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The aortic wall is perfused by the adventitial vasa vasorum (VV). Tissue hypoxia has previously been observed as a manifestation of enlarged abdominal aortic aneurysms (AAAs). We sought to determine whether hypoperfusion of the adventitial VV could develop AAAs. We created a novel animal model of adventitial VV hypoperfusion with a combination of a polyurethane catheter insertion and a suture ligation of the infrarenal abdominal aorta in rats. VV hypoperfusion caused tissue hypoxia and developed infrarenal AAA, which had similar morphological and pathological characteristics to human AAA. In human AAA tissue, the adventitial VV were stenotic in both small AAAs (30-49 mm in diameter) and in large AAAs (> 50 mm in diameter), with the sac tissue in these AAAs being ischemic and hypoxic. These results indicate that hypoperfusion of adventitial VV has critical effects on the development of infrarenal AAA.

A search in Scopus within “Article title, Abstract, Keywords” unveils 2,444 documents focused on the biomechanics of Abdominal Aortic Aneurysm (AAA), mostly on AAA wall stress. Only 24 documents investigated AAA kinematics, an important topic that could potentially offer significant insights into the biomechanics of AAA. In this paper, we present an image-based approach for patient-specific, in vivo, and non-invasive AAA kinematic analysis using patient’s time-resolved 3D computed tomography angiography (4D-CTA) images, with an objective to measure wall displacement and strain during the cardiac cycle. Our approach relies on regularized deformable image registration for estimating wall displacement, estimation of the local wall strain as the ratio of its normal displacement to its local radius of curvature, and local surface fitting with non-deterministic outlier detection for estimating the wall radius of curvature. We verified our approach against synthetic ground truth image data created by warping a 3D-CTA image of AAA using a realistic displacement field obtained from a finite element biomechanical model. We applied our approach to assess AAA wall displacements and strains in ten patients. Our kinematic analysis results indicated that the 99th percentile of circumferential wall strain, among all patients, ranged from 2.62% to 5.54%, with an average of 4.45% and a standard deviation of 0.87%. We also observed that AAA wall strains are significantly lower than those of a healthy aorta. Our work demonstrates that the registration-based measurement of AAA wall displacements in the direction normal to the wall is sufficiently accurate to reliably estimate strain from these displacements.

Repair of Abdominal Aortic Aneurysm This clinical trial compared endovascular with open repair of unruptured abdominal aortic aneurysm. An early survival advantage with endovascular repair was not sustained after 3 years. Aneurysm rupture remains a concern with this type of repair. Each year, 40,000 patients in the United States undergo elective procedures to repair abdominal aortic aneurysms. 1 These procedures result in about 1250 perioperative deaths — more than for any other general or vascular surgical procedure, with the exception of colectomy. 2 Endovascular repair was introduced in the 1990s as a less invasive method than traditional open repair. Randomized trials have shown that endovascular repair reduces perioperative mortality, 3 – 5 but in the United Kingdom Endovascular Aneurysm Repair 1 (EVAR 1) trial 3 and the Dutch Randomized Endovascular Aneurysm Management (DREAM) trial, 4 this advantage was lost within 2 years owing to excess late deaths . . .

Abdominal aortic aneurysms (AAAs) are currently one of the leading causes of death in developed countries. Inflammation is crucial in the disease progression, having a substantial impact on various determinants in AAAs development. Magnetic particle imaging (MPI) is an innovative imaging modality, enabling the highly sensitive detection of magnetic nanoparticles (MNPs), suitable as surrogate marker for molecular targeting of vascular inflammation. For this study, Apolipoprotein E-deficient-mice underwent surgical implantation of osmotic minipumps with constant Angiotensin II infusion. After 3 and 4 weeks respectively, in-vivo-magnetic resonance imaging (MRI), ex-vivo-MPI and ex-vivo-magnetic particle spectroscopy (MPS) were performed. The results were validated by histological analysis, immunohistology and laser ablation-inductively coupled plasma-mass spectrometry. MR-angiography enabled the visualization of aneurysmal development and dilatation in the experimental group. A close correlation (R = 0.87) with histological area assessment was measured. Ex-vivo-MPS revealed abundant iron deposits in AAA samples and ex-vivo histopathology measurements were in good agreement (R = 0.76). Ex-vivo-MPI and MPS results correlated greatly (R = 0.99). CD68-immunohistology stain and Perls’-Prussian-Blue-stain confirmed the colocalization of macrophages and MNPs. This study demonstrates the feasibility of ex-vivo-MPI for detecting inflammation in AAA. The quantitative ability for mapping MNPs establishes MPI as a promising tool for monitoring inflammatory progression in AAA in an experimental setting.

The stochastic rupture risk assessment of an abdominal aortic aneurysm (AAA) critically depends on sufficient data set size that would allow for the proper distribution estimate. However, in most published cases, the data sets comprise no more than 100 samples, which is deemed insufficient to describe the tails of AAA wall thickness distribution correctly. In this study, we propose a stochastic Bayesian model to merge thickness data from various groups. The thickness data adapted from the literature were supplemented by additional data from 81 patients. The wall thickness was measured at two different contact pressures for 34 cases, which allowed us to estimate the radial stiffness. Herein, the proposed stochastic model is formulated to predict the undeformed wall thickness. Furthermore, the model is able to handle data published solely as summary statistics. After accounting for the different contact pressures, the differences in the medians reported by individual groups decreased by 45%. Combined data can be fitted with a lognormal distribution with parameters μ = 0.85 and σ = 0.32 which can be further used in stochastic analyses.

PurposePerivascular adipose tissue (PVAT) surrounds the arterial adventitia and plays an important role in vascular homeostasis. PVAT expands in obesity, and inflamed PVAT can locally promote endothelial dysfunction and atherosclerosis. Here, using adipose tissue transplantation, we tested the hypothesis that expansion of PVAT can also remotely exacerbate vascular disease.MethodsFifty milligrams of abdominal aortic PVAT was isolated from high-fat diet (HFD)-fed wild-type mice and transplanted onto the abdominal aorta of lean LDL receptor knockout mice. Subcutaneous and visceral adipose tissues were used as controls. After HFD feeding for 10 weeks, body weight, glucose/insulin sensitivity, and lipid levels were measured. Adipocytokine gene expression was assessed in the transplanted adipose tissues, and the thoracic aorta was harvested to quantify atherosclerotic lesions by Oil-Red O staining and to assess vasorelaxation by wire myography.ResultsPVAT transplantation did not influence body weight, fat composition, lipid levels, or glucose/insulin sensitivity. However, as compared with controls, transplantation of PVAT onto the abdominal aorta increased thoracic aortic atherosclerosis. Furthermore, PVAT transplantation onto the abdominal aorta inhibited endothelium-dependent relaxation in the thoracic aorta. MCP-1 and TNF-α expression was elevated, while adiponectin expression was reduced, in the transplanted PVAT tissue, suggesting augmented inflammation as a potential mechanism for the remote vascular effects of transplanted PVAT.ConclusionsThese data suggest that PVAT expansion and inflammation in obesity can remotely induce endothelial dysfunction and augment atherosclerosis. Identifying the underlying mechanisms may lead to novel approaches for risk assessment and treatment of obesity-related vascular disease.

Abdominal aortic aneurysm (AAA) is a prevalent and potentially life threatening disease. Many animal models have been developed to simulate the natural history of the disease or test preclinical endovascular devices and surgical procedures. The aim of this review is to describe different methods of AAA induction in animal models and report on the effectiveness of the methods described in inducing an analogue of a human AAA. The PubMed database was searched for publications with titles containing the following terms “animal” or ‘‘animal model(s)’’ and keywords “research”, “aneurysm(s)’’, “aorta”, “pancreatic elastase’’, “Angiotensin”, “AngII” “calcium chloride” or “CaCl2”. Starting date for this search was set to 2004, since previously bibliography was already covered by the review of Daugherty and Cassis (2004). We focused on animal studies that reported a model of aneurysm development and progression. A number of different approaches of AAA induction in animal models has been developed, used and combined since the first report in the 1960’s. Although specific methods are successful in AAA induction in animal models, it is necessary that these methods and their respective results are in line with the pathophysiology and the mechanisms involved in human AAA development. A researcher should know the advantages/disadvantages of each animal model and choose the appropriate model.

Accurate reference values for abdominal aortic dimensions and wall thickness are crucial for the early detection and management of vascular diseases, particularly abdominal aortic aneurysms (AAAs). However, there is a lack of population-specific normative data for the Saudi population. A cross-sectional study was conducted on 347 adults [111 males, 236 females] aged 20-80 at King Fahad Medical City. Multidetector computed tomography (MDCT) was utilised to measure the abdominal aortic lumen area, diameter, and wall thickness at three standard anatomical levels. Pixel-based segmentation and image analysis using MATLAB allowed for precise quantification of wall thickness. Multiple linear regression was employed to assess associations with age, gender, and BMI. The average diameter of the aorta was 1.87 cm, the average wall thickness was 1.6 mm, and the average lumen area was 3.01 cm². Males generally had thicker aortic walls and larger dimensions than females, particularly in younger age groups. However, these gender differences became less pronounced with older age and increased BMI. A higher BMI was strongly linked to thicker aortic walls (p < 0.001) but was also associated with a reduced lumen area (p < 0.001). Importantly, aortic diameter did not significantly influence wall thickness. This study provides essential normative data for abdominal aortic measurements in the Saudi population, highlighting age and BMI as significant influencers of aortic morphology. The results support the adoption of population-specific diagnostic criteria and demonstrate the utility of advanced MDCT-based measurement techniques in vascular assessment.

We have previously shown that eNOS uncoupling mediates abdominal aortic aneurysm (AAA) formation in hph-1 mice. In the present study we examined whether recoupling of eNOS prevents AAA formation in a well-established model of Angiotensin II-infused apolipoprotein E (apoE) null mice by targeting some common pathologies of AAA. Infusion of Ang II resulted in a 92% incidence rate of AAA in the apoE null animals. In a separate group, animals were treated orally with folic acid (FA), which is known to recouple eNOS through augmentation of dihydrofolate reductase (DHFR) function. This resulted in a reduction of AAA rate to 19.5%. Imaging with ultrasound showed that FA markedly inhibited expansion of abdominal aorta. FA also abolished elastin breakdown and macrophage infiltration in the AAA animals. The eNOS uncoupling activity, assessed by L-NAME-sensitive superoxide production, was minimal at baseline but greatly exaggerated with Ang II infusion, which was completely attenuated by FA. This was accompanied by markedly improved tetrahydrobiopterin and nitric oxide bioavailability. Furthermore, the expression and activity of DHFR was decreased in Ang II-infused apoE null mice specifically in the endothelial cells, while FA administration resulted in its recovery. Taken together, these data further establish a significant role of uncoupled eNOS in mediating AAA formation, and a universal efficacy of FA in preventing AAA formation via restoration of DHFR to restore eNOS function.

Vascular calcification (VC) is a major risk factor for cardiovascular mortality in chronic renal failure (CRF) patients, but the pathogenesis remains partially unknown and effective therapeutic targets should be urgently explored. Here we pursued the therapeutic role of rapamycin in CRF-related VC. Mammalian target of rapamycin (mTOR) signal was activated in the aortic wall of CRF rats. As expected, oral rapamycin administration significantly reduced VC by inhibiting mTOR in rats with CRF. Further in vitro results showed that activation of mTOR by both pharmacological agent and genetic method promoted, while inhibition of mTOR reduced, inorganic phosphate-induced vascular smooth muscle cell (VSMC) calcification and chondrogenic/osteogenic gene expression, which were independent of autophagy and apoptosis. Interestingly, the expression of Klotho, an antiaging gene that suppresses VC, was reduced in calcified vasculature, whereas rapamycin reversed membrane and secreted Klotho decline through mTOR inhibition. When mTOR signaling was enhanced by either mTOR overexpression or deletion of tuberous sclerosis 1, Klotho mRNA was further decreased in phosphate-treated VSMCs, suggesting a vital association between mTOR signaling and Klotho expression. More importantly, rapamycin failed to reduce VC in the absence of Klotho by using either siRNA knockdown of Klotho or Klotho knockout mice. Thus, Klotho has a critical role in mediating the observed decrease in calcification by rapamycin in vitro and in vivo.