Mechanical properties of abdominal aortic aneurysm wall

There is a need to understand why and where the abdominal aortic aneurysm may rupture. Our goal therefore is to investigate whether the mechanical properties are different in different regions of the aneurysm. Aorta samples from five freshly excised whole aneurysms, &#85 5 cm in diameter, from five patients, average age 71 &#45 10 years, were subjected to uniaxial testing. We report the wall thickness, yield stress and strain, and parameters that describe nonlinear stress-strain curves for the anterior, lateral and posterior regions of the aneurysm. The posterior region was thicker than the anterior region ( 2.73 &#45 0.46 mm versus 2.09 &#45 0.51 mm). The stress-strain curves were described by &#134 = a &#107 b, where &#134 is true stress and &#107 is engineering strain. In the circumferential direction, the wall stiffness increased from posterior to anterior to lateral. In the longitudinal direction, the lateral and anterior regions showed greater wall stiffness than the posterior region. The wall stiffness was greater in the circumferential than longitudinal direction. The anterior region was the weakest, especially in the longitudinal direction (yield stress &#134 Y = 0.38 &#45 0.18 N mm -2 ). For a less complex model the aneurysmal wall could be considered orthotropic with &#134 = 12.89 &#107 2.92 and 4.95 &#107 2.84 in the circumferential and longitudinal directions. For the isotropic model, &#134 = 7.89 &#107 2.88. In conclusion, different regions of the aneurysm have different yield stress, yield strains, and other mechanical properties, and this must be considered in understanding where the rupture might occur.     

Histopathological analysis of cellular localization of cathepsins in abdominal aortic aneurysm wall

An important feature of abdominal aortic aneurysm (AAA) is the destruction of vessel wall, especially elastin and collagen. Besides matrix metalloproteinases, cathepsins are the most potent elastolytic enzymes. The expression of cathepsins with known elastolytic and collagenolytic activities in the individual cells within AAA has not yet been determined. The vessel wall of 32 AAA patients and 10 organ donors was analysed by immunohistochemistry for expression of cathepsins B, D, K, L and S, and cystatin C in all cells localized within AAA. Luminal endothelial cells (ECs) of AAA were positive for cathepsin D and partially for cathepsins B, K and S. Endothelial cells of the neovessels and smooth muscle cells in the media were positive for all cathepsins tested, especially for cathepsin B. In the inflammatory infiltrate all cathepsins were expressed in the following pattern: B > D = S > K = L. Macrophages showed the highest staining intensity for all cathepsins. Furthermore, weak overall expression of cystatin C was observed in all the cells localized in the AAA with the exception of the ECs. There is markedly increased expression of the various cathepsins within the AAA wall compared to healthy aorta. Our data are broadly consistent with a role for cathepsins in AAA; and demonstrate expression of cathepsins D, B and S in phagocytic cells in the inflammatory infiltrate; and also may reveal a role for cathepsin B in lymphocytes.     

In vitro evaluation of the effects of intraluminal thrombus on abdominal aortic aneurysm wall dynamics

The optimum time to treat abdominal aortic aneurysms (AAAs) still remains an uncertain issue. The decision to intervene does not take in account the effects that wall curvature, intraluminal thrombus (ILT) properties and thickness have on rupture. The role of ILT in aneurysm dynamics and rupture has been controversial. In vitro testing of four silicone AAA models incorporating the ILT and aortic bifurcation was studied under physiological conditions. Pressures (P) and diameters (D) were analysed for models with and without ILT at different locations. The diametral strain, compliance and P/D curves were influenced by the presence, elastic stiffness and thickness of the ILT. In this case, the inclusion of ILT reduced the lumen area by 77% that resulted in a 0.5–81% reduction in compliance depending on ILT properties. With an increase in ILT stiffness from 0.05 to 0.2 MPa, the compliance was reduced by 81%. In the region of maximum diameter, there was a reduction of diametral strain and compliance except for the softer ILT which was more compliant throughout the proximal region. The shifting of the maximum diametral strain and compliance to the proximal neck was pronounced by an increase in ILT stiffness, thus creating a possible rupture site.     

Quantitative assessment of abdominal aortic aneurysm geometry

Recent studies have shown that the maximum transverse diameter of an abdominal aortic aneurysm (AAA) and expansion rate are not entirely reliable indicators of rupture potential. We hypothesize that aneurysm morphology and wall thickness are more predictive of rupture risk and can be the deciding factors in the clinical management of the disease. A non-invasive, image-based evaluation of AAA shape was implemented on a retrospective study of 10 ruptured and 66 unruptured aneurysms. Three-dimensional models were generated from segmented, contrast-enhanced computed tomography images. Geometric indices and regional variations in wall thickness were estimated based on novel segmentation algorithms. A model was created using a J48 decision tree algorithm and its performance was assessed using ten-fold cross validation. Feature selection was performed using the χ²-test. The model correctly classified 65 datasets and had an average prediction accuracy of 86.6% (κ = 0.37). The highest ranked features were sac length, sac height, volume, surface area, maximum diameter, bulge height, and intra-luminal thrombus volume. Given that individual AAAs have complex shapes with local changes in surface curvature and wall thickness, the assessment of AAA rupture risk should be based on the accurate quantification of aneurysmal sac shape and size.     

Albert Einstein and his abdominal aortic aneurysm

The interesting case of Albert Einstein's abdominal aortic aneurysm is presented. He was operated on at age 69 and, finding that the large aneurysm could not be removed, the surgeon elected to wrap it with cellophane to prevent its growth. However, seven years later the aneurysm ruptured and caused the death of the famous scientist.     

腹主动脉瘤计算机仿真研究进展

腹主动脉瘤(abdominal aortic aneurysm,AAA)是腹主动脉较常见的疾病,破裂之后致死率极高,因此,及时发现和评估AAA破裂的风险就具有重要意义。近年来随着医学影像、计算机及血流动力学等理论和技术的快速发展,利用计算机模拟技术对AAA进行仿真研究已成为研究的热点,其模拟的结果趋于人体真实的动脉瘤,并在揭示AAA的发生及演变的机制方面发挥了重要作用。本文介绍了AAA仿真研究的原理及模型分类,详细地阐述了瘤体形态、瘤壁的结构及属性、血液及血流的属性、腔内血栓等相关因素在仿真研究中的作用,并对其目前的进展及局限性予以综述。     

Towards patient-specific risk assessment of abdominal aortic aneurysm

Diagnosis of vascular disease and selection and planning of therapy are to a large extent based on the geometry of the diseased vessel. Treatment of a particular vascular disease is usually considered if the geometrical parameter that characterizes the severity of the disease, e.g. % vessel narrowing, exceeds a threshold. The thresholds that are used in clinical practice are based on epidemiological knowledge, which has been obtained by clinical studies including large numbers of patients. They may apply “on average”, but they can be sub-optimal for individual patients. To realize more patient-specific treatment decision criteria, more detailed knowledge may be required about the vascular hemodynamics, i.e. the blood flow and pressure in the diseased vessel and the biomechanical reaction of the vessel wall to this flow and pressure. Over the last decade, a substantial number of publications have appeared on hemodynamic modeling. Some studies have provided first evidence that this modeling may indeed be used to support therapeutic decisions. The goal of the research reported in this paper is to go one step further, namely to investigate the feasibility of a patient-specific hemodynamic modeling methodology that is not only effective (improves therapeutic decisions), but that is also efficient (easy to use, fast, as much as possible automatic) and robust (insensitive to variation in the quality of the input data, same outcome for different users). A review is presented of our research performed during the last 5 years and the results that were achieved. This research focused on the risk assessment for one particular disease, namely abdominal aortic aneurysm, a life-threatening dilatation of the abdominal aorta.     

血管支架在腹主动脉瘤治疗中的应用及进展

腹主动脉瘤的发病率逐年上升,腹主动脉瘤患者若不及时治疗常可因瘤体破裂致死,手术治疗的死亡率及高并发症的风险对外科医师及患者均是一项严重的挑战,随着生物医学工程学的发展,运用血管支架的血管腔内治疗在腹主动脉瘤治疗中显示较低的死亡率和良好的近期效果从而占有越来越重要的地位,本文就血管支架在腹主动脉瘤治疗中的应用及进展进行综述.     

腹主动脉瘤的数值计算模型比较研究

目的分别采用纯流体模型和流固耦合模型来计算腹主动脉瘤的血流动力学特征,比较两种数值模型的不同,并讨论在研究腹主动脉瘤中的应用。方法使用Gambit 2.2.30和COMSOL Multiphysics 4.2建立腹主动脉瘤的理想模型,分别基于有限体的方法分析纯流体模型,基于任意拉格朗日-欧拉算法(Arbitrary Lagrangian-Eulerian)计算流固耦合模型。结果同样的入口速度下,纯流体模型出现4个涡流和6个局部压力集中;流固耦合模型只有2个涡流和局部压力集中,且涡流中心更接近腹主动脉瘤的远端。在边界层分离点、血流回帖位置以及腹主动脉瘤的近端和远端,两种模型均出现壁剪切力极值。血管壁的最大形变和最大壁应力出现在腹主动脉瘤的近端和远端。结论两种模型的涡流个数和涡流中心的位置均不一样,与瘤体的生长有着密切的关联;流固耦合模型中的最大壁剪切力比纯流体模型要小36%;最大壁应力和最大血管壁的形变量与出口血压呈正相关。在研究血管瘤生长与血流动力学的关系时需要考虑使用流固耦合模型。     

Evaluation of aortic aneurysm and dissection by abdominal echography

Aortic dissection and aneurysm are related to increased vulnerability of the aortic wall due to arteriosclerosis. Echographic findings of aortic sclerosis include irregularity and strong punctate echoes in the intima and meandering of the aorta. Unruptured abdominal aneurysms are often found incidentally by routine echography. The "maximum diameter" and "increase in the size" of aortic aneurysm on echography are important information closely related to the risk of its rupture. In the evaluation of acute aortic dissection, the flap length indicates the range of dissection. The presence or absence of blood flow in the false lumen must be examined simultaneously using color Doppler echography. Some aortic dissections and aneurysms require emergency treatment on detection, and the evaluation of their images on echography, which is often performed for screening of patients with back or abdominal pain, are important for the determination of the therapeutic approach. In patients who are treated conservatively or observed, echography is very useful for the follow-up. Such patients must also be diagnosed or followed up by combining echography with other imaging techniques depending on the condition and necessary information in each patient.     

Coronary artery aneurysm: management and association with abdominal aortic aneurysm.

BACKGROUND: Coronary artery aneurysm (CAA) is a dilatation that exceeds 1.5 times the diameter of a normal adjacent coronary artery. Several studies suggest that pathogenetic mechanisms involved in this disease and in abdominal aortic aneurysm (AAA) are similar. Surgery for CAA is mandatory when the aneurysm is three to four times larger than the original vessel diameter. We reviewed our experience in the surgical treatment of this unusual disease and analyzed its association with AAA. MATERIALS AND METHODS: Between October 1993 and March 2005, 11 patients (9 men; mean age=66 years) underwent surgery for CAA. In all cases, coronary aneurysms were diagnosed as incidental findings in coronary angiographies. The coronary aneurysms were isolated and longitudinally incised: the proximal and distal openings were identified and sutured. The sacs were obliterated with running sutures. Myocardial protection was achieved by retrograde cardioplegia only. Coronary artery bypass grafting was performed distally to the excluded aneurysms in all patients. RESULTS: One patient died of respiratory failure early after the operations; all other patients are alive, asymptomatic for angina, and free from repeated acute myocardial infarction after a median follow-up of 76 months (range=4-141 months). A total of six patients underwent surgical repair or endoprosthesis implantation because of AAAs. CONCLUSIONS: Our operative techniques ensured durable results. We recommend screening for abdominal aneurysms in all affected patients because of the frequent association between CAA and AAA as a result of their similar pathogenetic mechanism.     

异种移植建立的大鼠腹主动脉瘤形态学特征

目的: 建立和鉴定一种新型腹主动脉瘤动物模型, 为腹主动脉瘤的进一步研究提供基础。方法: 选取豚鼠肾下腹主动脉组织1 cm, 正位替换SD大鼠同长度腹主动脉; SD大鼠腹主动脉原位离断后吻合分别作为对照。分别于术后4周动态观测和比较移植腹主动脉直径、腔面积等形态学变化; 计算机图像技术半定量分析弹力纤维、胶原纤维及平滑肌变化。结果: 存活受体中88%移植腹部主动脉血流通畅, 无移植物或吻合口狭窄, 无腔内血栓形成。4周内, 异种移植组腹主动脉直径随时间延长逐渐扩张, 与对照组有显著差异; 腹主动脉扩张率与弹力蛋白、中膜平滑肌变化呈现显著负相关。结论: 免疫炎症损伤介导的豚鼠-SD大鼠异种移植腹主动脉瘤是一稳定可靠的动物模型。     

Inflammatory abdominal aortic aneurysm: report of six cases

Six cases of inflammatory aneurysm of the abdominal aorta are described. All patients were male, aged 59 to 80 years, and five had symptomatic atherosclerotic cerebrovascular or cardiovascular disease. In three the diagnosis of inflammatory aneurysm was suggested preoperatively on the basis of computed tomographic or ultrasonographic scanning. On gross examination the aneurysm wall was about 1 cm thick and included an inner narrow layer of atherosclerotic plaque, which was contiguous with the outer thick fibroinflammatory component. Microscopically, this component consisted of fibroblasts and collagen, which entrapped fat, nerves, and lymph nodes and was infiltrated by lymphocytes and plasma cells. Plasma cells, lymphocytes, and fibroblasts predominated in four patients, while two showed abundant dense collagen with fewer inflammatory cells and fibroblasts. There was associated vasculitis, predominantly phlebitis, in three. Inflammatory aneurysms represent a distinct group of abdominal aortic aneurysms.     

Inhibition of experimental abdominal aortic aneurysm progression by nifedipine

Agents to inhibit the renin-angiotensin system have been reported to suppress the progression of abdominal aortic aneurysm (AAA). However, the effects of calcium channel blockers (CCBs) are still unclear in terms of the inhibition of the progression of AAA. Recently, several effects of CCBs beyond those associated with blood pressure lowering have attracted much interest. In this study, we examined the effects of nifedipine on AAA progression. AAA was induced in rats by transient aortic perfusion with elastase. Then, nifedipine (10 mg/kg/day) and saline (control) were administered to rats by osmotic mini-pump. At 2 and 4 weeks, the size of the AAA, blood pressure and heart rate were measured. Then, to further explore the mechanisms of the progression of AAA, we used human vascular smooth muscle cells (VSMCs). Especially, we focused on NF-kappaB and matrix metalloproteinase-9 (MMP-9). Treatment with nifedipine resulted in a significant inhibition of the progression of AAA such as aneurismal dilation at 14 and 28 days compared to the control (week 2: control, 2.98+/-0.71 mm; nifedipine, 2.37+/-0.64 mm; p<0.05 and week 4: control, 3.28+/-0.98 mm; nifedipine, 2.41+/-0.17 mm; p<0.05). Neither nifedipine nor saline changed blood pressure and heart rate, significantly. Nifedipine (1 microM) significantly suppressed angiotensin II-induced (10(-6) M) NF-kappaB activity in VSMCs by reporter assay (p<0.01). Furthermore, nifedipine (1 microM) inhibited MMP-9 protein expression and activity. Saline did not show such inhibitory effects. Taken together, these results indicated that nifedipine inhibits the progression of experimental AAA possibly through suppression of NF-kappaB and MMP-9 activity, leading to protective effects against AAA beyond those associated with blood pressure lowering.