A Comparison of Diameter,Wall Stress,and Rupture Potential Index for Abdominal Aortic Aneurysm Rupture Risk Prediction

An abdominal aortic aneurysm (AAA) is a balloon-like dilation of the aorta, which is potentially fatal in case of rupture. Computational finite element (FE) analysis is a promising approach to a more accurate and patient-specific rupture risk prediction. AAA wall strength and rupture potential index (RPI) calculation are implemented in our FE software. Static structural FE simulations are performed on n = 30 non-ruptured asymptomatic, n = 9 non-ruptured symptomatic, and n = 14 ruptured AAAs. We calculate maximum values for diameter, wall displacement, strain, stress, and RPI as well as minimum wall strength for every AAA. All investigated quantities, except minimum strength, show statistically significant differences between non-ruptured asymptomatic and symptomatic/ruptured AAAs. Maximum wall stress and especially the RPI are notably increased for symptomatic and ruptured AAAs. The biggest difference is found to be the RPI (Δ = 44.9%, p = 8.0e−5). Lowest RPI obtained for symptomatic or ruptured AAAs is 0.3. The RPI of more than 55% of the investigated asymptomatic AAAs falls below this value. Maximum wall stress and maximum RPI criteria enable a reliable rupture risk evaluation for AAAs. Especially in the diameter range where surgical indication is not obvious, the RPI holds great potential for improvement of clinical decisions.     

The Role of Geometric and Biomechanical Factors in Abdominal Aortic Aneurysm Rupture Risk Assessment

The current clinical management of abdominal aortic aneurysm (AAA) disease is based to a great extent on measuring the aneurysm maximum diameter to decide when timely intervention is required. Decades of clinical evidence show that aneurysm diameter is positively associated with the risk of rupture, but other parameters may also play a role in causing or predisposing the AAA to rupture. Geometric factors such as vessel tortuosity, intraluminal thrombus volume, and wall surface area are implicated in the differentiation of ruptured and unruptured AAAs. Biomechanical factors identified by means of computational modeling techniques, such as peak wall stress, have been positively correlated with rupture risk with a higher accuracy and sensitivity than maximum diameter alone. The objective of this review is to examine these factors, which are found to influence AAA disease progression, clinical management and rupture potential, as well as to highlight on-going research by our group in aneurysm modeling and rupture risk assessment.     

Phosphorylation of AKT and Abdominal Aortic Aneurysm Formation

It is hypothesized that differential AKT phosphorylation between sexes is important in abdominal aortic aneurysm (AAA) formation. Male C57BL/6 mice undergoing elastase treatment showed a typical AAA phenotype (80% over baseline, P < 0.001) and significantly increased phosphorylated AKT-308 (p308) and total-AKT (T-AKT) at day 14 compared with female mice. Elastase-treated Raw cells produced increased p308 and significant amounts of matrix metalloproteinase 9 (MMP-9), and these effects were suppressed by {"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002 treatment, a known AKT inhibitor. Male and female rat aortic smooth muscle cells treated with elastase for 1, 6, or 24 hours demonstrated that the p308/T-AKT and AKT-Ser-473/T-AKT ratios peaked at 6 hours and were significantly higher in the elastase-treated cells compared with controls. Similarly, male cells had higher phosphorylated AKT/T-AKT levels than female cells. {"type":"entrez-nucleotide","attrs":{"text":"LY294002","term_id":"1257998346","term_text":"LY294002"}}LY294002 also inhibited elastase-induced p308 formation more in female smooth muscle cells than in males, and the corresponding cell media had less pro–MMP-9. AKT siRNA significantly decreased secretion of pro–MMP-9, as well as pro–MMP-2 and active MMP-2 from elastase-treated male rat aortic smooth muscle cells. IHC of male mice AAA aortas showed increased p308, AKT-Ser-473, and T-AKT compared with female mice. Aortas from male AAA patients had a significantly higher p308/T-AKT ratio than female AAA tissues. These data suggest that AKT phosphorylation is important in the upstream regulation of MMP activity, and that differential phosphorylation may be important in sex differences in AAA.Abdominal aortic aneurysm (AAA) formation is accompanied by chronic inflammation of the aorta wall, with males four times more likely to develop the disease than females.¹ The activation of matrix metalloproteinases (MMPs), especially MMP-2 and MMP-9, has long been known to play a vital role in the destruction of the aortic wall, leading to AAA development.^2–6 However, little is known about upstream modulation of the MMPs during AAA formation. Activation of the molecules of the mitogen-activated protein (MAP) kinase pathways is often observed in inflammatory diseases, such as in AAAs. Two MAP kinases in particular, c-Jun N-terminal kinase (JNK) and extracellular signal–regulated kinase (ERK), have been shown to be important in the activation of MMP-2 and MMP-9 in the aorta.^7–10 In addition to the MAP kinase cascade, the molecules of the phosphoinositide 3-kinase pathway are also known to be important for the modulation of MMPs.^9,11–15 Moreover, AKT, a key molecule in the phosphoinositide 3-kinase pathway, has been shown to play an important role in sex-specific differences of various diseases.^16–20 The role of AKT in the modulation of MMPs has not been studied in AAA formation. Therefore, using an in vivo mouse model of AAA and human AAA tissue, as well as in vitro experiments with rat aortic smooth muscle cells (RASMCs) and Raw cells, we show increased phosphorylation of AKT in males compared with females.     

The Novel Association of the Chemokine CCL22 with Abdominal Aortic Aneurysm

The aim of this study was to examine aortic biopsies with a cytokine array to identify new cytokines associated with abdominal aortic aneurysm (AAA). We assessed the relative expression of 79 cytokines using antibody-based cytokine arrays in a total of 12 AAA and 12 control aortic biopsies. Based on these findings we validated the findings for one cytokine by examining a further 11 AAA and 11 atherothrombosis biopsies and serum from 1028 men, 315 of whom had an AAA. Three cytokines (interleukins 1B and 8, and Chemokine CC motif ligand 22 [CCL22]) were consistently up-regulated in AAA biopsies. Since CCL22 had not previously been associated with aortic dilatation, we confirmed the upregulation of this cytokine in further tissue biopsies and serum using enzyme-linked immunosorbent assay. Median serum concentrations of CCL22 were greater in men with AAA (0.69 ng/ml) than controls (0.56 ng/ml, P < 0.01). Serum CCL22 was independently associated with both small (OR 1.51, 95% CI 1.21–1.88) and large AAA (OR 1.33, 95% CI 1.08–1.62) after adjusting for other risk factors. The association between CCL22 and AAA was also confirmed using immunohistochemistry. The results presented in this study demonstrate a novel association between CCL22 and AAA as well as illustrate how a protein array can be used to identify novel markers of potential pathogenic and diagnostic significance for AAA.Abdominal aortic aneurysm (AAA) is recognized as an important cause of mortality.¹ Marked accumulation of leukocytes, macrophages, B and T cells is a consistent finding in biopsies of human AAA.^2,3 The influx, migration, and effects of these cells are controlled by an array of pro-inflammatory cytokines, chemokines, and growth factors (referred to collectively as cytokines in this article).^4,5 High concentrations of various cytokines have been demonstrated in both AAA biopsies and within the circulation of patients with AAA.^6,7,8 Some cytokines, such as interleukin (IL) 6, have been shown to be present within the circulation at increased concentrations distal to AAAs, suggesting they are released directly from the aortic wall.⁸ At present, however, which cytokines are most relevant to AAA is not clear.We hypothesized that cytokines up-regulated within human AAA biopsies would also be present in increased concentrations within the circulation of patients. The aim of this study was to identify cytokines consistently up-regulated within human AAA biopsies using antibody arrays to measure relative expression of 79 proteins. The up-regulation of one cytokine in human AAA, not previously associated with aortic dilatation, was validated in additional aortic biopsies using alternative outcome techniques and further examined within the blood of 1028 men to assess any association between circulating levels and AAA.     

Perforin-Independent Extracellular Granzyme B Activity Contributes to Abdominal Aortic Aneurysm

Granzyme B (GZMB) is a serine protease that is abundantly expressed in advanced human atherosclerotic lesions and may contribute to plaque instability. Perforin is a pore-forming protein that facilitates GZMB internalization and the induction of apoptosis. Recently a perforin-independent, extracellular role for GZMB has been proposed. In the current study, the role of GZMB in abdominal aortic aneurysm (AAA) was assessed. Apolipoprotein E (APOE)^−/− × GZMB^−/− and APOE^−/− × perforin^−/− double knockout (GDKO, PDKO) mice were generated to test whether GZMB exerted a causative role in aneurysm formation. To induce aneurysm, mice were given angiotensin II (1000 ng/kg/min) for 28 days. GZMB was found to be abundant in both murine and human AAA specimens. GZMB deficiency was associated with a decrease in AAA and increased survival compared with APOE-KO and PDKO mice. Although AAA rupture was observed frequently in APOE-KO (46.7%; n = 15) and PDKO (43.3%; n = 16) mice, rupture was rarely observed in GDKO (7.1%; n = 14) mice. APOE-KO mice exhibited reduced fibrillin-1 staining compared with GDKO mice, whereas in vitro protease assays demonstrated that fibrillin-1 is a substrate of GZMB. As perforin deficiency did not affect the outcome, our results suggest that GZMB contributes to AAA pathogenesis via a perforin-independent mechanism involving extracellular matrix degradation and subsequent loss of vessel wall integrity.An aneurysm is a permanent focal dilatation of an artery that is associated with progressive weakening of the vessel wall. Approximately 80% of all aortic aneurysms occur in the abdominal region.¹ Abdominal aortic aneurysm (AAA) is an increasingly common and frequently fatal clinical condition, responsible for more than 15,000 deaths per year in the United States.¹ The most significant risk factors for AAA are male gender, cigarette smoking, age, family history, and atherosclerotic disease.^2,3 The incidence of AAA measuring 2.9 to 4.9 cm in diameter ranges from 1.3% in men 45 to 54 years of age to 12.5% in men 75 to 84 years of age. In women, prevalence ranges from 0% to 5.2% in the same age groups.² Rupture occurs in approximately 20% of AAA exceeding 5 cm in diameter but is expected in over 50% of AAA greater than 7 cm.² Currently, the only effective intervention is open surgical or endovascular repair, however operative mortality for elective open surgical repair is 5.6%.⁴ Endovascular repair is associated with lower operative mortality, but carries an increased risk of rupture after four years postsurgery and a greater probability of reintervention.⁵ Total mortality for rupture has been reported to be as high as 90%²; many such patients do not reach emergency treatment in time, and those who do have high surgical mortality.⁶ Because of the risk of rupture in combination with the asymptomatic nature of AAA, in 2006 the U.S. Congress passed the Screening for Abdominal Aortic Aneurysm (SAAAVE) Amendment for men over the age of 65 and men and women with a family history of AAA. Recently (September 2008), the Canadian Society for Vascular Surgery recommended a similar screening program. As such, as patient and provider awareness and education increases, it is anticipated that early-stage pharmaceutical options geared toward slowing or preventing aneurysm progression and rupture will be in great demand.¹The adventitia is thought to bear the brunt of the aortic circumferential wall stress and acts to restrict aneurysm expansion and rupture,⁷ whereas inflammation in this area may contribute to collagen degeneration, adventitial weakening, and AAA progression.⁸ Elastin degeneration, collagen fragmentation, stress distribution, and flow changes can all contribute to mechanical weakness in the aortic wall.^9,10,11 In human aortic aneurysmal tissue at the end stage of disease, medial thinning, elastic fiber degeneration, adventitial hypertrophy with an accumulation of T and B lymphocytes, atherosclerosis, and thrombi are observed.^12,13,14,15 Inflammation in the intraluminal thrombus adjacent to the AAA wall can also influence rupture as it is associated with increased vascular smooth muscle cell (VSMC) apoptosis, extracellular matrix (ECM) fragmentation, and perturbation of wall structural integrity and stability.¹⁶The proteolytic mechanisms that are associated with ECM degradation in AAA are areas of active investigation. Several types of proteases, including matrix metalloproteinases−2, −7, −9, −12, cathepsins, plasminogen activators, and elastases, have been proposed to contribute to the degradation of fibrillar ECM proteins.¹¹ In the aorta, microfibrils associate with elastin in the tunica media to form the concentric lamellae that separate individual SMC layers and confer elasticity to the aortic wall. Microfibrils also act to stabilize the vessel wall by connecting lamellar rings to one another, to SMC, and to the subendothelial basement membrane.¹⁷ Fibrillin-1 is the major scaffolding component of microfibrils and thus plays a key role in maintaining vessel wall stability.The present study examines the role of Granzyme B (GZMB) in AAA. GZMB is a 32-kDa serine protease that is secreted along with the membrane-disruptive protein perforin (PRF1) by cytotoxic lymphocytes to induce target cell apoptosis. PRF1 is a cytolytic protein that mediates the cytoplasmic entry of GZMB into target cells.¹⁸ Over the past two decades, the majority of research on GZMB has been focused on its role in apoptosis. However, GZMB may also exhibit extracellular proteolytic activity as in vitro assays have demonstrated that GZMB can cleave extracellular proteins such as fibronectin, vitronectin, laminin, fibrinogen, von Willebrand factor, and aggrecan.^19,20,21,22 Although GZMB expression was initially thought to be restricted to cytotoxic T lymphocytes and natural killer cells, it is now clear that, under conditions of cellular stress, aging, and disease, GZMB expression can be induced in other types of immune cells (macrophages, mast cells, neutrophils) in addition to nonimmune cells (keratinocytes, chondrocytes, VSMCs).^{23,24,25,26,27,28} As such, many cell types could potentially act as a source of GZMB in age-related degenerative diseases such as AAA.Elevated GZMB levels have been reported in advanced human atherosclerotic and allograft vasculopathy lesions but not in healthy coronary arteries.²³ In the latter study, GZMB was present in lymphocytes, macrophage foam cells, and medial and intimal SMCs, and it was found that extracellular staining increased with disease severity.²³ High GZMB levels in the plasma correspond to increased carotid artery plaque instability and increased cerebrovascular events in humans.²⁹ Furthermore, elevated GZMB production is observed in peripheral blood mononuclear cells isolated from patients with unstable angina pectoris compared with cells from patients with stable angina pectoris.³⁰The current study used a well-established mouse model of angiotensin II (Ang II)–induced AAA.³¹ In this model, macrophage accumulation in the media of the suprarenal aorta and dissection precede the formation of aneurysm and atherosclerosis in Ang II–infused apolipoprotein E–knockout (APOE-KO) mice. Although thrombi are usually constrained by adventitial tissue, rupture of the abdominal aorta and subsequent death attributable to abdominal bleeding is often observed.¹³ We hypothesize that GZMB is elevated in AAA and contributes to vessel wall instability and aneurysm formation. To test this, GZMB/APOE-DKO (GDKO) and PRF1/APOE-DKO (PDKO) mice were generated and infused with Ang II to induce AAA formation. In addition, human aneurysm tissues were assessed for the presence and localization of GZMB in clinical AAA and thoracic aortic aneurysm (TAA).     

腹主动脉瘤应力模型的建立及其应用

本研究用螺旋CT扫描腹主动脉瘤获得的断层图像合成腹主动脉瘤几何模型，通过设定瘤壁组织生物力学参数和边界条件，使用有限元分析的方法分析腹主动脉瘤瘤壁的应力分布。结果标明，本例腹主动脉瘤应力峰值位于远端分叉部位，瘤体应力峰值位于后壁，均小于瘤壁的承受极限。本研究所得结果对腹主动脉瘤应力模型有助于分析个体化腹主动脉瘤的破裂部位和生长方向，对研究疾病进程提供依据。     

Detection of Chlamydia pneumoniae DNA in Buffy-Coat Samples of Patients with Abdominal Aortic Aneurysm

 Recent studies have suggested that Chlamydia pneumoniae infection is a risk factor for abdominal aortic aneurysm. This study explores the presence of Chlamydia pneumoniae DNA in buffy-coat samples of control subjects and of patients with abdominal aortic aneurysm. The seroepidemiological association between abdominal aortic aneurysm and Chlamydia pneumoniae was also investigated. Buffy-coat samples and serum specimens were obtained from 88 patients and 88 control subjects. Detection of Chlamydia pneumoniae DNA in buffy-coat samples and measurement of IgG antibodies to Chlamydia pneumoniae in serum specimens were performed by polymerase chain reaction and microimmunofluorescence, respectively. Chlamydia pneumoniae DNA was detected in buffy-coat samples of 18 (20%) patients and 8 (9%) control subjects (adjusted odds ratio 2.9, 95% confidence interval 1–8.5). IgG antibodies to Chlamydia pneumoniae were detected in 85 (97%) patients and 71 (81%) control subjects (adjusted odds ratio 7.2, 95% confidence interval 1.7–31). The results show an association between abdominal aortic aneurysm and either the presence of Chlamydia pneumoniae DNA in buffy-coat samples or IgG antibodies to Chlamydia pneumoniae. These findings support the hypothesis that previous infection with Chlamydia pneumoniae might be a risk factor for abdominal aortic aneurysm.     

Evaluation of Texture for Classification of Abdominal Aortic Aneurysm After Endovascular Repair

The use of the endovascular prostheses in abdominal aortic aneurysm has proven to be an effective technique to reduce the pressure and rupture risk of aneurysm. Nevertheless, in a long-term perspective, complications such as leaks inside the aneurysm sac (endoleaks) could appear causing a pressure elevation and increasing the danger of rupture consequently. At present, computed tomographic angiography (CTA) is the most common examination for medical surveillance. However, endoleak complications cannot always be detected by visual inspection on CTA scans. The investigation on new techniques to detect endoleaks and analyse their effects on treatment evolution is of great importance for endovascular aneurysm repair (EVAR) technique. The purpose of this work was to evaluate the capability of texture features obtained from the aneurysmatic thrombus CT images to discriminate different types of evolutions caused by endoleaks. The regions of interest (ROIs) from patients with different post-EVAR evolution were extracted by experienced radiologists. Three techniques were applied to each ROI to obtain texture parameters, namely the grey level co-occurrence matrix (GLCM), the grey level run length matrix (GLRLM) and the grey level difference method (GLDM). The results showed that GLCM, GLRLM and GLDM features presented a good discrimination ability to differentiate between favourable or unfavourable evolutions. GLCM was the most efficient in terms of classification accuracy (93.41% ± 0.024) followed by GLRLM (90.17% ± 0.077) and finally by GLDM (81.98% ± 0.045). According to the results, we can consider texture analysis as complementary information to classified abdominal aneurysm evolution after EVAR.     

Chemical Mediators of Inflammation and Resolution in Post-Operative Abdominal Aortic Aneurysm Patients

Temporal–metabolomic studies of local mediators during inflammation and its resolution uncovered novel pathways and mediators, e.g., lipoxins, resolvins, and protectins that stimulate key resolution responses. Since these studies were carried out with isolated human cells and in animal models, it is important to determine in humans whether temporal profiles between pro-inflammatory mediators and pro-resolving mediators are demonstrable in vivo. To this end, we examined patients undergoing abdominal aortic aneurysm (AAA) surgery. Profiles of mediators including eicosanoids were assessed in addition to pro-resolving mediators. The results demonstrate temporal relationships for local-acting peptides (e.g., VEGF, IL-10, TGF_β) and lipid mediators (leukotrienes and resolvins). In addition, profiles obtained for AAA patients divided into two groups based on their temporal profile: one group consistent with a pro-inflammatory and another with a resolving profile. Together, these translational metabolomic profiles demonstrate for the first time the temporal relationships between local mediators in humans relevant in inflammation resolution.     

Screening for Abdominal Aortic Aneurysm during Transthoracic Echocardiography in Patients with Significant Coronary Artery Disease

Purpose

Coronary artery disease (CAD) shares several risk factors with abdominal aortic aneurysm (AAA). We evaluated the prevalence during transthoracic echocardiography (TTE) and risk factors of AAA in patients with CAD.

Materials and Methods

A total of 1300 CAD patients were screened from August 2009 to May 2010, and measurement of abdominal aorta size was feasible in 920 patients (71%) at the end of routine TTE. An AAA was defined as having a maximal diameter of ≥30 mm.

Results

Of the 920 patients, 22 (2.4% of the study population) were diagnosed with AAA; of these AAA patients, 86% were male, and 82% were over 65 years-old. Abdominal aortic size was weakly correlated with aortic root diameter (r=0.22, p<0.01). Although the proportions of male gender, hypertension, and dyslipidemia were higher in AAA patients, such differences were not statistically significant. Advanced age [odds ratio (OR)=1.07; 95% confidence interval (CI): 1.01-1.12; p<0.01], smoking (OR=3.44; 95% CI: 1.18-10.04; p=0.02), and peripheral arterial disease (OR=5.88; 95% CI: 1.38-25.05; p=0.01) were found to be associated with AAA.

Conclusion

Although prevalence of AAA is very low in the Asian population, the prevalence of AAA in Asian CAD patients is higher than the general population. Therefore, opportunistic examination of the abdominal aorta during routine TTE could be effective, especially for male CAD patients over 65 years with a history of smoking or peripheral arterial disease.     

Elevated MMP‐8 and Decreased Myeloperoxidase Concentrations Associate Significantly with the Risk for Peripheral Atherosclerosis Disease and Abdominal Aortic Aneurysm1

Matrix metalloproteinases are responsible for degradation and remodelling of extracellular matrix and exert important roles in initiation and progression of inflammatory diseases. We aimed to examine the role of Matrix metalloproteinases (MMPs) and their regulators in degenerative arterial diseases. Serum samples were collected from patients with arterial disease (n = 126), who underwent surgery because of symptomatic aorto‐occlusive disease (AOD, n = 18), carotid artery stenosis (n = 67) or abdominal arotic aneurysm (n = 41). Serum MMP‐1, MMP‐8, MMP‐13, TIMP‐1, myeloperoxidase (MPO) and neutrophil elastase (HNE) concentrations were determined by ELISA, and the molar ratio of MMP‐8 and TIMP‐1 was calculated. To get reference values, the determinations were done on samples of healthy blood donors (n = 100). In univariate analyses, the patients had higher MMP‐8 (P < 0.001), TIMP‐1 (P = 0.045), and MMP‐8/TIMP‐1 (P < 0.001), and lower MPO (P < 0.001) when compared with the blood donors. All three subgroups had higher MMP‐8 (P < 0.001) and MMP‐8/TIMP‐1 (P < 0.001), and lower MPO (P < 0.01, except AOD) levels when compared with the references. In multiple logistic regression analyses, the male gender (P < 0.01), age (P < 0.001), elevated MMP‐8 (P < 0.001) and decreased MPO (P < 0.001) concentrations associated significantly with the risk for arterial disease, and provided an area under curve (AUC) of 0.97 in the Receiver operating characteristics analyses. In multiple linear regression analyses, HNE correlated with both MMP‐8 (P < 0.001) and MPO (P = 0.008) concentrations. Combination of high MMP‐8 and low MPO level in serum eventually reflecting selectively modified neutrophil degranulation may indicate increased risk for arterial disease.     

腹主动脉瘤切除-人造血管置换术的麻醉管理

目的 总结腹主动脉瘤切除术及人造血管置换术的麻醉管理.方法 回顾20例腹主动脉瘤切除术及人造血管置换术的麻醉处理过程,对输液量、术中并发症、血压及心率等重要指标进行分析整理.结果 在主动脉阻断和开放时血流动力学波动比较剧烈,经处理后循环功能维持稳定,肾功能在术中未受到明显影响.所有患者都安全地度过了手术,无患者在术中发生死亡.结论 完善的麻醉监测、及时纠正代谢紊乱和维持循环稳定是患者安全度过围术期的有效保证.     

Effect of Variation in Intraluminal Thrombus Constitutive Properties on Abdominal Aortic Aneurysm Wall Stress

The abdominal aortic aneurysm (AAA) is a degenerating disease for which the end stage is the rupture of the vessel wall. Accurate prediction of the stresses acting on the aneurysm tissue may be used to determine the actual risk of rupture of a specific aneurysm. To accomplish this, a correct constitutive model for the aneurysmal aortic wall and any intraluminal thrombus (ILT) present within it are needed. Our laboratory has previously reported the mechanical properties of ILT. The aim of this work is to investigate the reliability of using population-mean values of ILT constitutive parameters to estimate AAA wall stress distribution. For this, a three-dimensional asymmetric model of an aneurysm including ILT was generated and a parametric study was conducted varying ILT constitutive properties within a physiological range. Results show that the presence of any ILT reduces and redistributes the stresses in the aortic wall markedly. Maximum variation in the peak wall stresses for all the models analyzed was 5%. Adopting a nonhomogeneous ILT did not alter the stress distribution. On the basis of these results, we infer that population mean parameters for ILT material characteristics can be used to reasonably estimate the wall stresses in patient specific aneurysm models. © 2003 Biomedical Engineering Society. PAC2003: 8719Rr, 8719Xx, 8710+e     

A Framework for the Automatic Generation of Surface Topologies for Abdominal Aortic Aneurysm Models

Patient-specific abdominal aortic aneurysms (AAAs) are characterized by local curvature changes, which we assess using a feature-based approach on topologies representative of the AAA outer wall surface. The application of image segmentation methods yields 3D reconstructed surface polygons that contain low-quality elements, unrealistic sharp corners, and surface irregularities. To optimize the quality of the surface topology, an iterative algorithm was developed to perform interpolation of the AAA geometry, topology refinement, and smoothing. Triangular surface topologies are generated based on a Delaunay triangulation algorithm, which is adapted for AAA segmented masks. The boundary of the AAA wall is represented using a signed distance function prior to triangulation. The irregularities on the surface are minimized by an interpolation scheme and the initial coarse triangulation is refined by forcing nodes into equilibrium positions. A surface smoothing algorithm based on a low-pass filter is applied to remove sharp corners. The optimal number of iterations needed for polygon refinement and smoothing is determined by imposing a minimum average element quality index with no significant AAA sac volume change. This framework automatically generates high-quality triangular surface topologies that can be used to characterize local curvature changes of the AAA wall.     

Mycotic Aortic Aneurysm Associated with Legionella anisa

Legionella anisa is rarely associated with human disease. Its gene was identified by broad-range PCR in whole blood and excised tissue from a patient with a culture-negative mycotic aneurysm and was considered as a possible pathogen. This case report is potentially useful for the future diagnosis of intravascular infection.     

A Systematic Review of Studies Examining Inflammation Associated Cytokines in Human Abdominal Aortic Aneurysm Samples

Objectives: Inflammation is critical in abdominal aortic aneurysm (AAA) but there is no current consensus on which inflammation related cytokines are important. The aim of this review was to systemically assess previous studies investigating the relative expression of inflammation associated cytokines within human AAA samples. Methods: The MEDLINE database was searched for studies which simultaneously examined an array of different inflammation associated cytokines in aortic samples in order to identify those associated with AAA. Focused searches were then conducted for further studies assessing relative concentrations of these cytokines in aortic samples in relation to AAA. Appropriate studies were assessed by two reviewers independently. Results: Eighteen studies were included. A number of different cytokines have been consistently found to be upregulated within AAA by comparison to aortic samples removed from patients without cardiovascular disease, however findings relative to samples of aortic athero-thrombosis were less consistent. TNFA and INFG appear to be the most consistently associated with AAA in studies using both normal and atherosclerotic controls. Cautious interpretation of these data is recommended due to a number of methodological problems. Conclusions: This systematic review suggests that TNFA and INFG are the most consistently upregulated cytokines in large AAAs. Further studies utilizing larger populations, new proteomic techniques and better patient matching are required.     

瘤颈角度对腹主动脉瘤腔内修复术后支架位移的影响

目的 研究瘤颈角度对腹主动脉瘤腔内修复术后支架位移的影响。方法 选用28名患者CT影像分别建立术前腹主动脉瘤(abdominal aortic aneurysm, AAA)模型、术后两次随访(postoperative follow-up)AAA模型和覆膜支架模型,并根据术前瘤颈角度将模型分为非严重成角组(n=14)和严重成角组(n=14)。测量每个模型的几何形态,分析手术前后AAA几何参数、术后支架位移变化。通过血流动力学模拟计算术后第1次随访模型的位移力。结果 两组患者在瘤长度、最大直径、位移力、瘤颈长度变化和瘤体积变化有明显差异(P<0.05)。支架重心位移和近端位移无显著差异(P>0.05)。在内漏发生情况上,未严重成角组中有2例,严重成角组中有4例(P>0.05)。结论 严重的瘤颈成角可导致支架位移力显著增加以及近端锚固区减小,进而增加支架位移发生的可能性。建议在临床方面医生应加强对严重瘤颈成角患者的术后随访,警惕远期内漏的发生。