Diet and the content of selenium and lead in patients with abdominal aortic aneurysm

VASA ◽  
2011 ◽  
Vol 40 (5) ◽  
pp. 381-389 ◽  
Author(s):  
Socha ◽  
Borawska ◽  
Gacko ◽  
Guzowski
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Healthy Volunteers ◽  
Arterial Wall ◽  
Aortic Wall ◽  
Dietary Habits ◽  
Absorption Spectrometry ◽  
Control Group ◽  
Abdominal Aortic ◽  
The Mean

Background: To evaluate the content of selenium (Se) and lead (Pb) and the influence of dietary habits and smoking in patients with abdominal aortic aneurysm (AAA). Patients and methods: Forty-nine patients with AAA prior to surgical procedures aged 42 - 81 years and a control group of 22 healthy volunteers aged 31 - 72 years and 17 aortic wall samples from deceased were included in the study. Food-frequency questionnaires were implemented in AAA patients to collect the dietary data. Se and Pb concentrations in the serum and blood, respectively, and in arterial wall and parietal thrombus samples were determined by the atomic absorption spectrometry method. Results: The mean Se level in serum of patients with AAA (60.37 ± 21.2 microg/L) was significantly (p < 0.008) lower than in healthy volunteers (75.87 ± 22.4 microg/L). We observed a significant correlation (r = 0.69, p < 0.0001) between the content of Se in serum and the parietal thrombus of examined patients. Se concentration in aortic wall was inversely correlated to the concentration of Pb (r = - 0.38, p < 0.02). We observed significantly lower (p < 0.05) concentrations of Se (39.14 ± 37.1 microg/g) and significantly higher (p < 0.05) concentrations of Pb (202.69 ± 180.6 microg/g) in aortic wall samples of smoking patients than in non-smoking patients (77.56 ± 70.0 microg/g, 73.09 ± 49.8 microg/g; respectively). Conclusions: Se serum level is lower in patients with AAA than in healthy volunteers. In aortic wall, Se concentration is inversely correlated with Pb concentration. Dietary habits and smoking have an influence on the Se and Pb status in patients with AAA.

scholarly journals Is Abdominal Aortic Aneurysm Behavior after Endovascular Repair Associated with Aneurysm Wall Density on Computed Tomography Angiography?

Medicina ◽  
2019 ◽  
Vol 55 (8) ◽  
pp. 406
Author(s):  
Skrebūnas ◽  
Lengvenis ◽  
Builytė ◽  
Žulpaitė ◽  
Bliūdžius ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Computed Tomography Angiography ◽  
Aortic Wall ◽  
Control Group ◽  
Density Score ◽  
Aneurysm Wall ◽  
Abdominal Aortic ◽  
Aortic Pathology

Background and objectives: Abdominal aortic aneurysm (AAA) growth is unpredictable after the endovascular aneurysm repair (EVAR). Continuing aortic wall degradation and weakening due to hypoxia may have a role in post-EVAR aneurysm sac growth. We aimed to assess the association of aortic wall density on computed tomography angiography (CTA) with aneurysm growth following EVAR. Materials and Methods: A total of 78 patients were included in the study. The control group consisted of 39 randomly assigned patients without aortic pathology. Post-EVAR aneurysm sac volumes on CTA were measured twice during the follow-up period to estimate aneurysm sac behavior. A maximum AAA sac diameter, aortic wall and lumen densities in Hounsfield units (HU) on CTA were measured. A relative aortic wall density (the ratio of aortic wall to lumen densities) was calculated. A statistical data analysis was performed using standard methods. Results: An increase in the AAA sac volume was observed in 12 (30.8%) cases. Median relative aortic wall density on CTA scores in both the patient and the control group at the level of the diaphragm were similar: 0.15 (interquartile range (IQR), 0.11–0.18) and 0.16 (IQR 0.11–0.18), p = 0.5378, respectively. The median (IQR) relative aortic wall density score at the level of the maximum AAA diameter in the patient group was lower than at the level below renal arteries in the control group: 0.10 (0.07–0.12) and 0.17 (0.12–0.23), p < 0.0001, respectively. The median (IQR) relative growing AAA sac wall density score was lower than a relative stable/shrinking AAA sac wall density score: 0.09 (0.06–0.10) and 0.11 (0.09–0.13), p = 0.0096, respectively. Conclusions: A lower aortic aneurysm wall density on CTA may be associated with AAA growth after EVAR.

Detection of Lumen, Thrombus and Outer Wall Boundaries of an Abdominal Aortic Aneurysm From 2D Medical Images Using Level Set Methods

2008 ◽  
Author(s):  
Georgios Kossioris ◽  
Yannis Papaharilaou ◽  
Christos Zohios
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Arterial Wall ◽  
Aortic Wall ◽  
Level Set Methods ◽  
Outer Wall ◽  
Surrounding Tissue ◽  
Patient Specific ◽  
Rupture Risk ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) is a localized dilatation of the aortic wall. Accurate geometric characterization is critical for a reliable patient specific estimate of AAA rupture risk. However, current imaging modalities do not provide sufficient contrast between thrombus, arterial wall and surrounding tissue thus making the task of segmenting these structures very challenging.

Abstract 297: Segmental Aortic Stiffening is a Mechanism Driving Early Abdominal Aortic Aneurysm Pathogenesis

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Uwe Raaz ◽  
Alexander M Zöllner ◽  
Ryuji Toh ◽  
Futoshi Nakagami ◽  
Isabel N Schellinger ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Ex Vivo ◽  
Wall Stress ◽  
Finite Elements Analysis ◽  
External Application ◽  
Abdominal Aortic ◽  
Aneurysm Growth ◽  
Aortic Stiffening

Stiffening of the aortic wall is a phenomenon consistently observed in abdominal aortic aneurysm (AAA). However, its role in AAA pathophysiology is largely undefined. Using an established murine elastase-induced AAA model, we demonstrate that segmental aortic stiffening (SAS) precedes aneurysm growth. Finite elements analysis (FEA)-based wall stress calculations reveal that early stiffening of the aneurysm-prone aortic segment leads to axial (longitudinal) stress generated by cyclic (systolic) tethering of adjacent, more compliant wall segments. Interventional stiffening of AAA-adjacent segments (via external application of surgical adhesive) significantly reduces aneurysm growth. These changes correlate with reduced segmental stiffness of the AAA-prone aorta (due to equalized stiffness in adjacent aortic segments), reduced axial wall stress, decreased production of reactive oxygen species (ROS), attenuated elastin breakdown, and decreased expression of inflammatory cytokines and macrophage infiltration, as well as attenuated apoptosis within the aortic wall. Cyclic pressurization of stiffened aortic segments ex vivo increases the expression of genes related to inflammation and extracellular matrix (ECM) remodeling. Finally, human ultrasound studies reveal that aging, a significant AAA risk factor, is accompanied by segmental infrarenal aortic stiffening. The present study introduces the novel concept of segmental aortic stiffening (SAS) as an early pathomechanism generating aortic wall stress and thereby triggering AAA growth. Therefore monitoring SAS by ultrasound might help to better identify patients at risk for AAA disease and better predict the susceptibility of small AAA to further growth. Moreover our results suggest that interventional mechanical stiffening of the AAA-adjacent aorta may be further tested as a novel treatment option to limit early AAA growth.

scholarly journals Identification of Novel Long Noncoding RNAs and Their Role in Abdominal Aortic Aneurysm

2020 ◽  
Vol 2020 ◽  
pp. 1-22
Author(s):  
Abulaihaiti Maitiseyiti ◽  
Hongbo Ci ◽  
Qingbo Fang ◽  
Sheng Guan ◽  
Alimujiang Shawuti ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Expression Profiles ◽  
Noncoding Rnas ◽  
Long Noncoding Rnas ◽  
Functional Enrichment ◽  
Pcr Analysis ◽  
Control Group ◽  
Abdominal Aortic

Objective. Long noncoding RNAs (lncRNAs) have emerged as critical molecular regulators in various diseases. However, the potential regulatory role of lncRNAs in the pathogenesis of abdominal aortic aneurysm (AAA) remains elusive. The aim of this study was to identify crucial lncRNAs associated with human AAA by comparing the lncRNA and mRNA expression profiles of patients with AAA with those of control individuals. Materials and Methods. The expression profiles of lncRNAs and mRNAs were analyzed in five dilated aortic samples from AAA patients and three normal aortic samples from control individuals using microarray technology. Functional annotation of the screened lncRNAs based on the differentially expressed genes was performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses. Results. Microarray results revealed 2046 lncRNAs and 1363 mRNAs. Functional enrichment analysis showed that the mRNAs significantly associated with AAA were enriched in the NOD-like receptor (NLR) and nuclear factor kappa-B (NF-κB) signaling pathways and in cell adhesion molecules (CAMs), which are closely associated with pathophysiological changes in AAA. The lncRNAs identified using microarray analysis were further validated using quantitative real-time polymerase chain reaction (qRT-PCR) analysis with 12 versus 11 aortic samples. Finally, three key lncRNAs (ENST00000566954, ENST00000580897, and T181556) were confirmed using strict validation. A coding-noncoding coexpression (CNC) network and a competing endogenous RNA (ceRNA) network were constructed to determine the interaction among the lncRNAs, microRNAs, and mRNAs based on the confirmed lncRNAs. Conclusions. Our microarray profiling analysis and validation of significantly expressed lncRNAs between patients with AAA and control group individuals may provide new diagnostic biomarkers for AAA. The underlying regulatory mechanisms of the confirmed lncRNAs in AAA pathogenesis need to be determined using in vitro and in vivo experiments.

scholarly journals The relationship between aortic wall distensibility and rupture of infrarenal abdominal aortic aneurysm

2003 ◽  
Vol 37 (1) ◽  
pp. 112-117 ◽  
Author(s):  
Katie A. Wilson ◽  
Amanda J. Lee ◽  
Amanda J. Lee ◽  
Peter R. Hoskins ◽  
F.Gerry R. Fowkes ◽  
...  
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Infrarenal Abdominal Aortic Aneurysm ◽  
Abdominal Aortic ◽  
The Relationship ◽  
Wall Distensibility

Abstract 667: The Role of Aortic Wall-Nuclear Factor- kappa B (NF-kB) Signaling in Formation of Dissecting Aortic Aneurysms

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Talha Ijaz ◽  
Hong Sun ◽  
Adrian Recinos ◽  
Ronald G Tilton ◽  
Allan R Brasier
Keyword(s):  
Flow Cytometry ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Aortic Rupture ◽  
Aortic Aneurysms ◽  
Tunel Staining ◽  
Abdominal Aortic ◽  
Significant Difference

Introduction: Abdominal aortic aneurysm is a devastating disease since it can lead to aortic rupture and instantaneous death. We previously demonstrated that IL-6 secreted from the aortic wall is necessary for the development of abdominal aortic aneurysm and dissection (AAD). Since IL-6 is a NF-kB/RelA dependant gene, we investigated the role of aortic wall- NF-kB/RelA signaling in the development of AAD. Methods and Results: To test the role of aortic wall-RelA, we utilized Cre-Lox technology to delete RelA from aortic cells. Tamoxifen-inducible, Col1a2-promoter driven Cre mice (Col1a2-Cre) were crossed with mT/mG Cre-reporter mice to determine which aortic cells undergo genetic recombination after Cre activation. Flow cytometry analysis of the aortic wall indicated that 88% of the genetically recombined cells were SMCs and 8% were fibroblasts. Next, RelA floxed (RelA f/f) mice, generated in our lab, were crossed with Col1a2-Cre mice. RelA f/f Cre+ and RelA f/f Cre- were stimulated with tamoxifen for 10 days to generate aortic-RelA deficient (Ao-RelA-/-) or wild-type (Ao-RelA+/+) transgenics. Flow cytometry, qRT-PCR, and immunohistochemistry analysis suggested a depletion of aortic-RelA greater than 60%. To test the role of Ao-RelA in AAD, Ao-RelA -/- (n= 20) and Ao-RelA +/+ (n=14) mice were infused with angiotensin II for 7 days. Surprisingly, 20% of Ao-RelA-/- mice died from development of AAD and aortic rupture while no deaths were observed in Ao-RelA+/+ group. In addition, 40% of Ao-RelA-/- mice developed AAD compared to 14% of Ao-RelA+/+ mice. There was no significant difference in TUNEL staining or ERTR7+ fibroblast population between the two groups. Conclusion: Our studies suggest that aortic wall-RelA may be necessary for protection from AAD.

P3114Protective effect of SOCS1-based therapy in experimental abdominal aortic aneurysm

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
S Bernal Uribe ◽  
L Lopez-Sanz ◽  
A Melgar ◽  
S La-Manna ◽  
L Jimenez-Castilla ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Aortic Wall ◽  
Janus Kinase ◽  
Toxic Dose ◽  
Altered Expression ◽  
Abdominal Aortic ◽  
Stat Pathway

Abstract Introduction Abdominal aortic aneurysm (AAA) is a multifactorial vascular disease characterized by chronic inflammation, oxidative stress and proteolytic activity in the aortic wall, which contribute to extracellular matrix degradation and aortic dilation. Altered expression and activation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) pathway have been implicated in several cardiovascular diseases including atherosclerosis and aneurysm formation. Suppressors of cytokine signaling (SOCS) are key negative regulators of JAK/STAT pathway and have been considered an attractive target for therapeutic intervention. AIM We hypothesize that SOCS1 protein could influence AAA development by inhibiting JAK activity and, consequently, STAT activation and target gene expression. Therefore, this study investigates the effect of a SOCS1-derived synthetic peptide in a rodent model of AAA and in cultured vascular smooth muscle cells (VSMC). Methods Experimental AAA was induced in C57BL/6 mice (males, 12 weeks old) by transient elastase perfusion of the aorta. Mice were randomly divided into control (vehicle, i.p.) and treatment (SOCS1 peptide, 3 mg/kg/day, i.p.) groups. Fourteen days after AAA induction, mice were sacrificed, and aorta segments were collected for histology (n=10/group) and mRNA and protein expression analysis (n=8/group). Results Compared to the AAA control group, SOCS1-treated mice exhibited a significant decrease in aortic diameter (68±6% vs. control; p<0.005) and aortic wall thickness, (67±3% vs. control; p<0.001). Histological analyses of aortic tissues showed a higher content of VSMC (α-actin) along with reduced leukocyte infiltration (macrophages, neutrophils and T-cells) and oxidative stress markers (superoxide anion and 8-hydroxyguanosine) in SOCS1-treated mice. SOCS1 therapy also attenuated the gene expression of inflammatory cytokines (CCL2, CCL5, TNF, IFNγ) and matrix metalloproteinases (MMP2, MMP9) in aortic lesions, and altered the expression levels of macrophage M1 (ArgII, iNOS) and M2 (ArgI, CD206) polarization markers. In vitro experiments in murine VSMC revealed that SOCS1 peptide prevented the expression of cytokines and chemokines induced by non-toxic dose of elastase (5 ug/ml, 24 hours). Effects of SOCS1 treatment were accompanied by a reduction in STAT1 and STAT3 phosphorylation and gene expression, both in AAA lesions and cultured VSMC. Conclusion Our results suggest that SOCS1 peptide presents protective effects in experimental AAA by suppressing JAK/STAT pathway-mediated inflammation. Acknowledgement/Funding MINECO-FEDER (SAF2015-63696-R), ISCII (FIS-FEDER PI17/01495), Spanish Society of Arteriosclerosis.

scholarly journals Genetic and Epigenetic Mechanisms Underlying Vascular Smooth Muscle Cell Phenotypic Modulation in Abdominal Aortic Aneurysm

2020 ◽  
Vol 21 (17) ◽  
pp. 6334
Author(s):  
Rijan Gurung ◽  
Andrew Mark Choong ◽  
Chin Cheng Woo ◽  
Roger Foo ◽  
Vitaly Sorokin
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Smooth Muscle Cells ◽  
Aortic Wall ◽  
Epigenetic Mechanisms ◽  
Phenotypic Modulation ◽  
Abdominal Aortic

Abdominal aortic aneurysm (AAA) refers to the localized dilatation of the infra-renal aorta, in which the diameter exceeds 3.0 cm. Loss of vascular smooth muscle cells, degradation of the extracellular matrix (ECM), vascular inflammation, and oxidative stress are hallmarks of AAA pathogenesis and contribute to the progressive thinning of the media and adventitia of the aortic wall. With increasing AAA diameter, and left untreated, aortic rupture ensues with high mortality. Collective evidence of recent genetic and epigenetic studies has shown that phenotypic modulation of smooth muscle cells (SMCs) towards dedifferentiation and proliferative state, which associate with the ECM remodeling of the vascular wall and accompanied with increased cell senescence and inflammation, is seen in in vitro and in vivo models of the disease. This review critically analyses existing publications on the genetic and epigenetic mechanisms implicated in the complex role of SMCs within the aortic wall in AAA formation and reflects the importance of SMCs plasticity in AAA formation. Although evidence from the wide variety of mouse models is convincing, how this knowledge is applied to human biology needs to be addressed urgently leveraging modern in vitro and in vivo experimental technology.

scholarly journals Routine open abdomen treatment compared with on-demand open abdomen or direct closure following open repair of ruptured abdominal aortic aneurysms: A propensity score–matched study

2019 ◽  
Vol 7 ◽  
pp. 205031211983350 ◽  
Author(s):  
Kristian Smidfelt ◽  
Joakim Nordanstig ◽  
Urban Wingren ◽  
Göran Bergström ◽  
Marcus Langenskiöld
Keyword(s):  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Propensity Score ◽  
Open Abdomen ◽  
Open Repair ◽  
Matched Control ◽  
University Hospital ◽  
Control Group ◽  
Ruptured Abdominal Aortic Aneurysm ◽  
Abdominal Aortic

Objective: To investigate whether a strategy of treatment with a primarily open abdomen improves outcome in terms of mortality and major complications in patients treated with open repair for a ruptured abdominal aortic aneurysm compared to a strategy of primary closure of the abdomen. Design: Retrospective cohort study. Methods: Patients treated with a primarily open abdomen at a centre where this strategy was routine in most ruptured abdominal aortic aneurysm patients were compared to a propensity score–matched control group of patients who had the abdomen closed at the end of the primary operation in a majority of the cases. Results: In total, 79 patients treated with a primarily open abdomen after open repair for ruptured abdominal aortic aneurysm at Sahlgrenska University Hospital were compared to a propensity score–matched control group of 148 patients. The abdomen was closed at the end of the procedure in 108 (73%) of the control patients. There was no difference in 30-day mortality between patients treated with a primarily open abdomen at Sahlgrenska University Hospital and the controls, 21 (26.6%) versus 49 (33.1%), p = 0.37. The adjusted odds ratio for mortality at 30 days was 0.66 (95% confidence interval: 0.35–1.25) in patients treated with a primarily open abdomen at Sahlgrenska University Hospital compared to the controls. No difference was observed between the groups regarding 90-day mortality, postoperative renal failure requiring renal replacement therapy, postoperative intestinal ischaemia necessitating bowel resection or postoperative bleeding requiring reoperation. Conclusions: The study did not show any survival advantage or difference in major complications between patients treated with a primarily open abdomen after open repair for ruptured abdominal aortic aneurysm and propensity-matched controls where the abdomen was primarily closed in a majority of the cases.

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