The aim of this study is to investigate the role of early postoperative CT texture analysis in aneurysm progression. Ninety-nine patients who had undergone post-endovascular aneurysm repair (EVAR) infra-renal abdominal aortic aneurysm CT serial scans were enrolled from July 2014 to December 2019. The clinical and traditional imaging features were obtained. Aneurysm texture analysis was performed using three methods-the grey-level co-occurrence matrix (GLCM), the grey-level run length matrix (GLRLM), and the grey-level difference method (GLDM). A multilayer perceptron neural network was applied as a classifier, and receiver operating characteristic (ROC) curve analysis and area under the curve (AUC) analysis were employed to illustrate the classification performance. No difference was found in the morphological and clinical features between the expansion (+) and (-) groups. GLCM yielded the best performance with an accuracy of 85.17% and an AUC of 0.90, followed by GLRLM with an accuracy of 87.23% and an AUC of 0.8615, and GLDM with an accuracy of 86.09% and an AUC of 0.8313. All three texture analyses showed superior predictive ability over clinical risk factors (accuracy: 69.41%; AUC: 0.6649), conventional imaging features (accuracy: 69.02%; AUC: 0.6747), and combined (accuracy: 75.29%; AUC: 0.7249). Early post-EVAR arterial phase-derived aneurysm texture analysis is a better predictor of later aneurysm expansion than clinical factors and traditional imaging evaluation combined.

This study is aimed at investigating the relationship between inflammation, the number of vasa vasorum, and the presence of lipoprotein (a) [Lp(a)] in the aortic aneurysm wall, as well as the relationships of these pathological processes with the development of aneurysm wall dissection. To that end, we examined segments of aortic aneurysm wall, consisting of intima, media, and adventitia, collected from patients during aneurysm prosthetics intervention. The material was collected from 23 men and eight women aged from 33 to 69 years. Monoclonal antibodies to Lp(a), markers of monocytes and macrophages (CD68), T cells (CD3, CD4, and CD8), von Willebrand factor, endothelium NO synthase, and smooth muscle α-actin were used for morphological and morphometric investigation. The present study demonstrated that Lp(a) is not often found in biopsies of patients with thoracic aortic aneurysm. Morphological and morphometric investigation shows the connection of aortic dissection with the process of damage to its wall caused by inflammatory infiltrates, medianecroses, and the appearance of newly formed vasa vasorum in media.

The self-healing phenomenon can be found in the elastase-induced abdominal aortic aneurysm (AAA) model, and an enlarging AAA model was successfully induced by coarctation. Unfortunately, aortic coarctation in these enlarging models is generally not found in human AAA disease. This study aimed to create an experiment model of enlarging AAA in rabbits to better mimic human aortic aneurysm disease. Eighty-four male New Zealand white rabbits were randomly divided into three equal groups: two aneurysm groups (A and B) and a SHAM group. Aneurysm group rabbits underwent extrinsic aortic stenosis below the right renal artery and received a 10-minute incubation of 60 μl elastase (1 unit/μl). Absorbable suture was used in Group A and nonabsorbable cotton thread was used in Group B. A sham operation was performed in the SHAM group. Aortic diameter was measured after 1, 3, 7, and 15 weeks; thereafter animals were sacrificed for histopathological, immunohistochemical and quantitative studies. Two rabbits died at 29 and 48 days, respectively, after operation in Group B. All aneurysms formed and enlarged progressively by 3 weeks in the Aneurysm groups. However, diameter enlargement in Group A was significantly lower than that in Group B at 7 weeks. Aneurysm groups developed intimal hyperplasia; intima-media thickness (IMT) increased significantly by week 7, and aortic media thickness and intima-media ratio (IMR) increased significantly by week 15. Marked destruction of elastin fibers and smooth muscle cells (SMCs) occurred 1 week later and increased progressively thereafter. Intimal hyperplasia and SMCs content in Group A increased significantly by week 15 compared with Group B. Aneurysm groups exhibited strong expression of matrix metalloproteinases 2 and 9 and RAM11 by week 1, and decreased progressively thereafter. In conclusion, this novel rabbit AAA model enlarges progressively without coarctation and is capable of better mimicking human aortic aneurysm disease.

Tuberculous aortic aneurysm (TBAA) is an exceedingly rare but severe manifestation of tuberculosis, with a high risk of sudden rupture of the aorta in absence of medical or surgical intervention. This review aimed to provide a detailed understanding of TBAA, including its associated complications, affected population, treatment measures, and outcomes.

The aim of this study was to assess if the complex anatomy of aortic aneurysm and aortic dissection can be accurately reproduced from a contrast-enhanced computed tomography (CT) scan into a three-dimensional (3D) printed model.

The pathogenesis of abdominal aortic aneurysm involves vascular inflammation and elastin degradation. Astragalusradix contains cycloastragenol, which is known to be anti-inflammatory and to protect against elastin degradation. We hypothesized that cycloastragenol supplementation inhibits abdominal aortic aneurysm progression. Abdominal aortic aneurysm was induced in male rats by intraluminal elastase infusion in the infrarenal aorta and treated daily with cycloastragenol (125 mg/kg/day). Aortic expansion was followed weekly by ultrasound for 28 days. Changes in aneurysmal wall composition were analyzed by mRNA levels, histology, zymography and explorative proteomic analyses. At day 28, mean aneurysm diameter was 37% lower in the cycloastragenol group (p < 0.0001). In aneurysm cross sections, elastin content was insignificantly higher in the cycloastragenol group (10.5% ± 5.9% vs. 19.9% ± 16.8%, p = 0.20), with more preserved elastin lamellae structures (p = 0.0003) and without microcalcifications. Aneurysmal matrix metalloprotease-2 activity was reduced by the treatment (p = 0.022). Messenger RNA levels of inflammatory- and anti-oxidative markers did not differ between groups. Explorative proteomic analysis showed no difference in protein levels when adjusting for multiple testing. Among proteins displaying nominal regulation were fibulin-5 (p = 0.02), aquaporin-1 (p = 0.02) and prostacyclin synthase (p = 0.007). Cycloastragenol inhibits experimental abdominal aortic aneurysm progression. The suggested underlying mechanisms involve decreased matrix metalloprotease-2 activity and preservation of elastin and reduced calcification, thus, cycloastragenol could be considered for trial in abdominal aortic aneurysm patients.

Abdominal aortic aneurysm (AAA) is a complex disease that requires regular imaging surveillance to monitor for aneurysm stability. Current imaging surveillance techniques use maximum diameter, often assessed by computed tomography angiography (CTA), to assess risk of rupture and determine candidacy for operative repair. However, maximum diameter measurements can be variable, do not reliably predict rupture risk and future AAA growth, and may be an oversimplification of complex AAA anatomy. Vascular deformation mapping (VDM) is a recently described technique that uses deformable image registration to quantify three-dimensional changes in aortic wall geometry, which has been previously used to quantify three-dimensional (3D) growth in thoracic aortic aneurysms, but the feasibility of the VDM technique for measuring 3D growth in AAA has not yet been studied. Seven patients with infra-renal AAAs were identified and VDM was used to identify three-dimensional maps of AAA growth. In the present study, we demonstrate that VDM is able to successfully identify and quantify 3D growth (and the lack thereof) in AAAs that is not apparent from maximum diameter. Furthermore, VDM can be used to quantify growth of the excluded aneurysm sac after endovascular aneurysm repair (EVAR). VDM may be a useful adjunct for surgical planning and appears to be a sensitive modality for detecting regional growth of AAAs.

Bicuspid aortic valve (BAV) can be both sporadic and hereditary, is phenotypically variable, and genetically heterogeneous. The clinical presentation of BAV is diverse and commonly associated with a high prevalence of valvular dysfunction producing altered hemodynamics and aortic abnormalities (e.g., aneurysm and dissection). The thoracic aortic aneurysm (TAA) in BAV frequently involves the proximal aorta, including the aortic root, ascending aorta, and aortic arch, but spares the aorta distal to the aortic arch. While the ascending aortic aneurysm might be affected by both aortopathy and hemodynamics, the aortic root aneurysm is considered to be more of a consequence of aortopathy rather than hemodynamics, especially in younger patients. The management of aortic aneurysm in BAV has been very controversial because the molecular mechanism is unknown. Increasing evidence points toward the BAV root phenotype [aortic root dilation with aortic insufficiency (AI)] as having a higher risk of catastrophic aortic complications. We propose more aggressive surgical approaches toward the BAV with root phenotype.

Screening for abdominal aortic aneurysms (AAA) is currently recommended by several vascular societies. In countries where it has been introduced the prevalence of AAAs differed greatly and was mainly related to cigarette smoking. The screening program also had an enormous impact on the decrease of AAA ruptures and reduced mortality rate. These facts have led to the introduction of the first screening program for AAAs in Poland.

Background. The coexistence of neoplasm and abdominal aortic aneurysm (AAA) presents a real management challenge. This paper reviews the literature on the prevalence, diagnosis, and management dilemmas of concurrent visceral malignancy and abdominal aortic aneurysm. Method. The MEDLINE and HIGHWIRE databases (1966-present) were searched. Papers detailing relevant data were assessed for quality and validity. All case series, review articles, and references of such articles were searched for additional relevant papers. Results. Current challenges in decision making, the effect of major body-cavity surgery on an untreated aneurysm, the effects of major vascular surgery on the treatment of malignancy, the use of EVAR (endovascular aortic aneurysm repair) as a fairly low-risk procedure and its role in the management of malignancy, and the effect of other challenging issues such as the use of adjuvant therapy, and patients informed decision-making were reviewed and discussed. Conclusion. In synchronous malignancy and abdominal aortic aneurysm, the most life-threatening lesion should be addressed first. Endovascular aneurysm repair where possible, followed by malignancy resection, is becoming the preferred initial treatment choice in most centres.

Abdominal aortic aneurysm (AAA) is a vascular disease characterized by weakening of the vascular walls. Male sex is a risk factor for AAA, and peak AAA incidence occurs in men 10 years earlier than in women. However, the growth rate of AAA is faster in women, and women have a higher mortality due to AAA rupture. The mechanisms underlying sex-related differences in AAA remain unknown. Herein, we evaluated the effects of ovariectomy (OVX) on AAA in rats. Upon evaluation of the effects of OVX and AAA induction, AAA incidence rate and the aneurysm diameter increased in the OVX group. However, the histopathology in the developed AAA wall was not different between groups. When the effects of OVX on the vascular wall without AAA induction were evaluated, elastin and collagen levels were significantly decreased. Furthermore, the level of matrix metalloproteinase-9 significantly increased in the OVX group. According to our results, it is speculated that decreased levels of collagen and elastin fibers induced by OVX might be involved in increased incidence rate and diameter of AAA. Weakening of the vascular wall before the onset of AAA might be one reason for the faster rate of AAA growth in women.

Background It is recognized that factors beyond aortic size are important in predicting outcome in abdominal aortic aneurysm (AAA) disease. AAA is characterized by the breakdown of elastin within the aortic tunica media, leading to aortic dilatation and rupture. The aim of this study was to investigate the association of plasma desmosine (pDES), an elastin-specific degradation product, with disease severity and clinical outcome in patients with AAA. Methods and Results We measured pDES and serum biomarker concentrations in 507 patients with AAAs (94% men; mean age, 72.4±6.1 years; mean AAA diameter, 48±8 mm) and 162 control subjects (100% men; mean age, 71.5±4.4 years) from 2 observational cohort studies. In the longitudinal cohort study (n=239), we explored the incremental prognostic value of pDES on AAA events. pDES was higher in patients with AAA compared with control subjects (mean±SD: 0.46±0.22 versus 0.33±0.16 ng/mL; P<0.001) and had the strongest correlation with AAA diameter (r=0.39; P<0.0001) of any serum biomarker. After adjustment for baseline AAA diameter, pDES was associated with an AAA event (hazard ratio, 2.03 per SD increase [95% CI, 1.02-4.02]; P=0.044). In addition to AAA diameter, pDES provided incremental improvement in risk stratification (continuous net reclassification improvement, 34.4% [95% CI, -10.8% to 57.5%; P=0.09]; integrated discrimination improvement, 0.04 [95% CI, 0.00-0.15; P=0.050]). Conclusions pDES concentrations predict disease severity and clinical outcomes in patients with AAA. Clinical Trial Registration http://www.isrctn.com. Unique identifier: ISRCTN76413758.

The pathogenesis of abdominal aortic aneurysm (AAA) is characterized to be inflammation-associated degeneration of vascular wall. Neovascularization is regularly found in human AAA and considered to play critical roles in the development and rupture of AAA. However, little is known about lymphangiogenesis in AAA. The purpose of this study was to demonstrate both angiogenesis and lymphangiogenesis in AAA. Abdominal aortic tissue was harvested either from autopsy (control group) and during open-repair surgery for AAA (AAA group). Adventitial lymphatic vasa vasorum was observed in both groups, but seemed to be no significant morphological changes in AAA. Immunohistochemical studies identified infiltration of lymphatic vessel endothelial hyaluronan receptor (LYVE) -1, vascular endothelial growth factor (VEGF)-C, and matrix metalloproteinase (MMP)-9-positive macrophages and podoplanin and Prox-1-positive microvessels in the intima/media in AAA wall, where hypoxia-inducible factors (HIF)-1α was expressed. VEGF-C and MMP-9 were not expressed in macrophages infiltrating in the adventitia. Intraoperative indocyanine green fluorescence lymphography revealed lymph stasis in intima/medial in AAA. Fluorescence microscopy of the collected samples also confirmed the accumulation of lymph in the intima/media but not in adventitia. These results demonstrate that infiltration of macrophages in intima/media is associated with lymphangiogenesis and angiogenesis in AAA. Lymph-drainage appeared to be insufficient in the AAA wall.

The usefulness of numerical modelling of a patient's cardiovascular system is growing in clinical treatment. Understanding blood flow mechanics can be crucial in identifying connections between haemodynamic factors and aortic wall pathologies.

Genetic causes for abdominal aortic aneurysm (AAA) have not been identified and the role of genes associated with familial thoracic aneurysms in AAA has not been explored. We analyzed nine genes associated with familial thoracic aortic aneurysms, the vascular Ehlers-Danlos gene COL3A1 and the MTHFR p.Ala222Val variant in 155 AAA patients. The thoracic aneurysm genes selected for this study were the transforming growth factor-beta pathway genes EFEMP2, FBN1, SMAD3, TGBF2, TGFBR1, TGFBR2, and the smooth muscle cells genes ACTA2, MYH11 and MYLK. Sanger sequencing of all coding exons and exon-intron boundaries of these genes was performed. Patients with at least one first-degree relative with an aortic aneurysm were classified as familial AAA (n = 99), the others as sporadic AAA. We found 47 different rare heterozygous variants in eight genes: two pathogenic, one likely pathogenic, twenty-one variants of unknown significance (VUS) and twenty-three unlikely pathogenic variants. In familial AAA we found one pathogenic and segregating variant (COL3A1 p.Arg491X), one likely pathogenic and segregating (MYH11 p.Arg254Cys), and fifteen VUS. In sporadic patients we found one pathogenic (TGFBR2 p.Ile525Phefs*18) and seven VUS. Thirteen patients had two or more variants. These results show a previously unknown association and overlapping genetic defects between AAA and familial thoracic aneurysms, indicating that genetic testing may help to identify the cause of familial and sporadic AAA. In this view, genetic testing of these genes specifically or in a genome-wide approach may help to identify the cause of familial and sporadic AAA.

Body composition (BC) may be associated with abdominal aortic aneurysm (AAA) growth, but the results of previous research are contradictory. This study aimed to explore the relationship between BC and postoperative aneurysm progression.

Bicuspid aortic valve (BAV) is a common congenital heart defect (population incidence, 1-2%)1-3 that frequently presents with ascending aortic aneurysm (AscAA)4. BAV/AscAA shows autosomal dominant inheritance with incomplete penetrance and male predominance. Causative gene mutations (for example, NOTCH1, SMAD6) are known for ≤1% of nonsyndromic BAV cases with and without AscAA5-8, impeding mechanistic insight and development of therapeutic strategies. Here, we report the identification of variants in ROBO4 (which encodes a factor known to contribute to endothelial performance) that segregate with disease in two families. Targeted sequencing of ROBO4 showed enrichment for rare variants in BAV/AscAA probands compared with controls. Targeted silencing of ROBO4 or mutant ROBO4 expression in endothelial cell lines results in impaired barrier function and a synthetic repertoire suggestive of endothelial-to-mesenchymal transition. This is consistent with BAV/AscAA-associated findings in patients and in animal models deficient for ROBO4. These data identify a novel endothelial etiology for this common human disease phenotype.

The most lethal complication of the abdominal aortic aneurysm (AAA) is rupture (rAAA). A triad of abdominal or back pain, a pulsating mass in the abdomen, and decrease in blood pressure is mostly diagnostic. However, this presentation may not be complete due to either an impalpable aneurysm or atypical symptoms which leads to difficulties in diagnosis and delayed management. Chronic contained rupture of AAA (CCR-AAA) is a rare but well-recognized condition. Its diagnosis may be difficult because of the atypical and chronic nature of the symptoms. The aim of this study is to investigate the incidence and to highlight the importance of this less common presentation of rAAA.

Variable imaging methods may add important information about abdominal aortic aneurysm (AAA) progression. The aim of this study is to assess available literature data regarding the predictive imaging factors of AAA growth.

Introduction: The life expectancy of patients who undergo ascending aortic replacement is unknown. The life expectancy of a population depends on a collection of environmental and socio-economic factors of the territory where they reside. Our aim was to compare the life expectancy of patients undergoing surgery for ascending aortic aneurysm with that of the general population matching by age, sex, and territory. In addition, we aimed to know the late complications, causes of death and risk factors. Methods: All patients who underwent elective replacement of an ascending aortic aneurysm at our institution between 2000 and 2019 were included. The long-term survival of the sample was compared with that of the general population using data of the National Institute of Statistics. Results: For patients who survived the postoperative period, observed cumulative survival at three, five and eight years was 94.07% (95% CI 91.87%-95.70%), 89.96% (95% CI 86.92%-92.33%) and 82.72% (95% CI 77.68%-86.71%). Cumulative survival of the general population at three, five and eight years was 93.22%, 88.30%, and 80.27%. Cancer and cardiac failure were the main causes of death. Conclusions: Long-term survival of patients undergoing elective surgery for ascending aortic aneurysm who survive the postoperative period completely recover their life expectancy.