IA-like conditions in vitro. Cell viability was detected using CCK-8 assays. Wound healing and Transwell assays were performed to detect cell motility. ROS production was determined by immunofluorescence using DCFH-DA probes. Western blotting and RT-qPCR were carried out to measure gene expression levels. Inflammation responses were determined by measuring inflammatory cytokines. Immunohistochemistry staining was conducted to measure α2-adrenergic receptor levels in tissue samples. DEX alleviated the H2O2-induced cytotoxicity, attenuated the promoting effects of H2O2 on cell malignancy, and protected VSMCs against H2O2-induced oxidative damage and inflammation response. DEX regulated the GSK-3β/MKP-1/NRF2 pathway via the α2AR. DEX alleviates the inflammatory responses and oxidative damage of VSMCs by regulating the GSK-3β/MKP-1/NRF2 pathway via the α2AR in IA.

Patient-specific modeling of hemodynamic characteristics associated with the formation of visceral artery aneurysms at uncommon locations.

ObjectiveHemodynamic characteristics play critical roles in aneurysm initiation and growth. This study aims to explore the effect of common hemodynamic parameters on the formation of visceral artery aneurysms (VAAs), especially those from the pancreaticoduodenal arteries or other uncommon locations, using real patients’ models.MethodsThree-dimension vessel models of 14 VAAs from 13 patients were selected and constructed from computed tomography angiography (CTA) images. Aneurysms were manually removed to perform computational fluid dynamics (CFD) simulations of the models before aneurysm formation. Flow field characteristics were obtained and compared at the aneurysm forming and para-aneurysm areas. Aneurysm forming models were categorized into high-wall-shear stress (WSS) and low-WSS groups according to WSS value at aneurysm forming versus para-aneurysm areas.ResultsComputational fluid dynamics analysis revealed that the high WSS group had significantly higher WSSmax (P = 0.038), higher time average WSS (TAWSS) (P = 0.011), higher WSS gradient (WSSG) (p = 0.036), as well as lower oscillatory shear index (OSI) (P = 0.022) compared to the low WSS group. Significant higher WSSmax (P = 0.003), TAWSS (P = 0.003), WSSG (P = 0.041) and lower OSI (P = 0.021) was observed at the aneurysm forming site compared to both upstream and downstream areas.ConclusionBoth local increase and decrease of WSS and WSS gradient were observed for the visceral artery aneurysm forming area. Computational fluid dynamics analysis could shed light on the pathogenesis of visceral artery aneurysms at uncommon vessel locations.

A machine learning model for non-invasive detection of atherosclerotic coronary artery aneurysm

PurposeAtherosclerosis plays a significant role in the initiation of coronary artery aneurysms (CAA). Although the treatment options for this kind of vascular disease are developing, there are challenges and limitations in both selecting and applying sufficient medical solutions. For surgical interventions, that are novel therapies, non-invasive specific patient-based studies could lead to obtaining more promising results. Despite medical and pathological tests, these pre-surgical investigations require special biomedical and computer-aided engineering techniques. In this study, a machine learning (ML) model is proposed for the non-invasive detection of atherosclerotic CAA for the first time.MethodsThe database for study was collected from hemodynamic analysis and computed tomography angiography (CTA) of 80 CAAs from 61 patients, approved by the Institutional Review Board (IRB). The proposed ML model is formulated for learning by a one-class support vector machine (1SVM) that is a field of ML to provide techniques for outlier and anomaly detection.ResultsThe applied ML algorithms yield reasonable results with high and significant accuracy in designing a procedure for the non-invasive diagnosis of atherosclerotic aneurysms. This proposed method could be employed as a unique artificial intelligence (AI) tool for assurance in clinical decision-making procedures for surgical intervention treatment methods in the future.ConclusionsThe non-invasive diagnosis of the atherosclerotic CAAs, which is one of the vital factors in the accomplishment of endovascular surgeries, is important due to some clinical decisions. Although there is no accurate tool for managing this kind of diagnosis, an ML model that can decrease the probability of endovascular surgical failures, death risk, and post-operational complications is proposed in this study. The model is able to increase the clinical decision accuracy for low-risk selection of treatment options.