A man in his 70s underwent an endovascular aneurysm repair(EVAR)for abdominal aortic aneurysm. Blood test revealed an anemia and an increased tumor marker. Enhanced computed tomography revealed the wall thickening in the sigmoid colon and the Type Ⅱ endoleak after EVAR. Colonoscopy showed the wall thickening in the sigmoid colon, and biopsy indicated a diagnosis of adenocarcinoma. We performed open sigmoid colectomy with D3 lymph node dissection and ileostomy. We performed intraoperative indocyanine green (ICG) fluorescence method for evaluating the blood flow in the colon before the high ligation of the inferior mesenteric artery and the creation of the anastomosis, and perfusion of the colon was visualized. He was discharged postoperative day 14, and was performed closure of ileostomy 5 months later. Intraoperative ICG fluorescence method was safety and useful for evaluating the blood flow in the colon.

Female patients with abdominal aortic aneurysms (AAAs) are usually less common and older than their male counterparts. We report on AAA disease in a Caribbean nation with respect to gender and review their outcomes relative to the male population. Data were collected prospectively and analyzed retrospectively for patients with AAAs who underwent surgery from 2001 to 2018. Sixty patients were diagnosed with AAA with 44 going on to have surgical repair of which 35 were males, aged 61 to 89 (mean age 73.4 years). Nine women ages 44 to 74 years (mean age 60.8 years) had surgical intervention, three being between 40 and 49 years. The size of aneurysms in these patients ranged from 4.3 to 11.0 cm in diameter (average 6.95 cm), female patients having an average diameter of 6.7 cm. Of the 44 patients, 43 underwent open and one endovascular repair. Thirty-three were elective cases and 11 were ruptured with 32 aorto-aortic and 13 aorto-iliac repairs. There were nine fatalities, three elective and six ruptured, with only one being female. Women had similar outcomes to men in all age groups with young patients having good results. Female AAA patients are usually older, undergo less surgical procedures especially if endovascular, and have worse outcomes than their male counterparts. Our study showed that the females were younger but had similar outcomes to the male patients. The female Caribbean patients may present at much younger ages than in continental populations and this may be due to genetic, ethnic, or lifestyle factors.

A robust, accurate, and standardized approach to measurement of the aorta is critical to improve the predictive accuracy of these aortic measurements, and to investigate other aortic imaging biomarkers. Developing a comprehensive and generic schema for characterization of the aorta to enable investigators to standardize data that are collected across all aorta research. A systematic review of the literature was conducted to identify and assess schemata of aortic measurement and description. The schemata were reported and discussed to guide the synthesis of a comprehensive schema. We propose the International College of Angiology Aortic Research Schema as a comprehensive design that fills the gaps left behind by previously reported schemata. It is intended to be applicable for all clinically relevant purposes, including endograft development for aneurysm repair and for the accurate characterization of the aortic anatomy. This schema divides the aorta into 14 segments and 2 sections (thoracic and abdominal aortas). The segmentation proposed can be used in addition to specific measurements taken for any aneurysm including the neck, and maximal and minimal diameters of the aneurysm.

Medical therapeutic options to prevent rupture of abdominal aortic aneurysm (AAA), a critical event, must be developed. Moreover, further understanding of the process of AAA development and rupture is crucial. Previous studies have revealed that aortic hypoperfusion can induce the development of AAA, and we successfully developed a hypoperfusion-induced AAA animal model. In this study, we examined the effects of medium-chain triglycerides (MCTs), tricaprylin (C8-TG) and tricaprin (C10-TG), on hypoperfusion-induced AAA rat model. We estimated the effects of MCTs on aortic pathologies, mechanical properties of the aorta, and development of AAA. C10-TG, but not C8-TG, significantly suppressed AAA development and completely prevented the rupture. We observed that C10-TG prevented the development and rupture of AAA, but not C8-TG. Additionally, regression of AAA diameter was observed in the C10-TG group. Pathological analysis revealed C10-TG improved the hypoperfusion-induced increase in hypoxia-inducible factor-1α levels, medial smooth muscle cells (SMCs) loss, degeneration of aortic elastin and collagen fibers, and loss of aortic wall elasticity. In addition, regression of the formed AAA was observed by administration of C10-TG after AAA formation. C10-TG administration after AAA formation improved degeneration of AAA wall including degradation of aortic elastin and collagen fibers, stenosis of vasa vasorum, and loss of medial SMCs. These data suggest C10-TG can prevent AAA by attenuating aortic hypoperfusion and degeneration. Considering the clinical safety of C10-TG, C10-TG can be a promising AAA drug candidate.

An abdominal aortic aneurysm (AAA) is a critical health condition with a risk of rupture, where the diameter of the aorta enlarges more than 50% of its normal diameter. The incidence rate of AAA has increased worldwide. Currently, about three out of every 100,000 people have aortic diseases. The diameter and geometry of AAAs influence the hemodynamic forces exerted on the arterial wall. Therefore, a reliable assessment of hemodynamics is crucial for predicting the rupture risk. Wall shear stress (WSS) is an important metric to define the level of the frictional force on the AAA wall. Excessive levels of WSS deteriorate the remodeling mechanism of the arteries and lead to abnormal conditions. At this point, WSS-related hemodynamic parameters, such as time-averaged WSS (TAWSS), oscillatory shear index (OSI), endothelial cell activation potential (ECAP), and relative residence time (RRT) provide important information to evaluate the shear environment on the AAA wall in detail. Calculation of these parameters is not straightforward and requires a physical understanding of what they represent. In addition, computational fluid dynamics (CFD) solvers do not readily calculate these parameters when hemodynamics is simulated. This review aims to explain the WSS-derived parameters focusing on how these represent different characteristics of disturbed hemodynamics. A representative case is presented for spatial and temporal formulation that would be useful for interested researchers for practical calculations. Finally, recent hemodynamics investigations relating WSS-related parameters with AAA rupture risk assessment are presented. This review will be useful to understand the physical representation of WSS-related parameters in cardiovascular flows and how they can be calculated practically for AAA investigations.

Background Angiotensin II type 1 receptor blockers (ARBs) have been shown to limit the growth of abdominal aortic aneurysm (AAA), but their efficacy is controversial. This study aimed to investigate the molecular mechanism underlying the protective effect of ARBs against AAA progression. Methods and Results Olmesartan, an ARB, was administered to wild-type and osteoprotegerin-knockout (Opg-KO) mice starting 2 weeks before direct application of CaCl2 to aortas to induce AAA. The protective effect of olmesartan against AAA in wild-type and Opg-KO mice was compared at 6 weeks after AAA induction. Olmesartan prevented AAA progression in Opg-KO mice, including excessive aortic dilatation and collapse of tunica media, but not in wild-type mice. Deficiency of the Opg gene is known to cause excessive activation of the tumor necrosis factor-related apoptosis-inducing ligand-induced c-Jun N-terminal kinase/matrix metalloproteinase 9 pathway, resulting in prolonged AAA progression. Olmesartan attenuated the upregulation of phosphorylated c-Jun N-terminal kinase and matrix metalloproteinase 9 expression in the aortic wall of Opg-KO mice. In cultured vascular smooth muscle cells, tumor necrosis factor-related apoptosis-inducing ligand-induced c-Jun N-terminal kinase phosphorylation and matrix metalloproteinase 9 expression were inhibited by angiotensin (1-7), the circulating levels of which are increased by ARBs. Furthermore, administering an angiotensin (1-7) antagonist to Opg-KO mice diminished the protective effect of olmesartan against AAA progression. Conclusions Olmesartan prevented AAA progression in Opg-KO mice by upregulating angiotensin (1-7), suggesting that angiotensin (1-7) may be a key factor that mediates the protective effect of ARBs.

To improve abdominal aortic aneurysm (AAA) rupture risk assessment, a large, longitudinal study on AAA hemodynamics and biomechanics is necessary, using personalized fluid-structure interaction (FSI) modeling. 3-dimensional, time-resolved ultrasound (3D+t US) is the preferred image modality to obtain the patient-specific AAA geometry for such a study, since it is safe, affordable and provides temporal information. However, the 3D+t US field-of-view (FOV) is limited and therefore often fails to capture the inlet and aorto-iliac bifurcation geometry. In this study, a framework was developed to add parametric inlet and bifurcation geometries to the abdominal aortic aneurysm geometry by employing dataset statistics and parameters of the AAA geometry. The impact of replacing the patient-specific inlet and bifurcation geometries, acquired using computed tomography (CT) scans, by parametric geometries was evaluated by examining the differences in hemodynamics (systolic and time-averaged wall shear stress and oscillatory shear index) in the aneurysm region. The results show that the inlet geometry has a larger effect on the AAA hemodynamics (median differences of 7.5 to 18.8%) than the bifurcation geometry (median differences all below 1%). Therefore, it is not feasible to replace the patient-specific inlet geometry by a generic one. Future studies should investigate the possibilities of extending the proximal FOV of 3D+t US. However, this study did show the feasibility of adding a parametric bifurcation geometry to the aneurysm geometry. After extending the proximal FOV, the obtained framework can be used to extract AAA geometries from 3D+t US for FSI simulations, despite the absence of the bifurcation geometry.

Macrophages play crucial roles in abdominal aortic aneurysm (AAA) formation through the inflammatory response and extracellular matrix degradation; therefore, regulating macrophages may suppress AAA formation. Interleukin-38 (IL-38) is a member of the IL-1 family, which binds to IL-36 receptor (IL1RL2) and has an anti-inflammation effect. Because macrophages express IL1RL2, we hypothesized that IL-38 suppresses AAA formation by controlling macrophages. We assessed a C57BL6/J mouse angiotensin II-induced AAA model with or without IL-38 treatment. RAW 264.7 cells were cultured with tumor necrosis factor-α and treated with or without IL-38. Because p38 has important roles in inflammation, we assessed p38 phosphorylation in vitro and in vivo. To clarify whether the IL-38 effect depends on the p38 pathway, we used SB203580 to inhibit p38 phosphorylation. IL1RL2+ macrophage accumulation along with matrix metalloproteinase (MMP)-2 and -9 expression was observed in mouse AAA. IL-38 reduced the incidence of AAA formation along with reduced M1 macrophage accumulation and MMP-2 and -9 expression in the AAA wall. Macrophage activities including inducible nitric oxide, MMP-2, and MMP-9 production and spindle-shaped changes were significantly suppressed by IL-38. Furthermore, we revealed that inhibition of p38 phosphorylation diminished the effects of IL-38 on regulating macrophages to reduce AAA incidence, indicating the protective effects of IL-38 depend on the p38 pathway. IL-38 plays protective roles against AAA formation through regulation of macrophage accumulation in the aortic wall and modulating the inflammatory phenotype. Using IL-38 may be a novel therapy for AAA patients.

In the cardiovascular diseased (CVD) conditions, it is essential to choose a suitable rheological model for capturing the correct physics behind the hemodynamic in the multiply afflicted diseased arterial network. This study investigates the effect of blood rheology on hemodynamics in a blood vessel with abdominal aortic aneurysm (AAA) and right internal iliac stenosis (RIIAS). A model with AAA and RIIAS is reconstructed from a human subject's computed tomography (CT) data. Localized mesh generation and pulsatile inflow condition are considered. Non-Newtonian models such as the Power-law, Carreau, Cross, and Herschel Berkley models are used in simulations. The outcome from a validated computational model is compared with the Newtonian model to identify the suitable model for dealing with pathological complications under consideration. The capabilities and significance of various rheological models are also examined via Wall Pressure (WP), Wall Shear Stress (WSS), velocity, Global non-Newtonian importance factor (IG), Vorticity Streamlines, and Swirling Strength. It is noted that during the entire cardiac cycle, the IG factor of the cross model is found to be relatively more significant. Power Law depicts larger IG factor during peak systole and early diastole. Also, the cross model depicts larger WSS, WPS, swirling strength distribution and vorticity during the peak systolic and diastolic phases It is noted that IG ∼0.02 is an appropriate non-Newtonian blood activity cut-off value in the descending abdominal artery having AAA and RIIAS. The critical important WSS values are in the range of 0-9 Pa which is stated in WSS contour plot.

Obstruction of the duodenum by an abdominal aortic aneurysm (AAA) (aortoduodenal syndrome) has rarely been reported. It presents with symptoms of upper gastrointestinal (GI) tract obstruction. Obstructive jaundice caused by an AAA is also extremely rare and requires high clinical suspicion. We present a unique case with informed consent of an elderly gentleman who presented with both rare presentations over a course of few months. After extensive literature search, we have found case reports of patients showing either of the two unusual presentations, but none were found to show them together.

Abdominal aortic aneurysm (AAA) is pathologically characterized by intimal atherosclerosis, disruption and attenuation of the elastic media, and adventitial inflammatory infiltrates. Although all these pathological events are possibly involved in the pathogenesis of AAA, the functional roles contributed by adventitial inflammatory macrophages have not been fully documented. Recent studies have revealed that increased expression of matrix metalloproteinase-12 (MMP-12) derived from macrophages may be particularly important in the pathogenesis of both atherosclerosis and AAA. In the current study, we developed a carrageenan-induced abdominal aortic adventitial inflammatory model in hypercholesterolemic rabbits and evaluated the effect of adventitial macrophage accumulation on the aortic remodeling with special reference to the influence of increased expression of MMP-12. To accomplish this, we compared the carrageenan-induced aortic lesions of transgenic (Tg) rabbits that expressed high levels of MMP-12 in the macrophage lineage to those of non-Tg rabbits. We found that the aortic medial and adventitial lesions of Tg rabbits were greater in degree than those of non-Tg rabbits, with the increased infiltration of macrophages and prominent destruction of elastic lamellae accompanied by the frequent appearance of dilated lesions, while the intimal lesions were slightly increased. Enhanced aortic lesions in Tg rabbits were focally associated with increased dilation of the aortic lumens. RT-PCR and Western blotting revealed high levels of MMP-12 in the lesions of Tg rabbits that were accompanied by elevated levels of MMP-2 and -3, which was caused by increased number of macrophages. Our results suggest that adventitial inflammation constitutes a major stimulus to aortic remodeling and increased expression of MMP-12 secreted from adventitial macrophages plays an important role in the pathogenesis of vascular diseases such as AAA.

Introduction: Chronic heart disease (CHD) is a common comorbidity of patients receiving endovascular aneurysm repair (EVAR) for abdominal aortic aneurysms (AAA). The explicit relationship between ventricular systolic function and EVAR complication of thrombotic events is unknown. Methods: In this study, we proposed a three-dimensional numerical model coupled with the lumped-elements heart model, which is capable of simulating thrombus formation in diverse systolic functions. The relation of cardiac functions and the predicted risk of thrombus formation in the aorta and/or endograft of 4 patients who underwent EVAR was investigated. Relative risks for thrombus formation were identified using machine-learning algorithms. Results: The computational results demonstrate that thrombus tended to form on the interior side of the aorta arch and iliac branches, and cardiac function can affect blood flow field and affect thrombus formation, which is consistent with the four patients' post-operative imaging follow-up. We also found that RRT, OSI, TAWSS in thrombosis area are lower than whole average. In addition, we found that the thrombus formation has negative correlations with the maximum ventricular contractile force (r = -.281 ± .101) and positive correlations with the minimum ventricular contractile force (r = .238 ± .074), whereas the effect of heart rate (r = -.015 ± .121) on thrombus formation is not significant. Conclusion: In conclusion, changes in ventricular systolic function may alter the risk of thrombotic events after EVAR repair, which could provide insight into the selection of adjuvant therapy strategies for AAA patients with CHD.

Introduction: Aortic aneurysm is a life-threatening disease resulted from progressive dilatation of the aorta, which can be subdivided into thoracic and abdominal aortic aneurysms. Sustained subcutaneous angiotensin II infusion can induce aortic aneurysms in mice. However, the relevance of using angiotensin II induction model to study aneurysm disease and the degree of commonality between species remain elusive. Methods: We utilized scRNA-seq to infer aortic cell sub-structures and transcriptional profiles in clinical patient TAAs and AAAs, as well as mouse models of corresponding diseases (Ang II induction) and in healthy mouse aorta. Unbiased comparison between mice and humans explored the possible reasonability and utility of mouse Ang II-induced aortic aneurysm as a model for human aortic aneurysm diseases. Meanwhile, we performed comparative analysis of aortic aneurysms between TAA and AAA in both organisms. Results and Discussion: We demonstrated similarities and differences of changes in the components of human and mouse cell types, and our unbiased comparison between mouse and human identified well conserved subpopulations of SMCs and macrophages. Furthermore, the results of our comparative analyses suggested different biological functions and distinct potential pathogenic genes for thoracic and abdominal aortic aneurysms. MIF and SPP1 signaling networks participated in aortic aneurysm in both organisms. This study maps aortic aneurysm and offers opportunities for future researches to investigate the potential of subpopulations or marker genes as therapy targets.