Journal articles on the topic 'Adominal aortic aneurysms (AAAs)'
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1
Salmon, Morgan. "NADPH Oxidases in Aortic Aneurysms." Antioxidants 11, no. 9 (September 16, 2022): 1830. http://dx.doi.org/10.3390/antiox11091830.
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Abdominal aortic aneurysms (AAAs) are a progressive dilation of the infrarenal aorta and are characterized by inflammatory cell infiltration, smooth muscle cell migration and proliferation, and degradation of the extracellular matrix. Oxidative stress and the production of reactive oxygen species (ROS) have been shown to play roles in inflammatory cell infiltration, and smooth muscle cell migration and apoptosis in AAAs. In this review, we discuss the principles of nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase/NOX) signaling and activation. We also discuss the effects of some of the major mediators of NOX signaling in AAAs. Separately, we also discuss the influence of genetic or pharmacologic inhibitors of NADPH oxidases on experimental pre-clinical AAAs. Experimental evidence suggests that NADPH oxidases may be a promising future therapeutic target for developing pharmacologic treatment strategies for halting AAA progression or rupture prevention in the management of clinical AAAs.
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Lu, Hong, Debra L. Rateri, Dennis Bruemmer, Lisa A. Cassis, and Alan Daugherty. "Involvement of the renin–angiotensin system in abdominal and thoracic aortic aneurysms." Clinical Science 123, no. 9 (July 13, 2012): 531–43. http://dx.doi.org/10.1042/cs20120097.
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Aortic aneurysms are relatively common maladies that may lead to the devastating consequence of aortic rupture. AAAs (abdominal aortic aneurysms) and TAAs (thoracic aortic aneurysms) are two common forms of aneurysmal diseases in humans that appear to have distinct pathologies and mechanisms. Despite this divergence, there are numerous and consistent demonstrations that overactivation of the RAS (renin–angiotensin system) promotes both AAAs and TAAs in animal models. For example, in mice, both AAAs and TAAs are formed during infusion of AngII (angiotensin II), the major bioactive peptide in the RAS. There are many proposed mechanisms by which the RAS initiates and perpetuates aortic aneurysms, including effects of AngII on a diverse array of cell types and mediators. These experimental findings are complemented in humans by genetic association studies and retrospective analyses of clinical data that generally support a role of the RAS in both AAAs and TAAs. Given the lack of a validated pharmacological therapy for any form of aortic aneurysm, there is a pressing need to determine whether the consistent findings on the role of the RAS in animal models are translatable to humans afflicted with these diseases. The present review compiles the recent literature that has shown the RAS as a critical component in the pathogenesis of aortic aneurysms.
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Fairman, Alexander S., and Grace J. Wang. "Endovascular Treatment of Ruptured Abdominal Aortic Aneurysms." Seminars in Interventional Radiology 37, no. 04 (October 2020): 382–88. http://dx.doi.org/10.1055/s-0040-1715872.
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AbstractSince its inception in the 1990s, endovascular aortic repair has quickly replaced traditional open aortic repair (OAR) as the most common method for elective treatment of abdominal aortic aneurysms (AAA). After numerous iterations and failures of different endografts, the technology has undergone dramatic improvements with evidence pointing to this technology serving as a safe and durable modality, albeit with the requirement of routine surveillance. Not surprisingly, the ability to treat patients with AAAs with minimally invasive technology that could theoretically mitigate some of the risks associated with OAR, such as aortic cross clamping and significant blood loss, was also adopted in patients with ruptured AAAs and is now the preferred treatment method if anatomically feasible.
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Siika, Antti, Moritz Lindquist Liljeqvist, Rebecka Hultgren, T. Christian Gasser, and Joy Roy. "Aortic Lumen Area Is Increased in Ruptured Abdominal Aortic Aneurysms and Correlates to Biomechanical Rupture Risk." Journal of Endovascular Therapy 25, no. 6 (October 24, 2018): 750–56. http://dx.doi.org/10.1177/1526602818808292.
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Purpose: To investigate how 2-dimensional geometric parameters differ between ruptured and asymptomatic abdominal aortic aneurysms (AAAs) and provide a biomechanical explanation for the findings. Methods: The computed tomography angiography (CTA) scans of 30 patients (mean age 77±10 years; 23 men) with ruptured AAAs and 60 patients (mean age 76±8 years; 46 men) with asymptomatic AAAs were used to measure maximum sac diameter along the center lumen line, the cross-sectional lumen area, the total vessel area, the intraluminal thrombus (ILT) area, and corresponding volumes. The CTA data were segmented to create 3-dimensional patient-specific models for finite element analysis to compute peak wall stress (PWS) and the peak wall rupture index (PWRI). To reduce confounding from the maximum diameter, 2 diameter-matched groups were selected from the initial patient cohorts: 28 ruptured AAAs and another with 15 intact AAAs (diameters 74±12 vs 73±11, p=0.67). A multivariate model including the maximum diameter, the lumen area, and the ILT area of the 60 intact aneurysms was employed to predict biomechanical rupture risk parameters. Results: In the diameter-matched subgroup comparison, ruptured AAAs had a significantly larger cross-sectional lumen area (1954±1254 vs 1120±623 mm2, p=0.023) and lower ILT area ratio (55±24 vs 68±24, p=0.037). The ILT area (2836±1462 vs 2385±1364 mm2, p=0.282) and the total vessel area (3956±1170 vs 4338±1388 mm2, p=0.384) did not differ statistically between ruptured and intact aneurysms. The PWRI was increased in ruptured AAAs (0.80 vs 0.48, p<0.001), but the PWS was similar (249 vs 284 kPa, p=0.194). In multivariate regression analysis, lumen area was significantly positively associated with both PWS (p<0.001) and PWRI (p<0.01). The ILT area was also significantly positively associated with PWS (p<0.001) but only weakly with PWRI (p<0.01). The lumen area conferred a higher risk increase in both PWS and PWRI when compared with the ILT area. Conclusion: The lumen area is increased in ruptured AAAs compared to diameter-matched asymptomatic AAAs. Furthermore, this finding may in part be explained by a relationship with biomechanical rupture risk parameters, in which lumen area, irrespective of maximum diameter, increases PWS and PWRI. These observations thus suggest a possible method to improve prediction of rupture risk in AAAs by measuring the lumen area without the use of computational modeling.
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Paraskevas, Kosmas I., Dimitri P. Mikhailidis, and Athanasios D. Giannoukas. "Additional Issues on Screening, Prevention, and Treatment of Abdominal Aortic Aneurysms." American Journal of Men's Health 7, no. 6 (March 28, 2013): 472–74. http://dx.doi.org/10.1177/1557988313483306.
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The prevalence of abdominal aortic aneurysms (AAAs) and AAA-related deaths are steadily declining in some countries as a result of the reduction in smoking rates. It was thus suggested that screening programs that do not target high-risk populations are likely to have very low AAA detection rates. However, this may not apply to other countries that do not exhibit similar reductions in smoking rates. It was assumed that by using the U.S. Preventive Services Task Force screening criteria (men 65-75 years with smoking history) less than 30% of AAAs would be captured. A more extensive scoring system that includes additional risk factors such as the presence of carotid artery or peripheral arterial disease, obesity, hypertension, and so on, may identify almost 90% of AAAs. This article discusses this and other issues on screening, prevention, and treatment of AAAs.
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Zarins, Christopher K., and E. John Harris. "Operative Repair for Aortic Aneurysms: The Gold Standard." Journal of Endovascular Therapy 4, no. 3 (August 1997): 232–41. http://dx.doi.org/10.1177/152660289700400302.
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Surgical treatment of abdominal aortic aneurysm (AAA) is being challenged by newer, minimally invasive therapies. Such new treatment strategies will need to prove themselves against concurrent results of standard operative AAA repair, within defined medical risk and aneurysm morphological categories. We review the natural history of AAAs, the medical risk levels for elective AAA repair, aneurysm morphology and its impact on operative mortality, the issue of high-risk patient treatment, and the current standard of care for AAAs based on single-center, multicenter, and population-based statistics. In good-risk patients, aneurysms > 5 cm in diameter are best treated by replacement with a prosthetic graft. Operative mortality should be < 5% and 1-year survival > 90%. Aortic endograft techniques must meet or exceed these standards if they are to supplant standard surgical repair.
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Liu, Haole, Panpan Wei, Weilai Fu, Congcong Xia, Yankui Li, Kangli Tian, Yafeng Li, et al. "Dapagliflozin Ameliorates the Formation and Progression of Experimental Abdominal Aortic Aneurysms by Reducing Aortic Inflammation in Mice." Oxidative Medicine and Cellular Longevity 2022 (January 28, 2022): 1–11. http://dx.doi.org/10.1155/2022/8502059.
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Background. Dapagliflozin, a sodium glucose transporter protein-2 (SGLT-2) inhibitor, reduces the risk for cardiovascular diseases. However, the influence of dapagliflozin on nondissecting abdominal aortic aneurysms (AAAs) remains unclear. Methods. AAAs were created in male C57BL/6 mice via intra-aortic porcine pancreatic elastase (PPE) infusion. Mice were daily treated with dapagliflozin (1 or 5 mg/kg body weight) or an equal volume of vehicle through oral gavage beginning one day prior to PPE infusion for 14 days. To investigate its translational value, dapagliflozin or vehicle was also administered to mice with existing AAAs in another cohort. Aortic diameters were measured prior to (day 0 for baseline) and 14 days after PPE infusion. After sacrifice, mice aortae were collected, and following histological analyses were performed. Results. Dapagliflozin treatment significantly reduced aneurysmal aortic expansion following PPE infusion as compared to vehicle treatment especially at 5 mg/kg body weight (approximately 21% and 33% decreases in 1 and 5 mg/kg treatment groups, respectively). The dose-dependent attenuation of AAAs by dapagliflozin was also confirmed on histological analyses. Dapagliflozin remarkably reduced aortic accumulation of macrophages, CD4+ T cells, and B cells particularly following dapagliflozin treatment at 5 mg/kg. Dapagliflozin treatment also markedly attenuated medial SMC loss. Though the difference was not significant, dapagliflozin treatment tended to attenuate CD8+ T cells and elastin degradation. Dapagliflozin treatment at 5 mg/kg caused a 53% reduction in neovessel density. Furthermore, dapagliflozin treatment mitigated further progress of existing AAAs. Conclusion. Dapagliflozin treatment ameliorated PPE-induced AAAs by inhibiting aortic leukocytes infiltration and angiogenesis.
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Li, Zong-Zhuang, and Qiu-Yan Dai. "Pathogenesis of Abdominal Aortic Aneurysms: Role of Nicotine and Nicotinic Acetylcholine Receptors." Mediators of Inflammation 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/103120.
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Inflammation, proteolysis, smooth muscle cell apoptosis, and angiogenesis have been implicated in the pathogenesis of abdominal aortic aneurysms (AAAs), although the well-defined initiating mechanism is not fully understood. Matrix metalloproteinases (MMPs) such as MMP-2 and -9 and other proteinases degrading elastin and extracellular matrix are the critical pathogenesis of AAAs. Among the risk factors of AAAs, cigarette smoking is an irrefutable one. Cigarette smoke is practically involved in various aspects of the AAA pathogenesis. Nicotine, a major alkaloid in tobacco leaves and a primary component in cigarette smoke, can stimulate the MMPs expression by vascular SMCs, endothelial cells, and inflammatory cells in vascular wall and induce angiogenesis in the aneurysmal tissues. However, for the inflammatory and apoptotic processes in the pathogenesis of AAAs, nicotine seems to be moving in just the opposite direction. Additionally, the effects of nicotine are probably dose dependent or associated with the exposure duration and may be partly exerted by its receptors—nicotinic acetylcholine receptors (nAChRs). In this paper, we will mainly discuss the pathogenesis of AAAs involving inflammation, proteolysis, smooth muscle cell apoptosis and angiogenesis, and the roles of nicotine and nAChRs.
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Romary, Daniel J., Alycia G. Berman, and Craig J. Goergen. "High-frequency murine ultrasound provides enhanced metrics of BAPN-induced AAA growth." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 5 (November 1, 2019): H981—H990. http://dx.doi.org/10.1152/ajpheart.00300.2019.
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An abdominal aortic aneurysm (AAA), defined as a pathological expansion of the largest artery in the abdomen, is a common vascular disease that frequently leads to death if rupture occurs. Once diagnosed, clinicians typically evaluate the rupture risk based on maximum diameter of the aneurysm, a limited metric that is not accurate for all patients. In this study, we worked to evaluate additional distinguishing factors between growing and stable murine aneurysms toward the aim of eventually improving clinical rupture risk assessment. With the use of a relatively new mouse model that combines surgical application of topical elastase to cause initial aortic expansion and a lysyl oxidase inhibitor, β-aminopropionitrile (BAPN), in the drinking water, we were able to create large AAAs that expanded over 28 days. We further sought to develop and demonstrate applications of advanced imaging approaches, including four-dimensional ultrasound (4DUS), to evaluate alternative geometric and biomechanical parameters between 1) growing AAAs, 2) stable AAAs, and 3) nonaneurysmal control mice. Our study confirmed the reproducibility of this murine model and found reduced circumferential strain values, greater tortuosity, and increased elastin degradation in mice with aneurysms. We also found that expanding murine AAAs had increased peak wall stress and surface area per length compared with stable aneurysms. The results from this work provide clear growth patterns associated with BAPN-elastase murine aneurysms and demonstrate the capabilities of high-frequency ultrasound. These data could help lay the groundwork for improving insight into clinical prediction of AAA expansion. NEW & NOTEWORTHY This work characterizes a relatively new murine model of abdominal aortic aneurysms (AAAs) by quantifying vascular strain, stress, and geometry. Furthermore, Green-Lagrange strain was calculated with a novel mapping approach using four-dimensional ultrasound. We also compared growing and stable AAAs, finding peak wall stress and surface area per length to be most indicative of growth. In all AAAs, strain and elastin health declined, whereas tortuosity increased.
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Han, Yanshuo, Hao Zhang, Ce Bian, Chen Chen, Simei Tu, Jiahui Guo, Yihao Wu, Dittmar Böckler, and Jian Zhang. "Circular RNA Expression: Its Potential Regulation and Function in Abdominal Aortic Aneurysms." Oxidative Medicine and Cellular Longevity 2021 (June 29, 2021): 1–21. http://dx.doi.org/10.1155/2021/9934951.
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Abdominal aortic aneurysms (AAAs) have posed a great threat to human life, and the necessity of its monitoring and treatment is decided by symptomatology and/or the aneurysm size. Accumulating evidence suggests that circular RNAs (circRNAs) contribute a part to the pathogenesis of AAAs. circRNAs are novel single-stranded RNAs with a closed loop structure and high stability, having become the candidate biomarkers for numerous kinds of human disorders. Besides, circRNAs act as molecular “sponge” in organisms, capable of regulating the transcription level. Here, we characterize that the molecular mechanisms underlying the role of circRNAs in AAA development were further elucidated. In the present work, studies on the biosynthesis, bibliometrics, and mechanisms of action of circRNAs were aims comprehensively reviewed, the role of circRNAs in the AAA pathogenic mechanism was illustrated, and their potential in diagnosing AAAs was examined. Moreover, the current evidence about the effects of circRNAs on AAA development through modulating endothelial cells (ECs), macrophages, and vascular smooth muscle cells (VSMCs) was summarized. Through thorough investigation, the molecular mechanisms underlying the role of circRNAs in AAA development were further elucidated. The results demonstrated that circRNAs had the application potential in the diagnosis and prevention of AAAs in clinical practice. The study of circRNA regulatory pathways would be of great assistance to the etiologic research of AAAs.
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Chang, Tiffany W., Adam S. A. Gracon, Michael P. Murphy, and David S. Wilkes. "Exploring autoimmunity in the pathogenesis of abdominal aortic aneurysms." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 5 (September 2015): H719—H727. http://dx.doi.org/10.1152/ajpheart.00273.2015.
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The abdominal aortic aneurysm (AAA) is a disease process that carries significant morbidity and mortality in the absence of early identification and treatment. While current management includes surveillance and surgical treatment of low- and high-risk aneurysms, respectively, our narrow understanding of the pathophysiology of AAAs limits our ability to more effectively manage and perhaps even prevent the occurrence of this highly morbid disease. Over the past couple of decades, there has been considerable interest in exploring the role of autoimmunity as an etiological component of AAA. This review covers the current literature pertaining to this immunological process, focusing on research that highlights the local and systemic immune components found in both human patients and murine models. A better understanding of the autoimmune mechanisms in the pathogenesis of AAAs can pave the way to novel and improved treatment strategies in this patient population.
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Sprynger, Muriel, Michel Willems, Hendrik Van Damme, Benny Drieghe, J. C. Wautrecht, and Marie Moonen. "Screening Program of Abdominal Aortic Aneurysm." Angiology 70, no. 5 (January 17, 2019): 407–13. http://dx.doi.org/10.1177/0003319718824940.
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In Europe, the prevalence of abdominal aortic aneurysms (AAAs) in the elderly population (≥65 year old) has declined in the past decades to <4%. Aneurysmal degeneration of the aorta is a serious and potentially life-threatening vascular disease. Abdominal aortic aneurysms typically develop subclinically and often only become symptomatic when complicated by impending rupture. Most AAAs are discovered incidentally while investigating for an unrelated pathology. Ruptured AAA is the tenth leading cause of death in Belgium (0.32% of all deaths in 2014). Health-care providers have emphasized the importance of early detection of AAA and elective repair when the rupture risk outweighs operative risk (usual diameter threshold of 55 mm). Routine AAA screening programs, consisting of a single abdominal ultrasonography at the age of 65 years, aim to reduce the number of AAA-related deaths. Does population-based ultrasound screening for AAA achieve its objective and is it cost-effective? This literature review tries to answer these challenging questions.
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Makrygiannis, Georgios, Evanthia Mourmoura, Konstantinos Spanos, Nikolaos Roussas, Helena Kuivaniemi, Natzi Sakalihasan, Aspasia Tsezou, and Athanasios Giannoukas. "Risk Factor Assessment in a Greek Cohort of Patients With Large Abdominal Aortic Aneurysms." Angiology 70, no. 1 (May 8, 2018): 35–40. http://dx.doi.org/10.1177/0003319718774474.
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Environmental and genetic risk factors contribute to the etiology of abdominal aortic aneurysms (AAAs). Matrix metalloproteinases (MMPs) have been associated with the pathophysiology of AAAs. A prospective, nonrandomized case–control study was undertaken to investigate the risk factors for large AAAs (≥5.5 cm) among 175 male Greek AAA patients and to compare the results with a cohort of 166 male controls free from any aortic dilatation, as confirmed by ultrasonography from an existing AAA screening program in the same region. We also assessed the potential association between 2 functional single nucleotide polymorphisms in the genes MMP9 (−1561C/T; rs3918242) and MMP13 (−77A/G; rs2252070), and the presence of large AAAs. Multiple logistic regression analysis revealed AAA family history ( P = .028), hypercholesterolemia ( P < .001), and current smoking ( P < .001) as AAA risk factors. Statistical difference was reached in genotype ( P = .047) and allele ( P = .037) frequencies for rs2252070, but the results did not remain significant after correction for multiple testing. No significant differences in genotype or allele frequencies for rs3918242 were detected. In summary, AAA family history, hypercholesterolemia, and current smoking were found to be risk factors for large AAAs.
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Finol, Ender A., and Cristina H. Amon. "Blood Flow in Abdominal Aortic Aneurysms: Pulsatile Flow Hemodynamics." Journal of Biomechanical Engineering 123, no. 5 (May 15, 2001): 474–84. http://dx.doi.org/10.1115/1.1395573.
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Numerical predictions of blood flow patterns and hemodynamic stresses in Abdominal Aortic Aneurysms (AAAs) are performed in a two-aneurysm, axisymmetric, rigid wall model using the spectral element method. Physiologically realistic aortic blood flow is simulated under pulsatile conditions for the range of time-averaged Reynolds numbers 50⩽Rem⩽300, corresponding to a range of peak Reynolds numbers 262.5⩽Repeak⩽1575. The vortex dynamics induced by pulsatile flow in AAAs is characterized by a sequence of five different flow phases in one period of the flow cycle. Hemodynamic disturbance is evaluated for a modified set of indicator functions, which include wall pressure pw, wall shear stress τw, and Wall Shear Stress Gradient (WSSG). At peak flow, the highest shear stress and WSSG levels are obtained downstream of both aneurysms, in a pattern similar to that of steady flow. Maximum values of wall shear stresses and wall shear stress gradients obtained at peak flow are evaluated as a function of the time-average Reynolds number resulting in a fourth order polynomial correlation. A comparison between predictions for steady and pulsatile flow is presented, illustrating the importance of considering time-dependent flow for the evaluation of hemodynamic indicators.
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Georgakarakos, Efstratios, George S. Georgiadis, Evagelos Nikolopoulos, George Trellopoulos, Konstantinos Kapoulas, and Miltos Lazarides. "Technical Advances With Newer Aortic Endografts Provide Additional Support to Withhold the Early Endovascular Repair of Small Abdominal Aortic Aneurysms Until it is Really Needed." Vascular and Endovascular Surgery 46, no. 5 (May 15, 2012): 374–77. http://dx.doi.org/10.1177/1538574412445601.
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The idea of early endovascular aortic repair (EVAR) of “small” abdominal aortic aneurysms (AAAs) has gained attention over “watchful waiting,” mostly due to the concern for losing the anatomic suitability for endovascular repair over time. Generally, small AAAs have longer, smaller, less angulated necks, and less tortuous iliac arteries than larger ones. Though the borderline anatomic characteristics were assumed to be contraindications for older generation endografts, the modifications of modern devices seem promising to overcome those limitations, in order to treat the small AAAs when reaching the 5.5 cm threshold. Moreover, early endovascular intervention has been proven neither cost effective nor beneficial for the patients’ quality of life. This article evaluates the technical progress that could overcome the difficulties of those small AAAs that present technically demanding anatomies, thus advocating endovascular intervention when they reach the diameter threshold.
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Nordon, Ian M., Robert J. Hinchliffe, Peter J. Holt, Ian M. Loftus, and Matthew M. Thompson. "Review of Current Theories for Abdominal Aortic Aneurysm Pathogenesis." Vascular 17, no. 5 (January 1, 2009): 253–63. http://dx.doi.org/10.2310/6670.2009.00046.
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Atherosclerotic plaques are a feature of abdominal aortic aneurysms (AAAs). Atherosclerosis and AAA appear to share similar risk factors. These observations have led to the conclusion that AAAs are a consequence of advanced atherosclerosis. This review explores current theories regarding the pathogenesis of AAA and their implications for treatment. A systematic literature search was conducted using the search terms abdominal aortic aneurysm, atherosclerosis, pathogenesis, and systemic disease. Articles were categorized according to the association of AAAs with atherosclerosis, arteriomegaly, peripheral aneurysm, systemic expression, genetics, autoimmunity, oxidative stress, and systemic disease. Twenty-nine articles reporting changes in the systemic vasculature associated with AAA and 12 articles examining the shared risk factor hypothesis were identified. There is insufficient evidence to confirm that AAAs are the result of advanced atherosclerosis. The bulk of evidence points to AAA disease being a systemic disease of the vasculature, with a predetermined genetic susceptibility leading to a phenotype governed by environmental factors.
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Finol, E. A., K. Keyhani, and C. H. Amon. "The Effect of Asymmetry in Abdominal Aortic Aneurysms Under Physiologically Realistic Pulsatile Flow Conditions." Journal of Biomechanical Engineering 125, no. 2 (April 1, 2003): 207–17. http://dx.doi.org/10.1115/1.1543991.
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In the abdominal segment of the human aorta under a patient’s average resting conditions, pulsatile blood flow exhibits complex laminar patterns with secondary flows induced by adjacent branches and irregular vessel geometries. The flow dynamics becomes more complex when there is a pathological condition that causes changes in the normal structural composition of the vessel wall, for example, in the presence of an aneurysm. This work examines the hemodynamics of pulsatile blood flow in hypothetical three-dimensional models of abdominal aortic aneurysms (AAAs). Numerical predictions of blood flow patterns and hemodynamic stresses in AAAs are performed in single-aneurysm, asymmetric, rigid wall models using the finite element method. We characterize pulsatile flow dynamics in AAAs for average resting conditions by means of identifying regions of disturbed flow and quantifying the disturbance by evaluating flow-induced stresses at the aneurysm wall, specifically wall pressure and wall shear stress. Physiologically realistic abdominal aortic blood flow is simulated under pulsatile conditions for the range of time-average Reynolds numbers 50⩽Rem⩽300, corresponding to a range of peak Reynolds numbers 262.5⩽Repeak⩽1575. The vortex dynamics induced by pulsatile flow in AAAs is depicted by a sequence of four different flow phases in one period of the cardiac pulse. Peak wall shear stress and peak wall pressure are reported as a function of the time-average Reynolds number and aneurysm asymmetry. The effect of asymmetry in hypothetically shaped AAAs is to increase the maximum wall shear stress at peak flow and to induce the appearance of secondary flows in late diastole.
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Gomes, Giovanna Ricarte Granja, Marcos Cordeiro D’Ornellas, and Gustavo Nogara Dotto. "Direct and virtual measurements of abdominal aortic aneurysms: three-dimensional printed models." Radiologia Brasileira 54, no. 1 (February 2021): 21–26. http://dx.doi.org/10.1590/0100-3984.2019.0117.
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Abstract Objective: To validate the use of a three-dimensional printing system for metric and volumetric analysis of the segments of an abdominal aortic aneurysm (AAA). Materials and Methods: In patients scheduled to undergo endovascular AAA repair, the computed tomography angiography (CTA) measurements obtained during the preoperative assessment of the patients were compared with those obtained by computed tomography of individualized three-dimensional biomodels. Results: The volumetric assessment showed a discrepancy of 3-12%, and the difference between the areas was 10-16%. Conclusion: Computed tomography measurements of 3D-printed biomodels of AAAs appear to be comparable to those of threedimensional CTA measurements of the same AAAs, in terms of the metric and volumetric dimensions.
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Galiñanes, Edgar Luis, Eduardo A. Hernandez-Vila, and Zvonimir Krajcer. "EndoAnchors Minimize Endoleaks in Chimney-Graft Endovascular Repair of Juxtarenal Abdominal Aortic Aneurysms." Texas Heart Institute Journal 46, no. 3 (June 1, 2019): 183–88. http://dx.doi.org/10.14503/thij-17-6520.
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Juxtarenal abdominal aortic aneurysms (AAAs) are difficult to treat because they often have little or no proximal aortic neck. Patients with this complex anatomy are not usually candidates for an endovascular aneurysm repair (EVAR). Chimney-graft EVAR has been introduced, but type Ia endoleak is a typical risk. We have begun using EndoAnchors to determine whether this risk can be reduced. From July 2013 through July 2014, we used the chimney-graft EVAR technique in 5 patients whose juxtarenal AAAs had a short or no proximal aortic neck. During the procedure, we implanted EndoAnchors as needed. Postprocedurally, at 30 days, and through end of follow-up (duration, 11–18 mo), all patients had patent endografts without type Ia endoleak (our primary endpoint), visceral stent-graft thrombosis, or renal complications. One patient who received 4 chimney grafts had a postprocedural type II endoleak, which was treated with embolization. We found it feasible to use EndoAnchors with the chimney-graft technique to prevent type Ia endoleaks in the treatment of juxtarenal AAAs. Further studies are needed to validate this adjunctive technique and to determine its durability.
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Moniaci, D., P. Brustia, A. Renghi, F. Casella, L. De Simeis, G. Guzzardi, R. Fossaceca, and L. Gramaglia. "Abdominal aortic aneurysm treatment: minimally invasive fast-track surgery and endovascular technique." Vascular 19, no. 5 (September 8, 2011): 233–41. http://dx.doi.org/10.1258/vasc.2010.oa0271.
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In our department we started a program in order to offer a mini-invasive approach to all patients affected by abdominal aortic aneurysms (AAAs), trying to offer this option also to patients not eligible for endovascular aneurysm repair (EVAR) due to unfavorable anatomy, age under 65 years and aorto-iliac occlusive disease, considering nowadays EVAR is the gold-standard for the mini-invasive treatment of AAAs. The aim of this study was to compare endovascular versus fast-track surgical treatment in patients undergoing elective surgery for AAAs. We wanted to verify if it was possible to be totally mini-invasive in the treatment of AAAs. A total of 128 patients were chosen for the study. Ninety-four patients were enrolled in the OPEN group and 34 were enrolled in the EVAR group. This study demonstrates that minimally invasive treatment with the fast-track protocol may be a valid alternative to EVAR.
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Weiss, Norbert, Roman N. Rodionov, and Adrian Mahlmann. "Medical management of abdominal aortic aneurysms." Vasa 43, no. 6 (November 1, 2014): 415–21. http://dx.doi.org/10.1024/0301-1526/a000388.
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Abdominal aortic aneurysms (AAA) are the most common arterial aneurysms. Endovascular or open surgical aneurysm repair is indicated in patients with large AAA ≥ 5.5 cm in diameter as this prevents aneurysm rupture. The presence even of small AAAs not in need of immediate repair is associated with a very high cardiovascular risk including myocardial infarction, stroke or cardiovascular death. This risk by far exceeds the risk of aneurysm rupture. These patients therefore should be considered as high-risk patients and receive optimal medical treatment and life-style modificiation of their cardiovascular risk factors to improve their prognosis. In addition, these patients should be followed-up for aneurysm growth and receive medical treatment to decrease aneurym progression and rupture rate. Treatment with statins has been shown to reduce cardiovascular mortality in these patients, and also slows the rate of AAA growth. Use of beta-blockers, ACE inhibitors and AT1-receptor antagonists does not affect AAA growth but may be indicated for comorbidities. Antibiotic therapy with roxithromycin has a small effect on AAA growth, but this effect must be critically weighed against the potential risk of wide-spread use of antibiotics.
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Di Achille, P., G. Tellides, C. A. Figueroa, and J. D. Humphrey. "A haemodynamic predictor of intraluminal thrombus formation in abdominal aortic aneurysms." Proceedings of the Royal Society A: Mathematical, Physical and Engineering Sciences 470, no. 2172 (December 8, 2014): 20140163. http://dx.doi.org/10.1098/rspa.2014.0163.
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Intraluminal thrombus (ILT) is present in over 75% of all abdominal aortic aneurysms (AAAs) and probably contributes to the complex biomechanics and pathobiology of these lesions. A reliable predictor of thrombus formation in enlarging lesions could thereby aid clinicians in treatment planning. The primary goal of this work was to identify a new phenomenological metric having clinical utility that is motivated by the hypothesis that two basic haemodynamic features must coincide spatially and temporally to promote the formation of a thrombus on an intact endothelium—platelets must be activated within a shear flow and then be presented to a susceptible endothelium. Towards this end, we propose a new thrombus formation potential (TFP) that combines information on the flow-induced shear history experienced by blood-borne particles that come in close proximity to the endothelium with information on both the time-averaged wall shear stress (WSS) and the oscillatory shear index (OSI) that locally affect the endothelial mechanobiology. To illustrate the possible utility of this new metric, we show computational results for 10 carotid arteries from five patients where regions of low WSS and high OSI tend not to be presented with activated platelets (i.e. they have a low TFP), consistent with the thrombo-resistance of the healthy carotid despite its complex haemodynamics. Conversely, we show results for three patients that high TFP co-localizes with regions of observed thin thrombus in AAAs, which contrasts with findings of low TFP for the abdominal aorta of three healthy subjects. We submit that these promising results suggest the need for further consideration of the TFP, or a similar combined metric, as a potentially useful clinical predictor of the possible formation of ILT in AAAs.
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Tian, Kangli, Congcong Xia, Haole Liu, Boyu Xu, Panpan Wei, Weilai Fu, Ming Lu, et al. "Temporal and Quantitative Analysis of Aortic Immunopathologies in Elastase-Induced Mouse Abdominal Aortic Aneurysms." Journal of Immunology Research 2021 (November 16, 2021): 1–10. http://dx.doi.org/10.1155/2021/6297332.
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Objective. Elastase-induced abdominal aortic aneurysm (AAA) model is widely used for aneurysmal pathogenesis and translational research. However, temporal alternations in aneurysmal histologies remain unknown. This study is aimed at analyzing temporal immunopathologies of aneurysmal aorta following experimental AAA induction. Methods. Male C57BL/6J mice at the age of 10-14 weeks received intra-aortic infusion of elastase to induce AAAs. Aortic diameters at the baseline and indicated days after AAA induction were measured, and aortae were collected for histopathological analysis. Results. Aorta diameters increased from 0.52 mm at the baseline levels to 0.99 mm, 1.34 mm, and 1.41 mm at days 7, 14, and 28, respectively, corresponding 90%, 158%, and 171% increases over the baseline level. Average aortic diameters did not differ between days 14 and 28. Severe elastin degradation and smooth muscle cell depletion were found at days 14 and 28 as compared to the baseline and day 7. No difference in the scores of medial elastin and SMC destruction was noted between days 14 and 28. Consistent results were found for leukocyte accumulation, neoangiogenesis, and matrix metalloproteinase expression. Twenty-eight days after AAA induction, all aneurysmal pathologies showed an attenuated trend, although most histopathological parameters did no differ between days 14 and 28. Conclusion. Our data suggest that almost aneurysmal immunohistopathologies reach maximal 14 days following AAA induction. Analysis of day 14 histologies is sufficient for AAA pathogenesis and translational studies in elastase-induced mouse experimental AAAs.
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Blackstock, Christopher D., and Benjamin M. Jackson. "Open Surgical Repair of Abdominal Aortic Aneurysms Maintains a Pivotal Role in the Endovascular Era." Seminars in Interventional Radiology 37, no. 04 (October 2020): 346–55. http://dx.doi.org/10.1055/s-0040-1715881.
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AbstractSince the advent of endovascular aortic repair (EVAR) nearly three decades ago, there has been a paradigm shift in the treatment of the abdominal aortic aneurysm (AAA) to favor EVAR due to its reduced operative mortality, less invasive nature, and faster recovery times. However, more recently there has been an accumulation of data from large meta-analyses and randomized clinical trials revealing that EVAR has no survival benefit after approximately 2 years and is associated with substantially higher rates of reintervention and aneurysm rupture in the long term. These findings call into question the durability of EVAR compared with open aortic repair and emphasize the need for surgeons to remain competent with open aortic surgery in the modern era. This article will provide comprehensive review of a large body of literature comparing endovascular repair to open aortic surgery for the management of AAAs, and it will offer an overview of the open surgical repair technique for AAAs.
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Greenberg, Roy K., Sunita D. Srivastava, Kenneth Ouriel, David Waldman, Krasnodar Ivancev, Karl A. Illig, Cynthia Shortell, and Richard M. Green. "An Endoluminal Method of Hemorrhage Control and Repair of Ruptured Abdominal Aortic Aneurysms." Journal of Endovascular Therapy 7, no. 1 (February 2000): 1–7. http://dx.doi.org/10.1177/152660280000700101.
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Purpose: To report our initial experience with endovascular grafting to treat ruptured abdominal aortic aneurysms (AAAs). Methods: Three consecutive patients with severe comorbid illnesses and symptoms of aneurysm rupture and hemodynamic instability were treated with aortomonoiliac grafts. The Z-stent—based devices were implanted with the assistance of an occlusion balloon placed in the distal descending thoracic aorta. Results: All patients survived the procedure with successfully excluded AAAs. Two patients had relatively short hospital stays (4 and 14 days), while the third required prolonged treatment for pre-existing conditions. All patients required blood transfusions; 2 developed significant coagulopathies. Definitive management was delayed significantly by imaging protocols and graft construction. Conclusions: Endovascular repair of ruptured aortic aneurysms is feasible. Proximal aortic control is readily attainable with the use of an aortic occlusion balloon placed through the left axillary artery. The absence of a laparotomy, extensive retroperitoneal dissection, and aortic cross-clamping likely contributes to patient survival; however, the delay in operative therapy to obtain adequate imaging and construct an endograft could be a hindrance to the ultimate success of this approach. The concepts of alternative aortic imaging techniques and endograft design, construction, and storage must be addressed.
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Xu, Baohui, Hongping Deng, Gang Li, Naoki Fujimura, Yuko Furusho, and Ronald L. Dalman. "Deletion of CCL2 in mesenchymal stem cells suppresses experimental aortic aneurysms." Journal of Immunology 198, no. 1_Supplement (May 1, 2017): 69.3. http://dx.doi.org/10.4049/jimmunol.198.supp.69.3.
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Abstract Abdominal aortic aneurysm (AAA) is a macrophage-mediated chronic inflammatory disease. Aortic mural macrophages arise from bone marrow-derived circulating monocytes, recruited to the aneurysmal aorta by CCL2/CCR2 signaling. Given the importance of mesenchymal stem cell (MSC)-derived CCL2 in bone marrow monocyte mobilization, we hypothesized that MSC-derived CCL2 contributes to AAA pathogenesis. AAAs were created in 10–12 weeks old, male MSC-specific CCL2 knockout (Nestin+/CCL2 Flox+/+) and wild type (CCL2 Flox+/+) mice via intra-aortic elastase infusion. AAA incidence and progression were assessed via serial in vivo ultrasound aortic diameter measurements and histopathological analysis at sacrifice. MSC cell-specific CCL2 ablation significantly reduced circulating Ly-6Chigh inflammatory monocytes at baseline as well as 3 hours following lipopolysaccharide injection. Following elastase infusion, wild type mice demonstrated progressive, time-dependent aortic enlargement beginning on day 3. In MSC-specific CCL2 knockout mice, elastase-induced aortic enlargement was substantially suppressed, and medial elastin lamellae and smooth muscle cell cellularity were preserved compared to that demonstrated in wild type AAA mice. Mural macrophages, T and B cell infiltration were all also significantly attenuated in knockout, as compared to wild type, mice. Additionally, aortic neoangiogenesis, as defined by mural CD31+ capillary vessel density, was significantly reduced in knockout mice. Taken together, this evidence suggests that MSC-specific CCL2 deletion suppresses progression of experimental AAAs, in conjunction with attenuation of aortic mural inflammation and angiogenesis.
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Ammar, Alex D. "Mortality for Open Abdominal Aortic Aneurysm Repair before and after Endovascular Aortic Repair (EVAR)." American Surgeon 85, no. 12 (December 2019): 1341–44. http://dx.doi.org/10.1177/000313481908501226.
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The purpose of this study was to determine whether endovascular aortic repair (EVAR) has impacted inhospital mortality for patients undergoing open repair (OR). From 1982 through 2016, 1572 repairs were performed for abdominal aortic aneurysms (AAAs). Both ORs and EVARs were performed by the author at two large, tertiary-care, community-based hospitals. In Period I (1982–1999, n = 863), all AAA repairs were performed open. In Period II (2000–2016; n = 709), repairs were performed both by ORs and EVARs. Demographics were similar between study groups. Mortality for elective repairs in Periods I and II were as follows: I = 1.2 per cent (open, n = 9/756) versus II = 1.7 per cent (open, n = 4/241) versus II = 1.2 per cent (EVAR, n = 5/420). Mortality for patients with ruptured AAAs in Periods I and II were as follows: I = 31.8 per cent (open, n = 34/107) versus II = 32 per cent (open, n = 8/25) versus II = 13 per cent (EVAR, n = 3/23). The results of this study demonstrate that the introduction of EVARs has not negatively impacted the inhospital mortality for elective ORs or emergent AAAs for one vascular surgeon who completed training before EVARs became available.
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Police, Sara B., Kelly Putnam, Sean Thatcher, Frederique Batifoulier-Yiannikouris, Alan Daugherty, and Lisa A. Cassis. "Weight loss in obese C57BL/6 mice limits adventitial expansion of established angiotensin II-induced abdominal aortic aneurysms." American Journal of Physiology-Heart and Circulatory Physiology 298, no. 6 (June 2010): H1932—H1938. http://dx.doi.org/10.1152/ajpheart.00961.2009.
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Previous studies demonstrated that obesity increases inflammation in periaortic adipose tissue and promotes angiotensin II (ANG II)-induced abdominal aortic aneurysms (AAAs). We sought to determine whether weight loss of obese C57BL/6 mice would influence the progression of established AAAs. Male C57BL/6 mice were fed a high-fat diet (HF) for 4 mo and then infused with either saline or ANG II (1,000 ng·kg−1·min−1) for 3 mo. Mice with dilated suprarenal aortas at 28 days of ANG II infusion were designated to groups fed the HF (HF/HF) or a low-fat diet (LF; 10% kcal as fat; HF/LF) to induce weight loss for the last 2 mo of infusions. Suprarenal aortic lumen diameters of obese mice were increased by ANG II infusion at day 28 ( day 0: 1.03 ± 0.02; day 28: 1.86 ± 0.14 mm; P < 0.05), but did not progress with continued infusion in HF/HF mice. Moreover, aortic lumen diameters were not different between groups (HF/HF: 1.89 ± 0.15; HF/LF: 1.79 ± 0.18 mm). However, maximal diameters of excised AAAs were decreased with weight loss (HF/HF: 2.00 ± 0.11; HF/LF: 1.55 ± 0.13 mm; P < 0.05) and had reduced adventitial areas (HF/HF: 1.18 ± 0.10; HF/LF: 0.54 ± 0.02 mm2; P < 0.05). Neovascularization of aortic adventitias was strikingly decreased in HF/LF mice (HF/HF: 43 ± 5; HF/LF: 12 ± 2 endothelial cells/adventitial area; P < 0.05). ANG II-induced elevations in adipose mRNA abundance of CD105, an adipose-derived stem cell marker, were abolished with weight loss. These results demonstrate that weight loss limits adventitial expansion of ANG II-induced AAAs. Reduced neovascularization from weight loss may limit progression of AAAs.
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Kim, Hyangkyoung, Sungsin Cho, Natzi Sakalihasan, Rebecka Hultgren, and Jin Hyun Joh. "Prevalence and Risk Factors of Abdominal Aortic Aneurysms Detected with Ultrasound in Korea and Belgium." Journal of Clinical Medicine 12, no. 2 (January 6, 2023): 484. http://dx.doi.org/10.3390/jcm12020484.
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The objective was to investigate the prevalence of abdominal aortic aneurysms (AAAs) and the diameters of the aorta and common iliac arteries (CIAs) in a Korean cohort and secondly to analyze the differences in aortic diameter by comparison with a European cohort. The Korean cohort included participants ≥ 50 years who consented to AAA screening and data were analysed retrospectively. Aortic and common iliac diameters were measured using the outer-to-outer diameter method and prevalence rates were calculated. Common risk factors such as smoking, body mass index, pulmonary disease, hypertension, diabetes, hyperlipidaemia, ischaemic heart disease, and cerebrovascular disease were reported in association with AAA occurrence and AAA development. The aortic diameters were then compared with those in a Belgian cohort of 2487 participants identified in the Liège AAA Screening Program. An aortic size index (ASI) was also calculated to account for the potential size differences in the Belgian and Korean populations. A total of 3124 Korean participants were examined using ultrasound. The prevalence of AAAs in this cohort was 0.7%. The combined prevalence of subaneurysmal dilatation and AAA was 1.5%. The prevalence in male smokers older than 65 years was 2.7% (19/715). The mean infrarenal aortic diameter was 17.3 ± 3.1 mm in men and 15.7 ± 2.7 mm in women; the corresponding values in Belgian participants were 19.4 ± 3.0 mm in men and 17.9 ± 2.4 mm in women. The median aortic size index was 0.99 (interquartile range 0.88–1.12). The mean infrarenal aortic diameter was significantly smaller in the Korean cohort than in the Belgian cohort. Considering the observed prevalence of AAAs in different age groups, the age groups which would contribute to most cases was male persons above 66 years in both cohorts.
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Daugherty, Alan, Debra L. Rateri, Israel F. Charo, A. Phillip Owens, Deborah A. Howatt, and Lisa A. Cassis. "Angiotensin II infusion promotes ascending aortic aneurysms: attenuation by CCR2 deficiency in apoE−/− mice." Clinical Science 118, no. 11 (March 9, 2010): 681–89. http://dx.doi.org/10.1042/cs20090372.
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AngII (angiotensin II) induces atherosclerosis and AAAs (abdominal aortic aneurysms) through multiple proposed mechanisms, including chemotaxis. Therefore, we determined the effects of whole-body deficiency of the chemokine receptor CCR2 (CC chemokine receptor 2) on these diseases. To meet this objective, apoE (apolipoprotein E)−/− mice that were either CCR2+/+ or CCR2−/−, were infused with either saline or AngII (1000 ng·kg−1 of body weight·min−1) for 28 days via mini-osmotic pumps. Deficiency of CCR2 markedly attenuated both atherosclerosis and AAAs, unrelated to systolic blood pressure or plasma cholesterol concentrations. During the course of the present study, we also observed that AngII infusion led to large dilatations that were restricted to the ascending aortic region of apoE−/− mice. The aortic media in most of the dilated area was thickened. In regions of medial thickening, distinct elastin layers were discernable. There was an expansion of the distance between elastin layers in a gradient from the intimal to the adventitial aspect of the media. This pathology differed in a circumscribed area of the anterior region of ascending aortas in which elastin breaks were focal and almost transmural. All regions of the ascending aorta of AngII-infused mice had diffuse medial macrophage accumulation. Deficiency of CCR2 greatly attenuated the AngII-induced lumen dilatation in the ascending aorta. This new model of ascending aortic aneurysms has pathology that differs markedly from AngII-induced atherosclerosis or AAAs, but all vascular pathologies were attenuated by CCR2 deficiency.
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Shoji, Takahiro, Jia Guo, Yingbin Ge, Yankui Li, Gang Li, Toru Ikezoe, Wei Wang, et al. "Type I Interferon Receptor Subunit 1 Deletion Attenuates Experimental Abdominal Aortic Aneurysm Formation." Biomolecules 12, no. 10 (October 21, 2022): 1541. http://dx.doi.org/10.3390/biom12101541.
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Objective: Type I interferon receptor signaling contributes to several autoimmune and vascular diseases such as lupus, atherosclerosis and stroke. The purpose of this study was to assess the influence of type I interferon receptor deficiency on the formation and progression of experimental abdominal aortic aneurysms (AAAs). Methods: AAAs were induced in type I interferon receptor subunit 1 (IFNAR1)-deficient and wild type control male mice via intra-infrarenal aortic infusion of porcine pancreatic elastase. Immunostaining for IFNAR1 was evaluated in experimental and clinical aneurysmal abdominal aortae. The initiation and progression of experimental AAAs were assessed via ultrasound imaging prior to (day 0) and days 3, 7 and 14 following elastase infusion. Aneurysmal histopathology was analyzed at sacrifice. Results: Increased aortic medial and adventitial IFNAR1 expression was present in both clinical AAAs harvested at surgery and experimental AAAs. Following AAA induction, wild type mice experienced progressive, time-dependent infrarenal aortic enlargement. This progression was substantially attenuated in IFNAR1-deficient mice. On histological analyses, medial elastin degradation, smooth muscle cell depletion, leukocyte accumulation and neoangiogenesis were markedly diminished in IFNAR1-deficient mice in comparison to wild type mice. Conclusion: IFNAR1 deficiency limited experimental AAA progression in response to intra-aortic elastase infusion. Combined with clinical observations, these results suggest an important role for IFNAR1 activity in AAA pathogenesis.
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Sansone, Fabrizio, Edoardo Zingarelli, Fabrizio Ceresa, and Francesco Patanè. "Partial Aortic Root Remodeling in Case of Ascending Aortic Aneurysms." Innovations: Technology and Techniques in Cardiothoracic and Vascular Surgery 8, no. 4 (June 2013): 1–5. http://dx.doi.org/10.1097/imi.0b013e3182a754b6.
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Objective In degenerative ascending aortic aneurysms (AAAs), the pathological process may extend into the aortic root, causing aortic regurgitation (AR). As often one or two sinuses are involved, ascending aorta replacement should be associated with selected sinus replacement. Methods Thirty patients (21 men and 9 women; mean ± SD age, 70.0 ± 10.4) were operated on for ascending aorta and selected sinus replacement. All patients had degenerative AAA with sinotubular junction and partial root dilatation: one or two sinuses of Valsalva were involved. Mild to moderate-severe AR was present in all patients. The mean ± SD logistic EUROscore 1 was 15.4 ± 12.5. Twenty patients had ascending aorta replacement associated with noncoronary sinus replacement; 8 patients, associated with both right and noncoronary sinuses; 1 patient, associated with both left and noncoronary sinuses; and 1 patient, associated with left coronary sinus alone. Results There were no hospital or late deaths. No thromboembolic event or bleeding complications were reported. Postoperative echocardiography did not show significant AR, and computed tomographic scanning revealed a normal positioning of the vascular graft in the ascending aorta. Conclusions Remodeling of the sinotubular junction with selected sinus replacement in degenerative AAA is a valuable approach for aortic root remodeling, leading to a significant reduction of AR when the aortic leaflets are normal.
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Davidović, Lazar. "Open surgical treatment of abdominal aortic aneurysms in the endovascular era." Galenika Medical Journal 1, no. 1 (2022): 9–14. http://dx.doi.org/10.5937/galmed2201009d.
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In addition to the well-known benefits, endovascular treatment (EVAR) of abdominal aortic aneurysms has its drawbacks and limitations. That is why open surgery (OS) still has a very important place. OS should be considered as the first treatment option for degenerative AAAs with either favorable or unfavorable anatomy in low-risk patients with long life expectancy. When it comes to inflammatory AAA, OS is indicated only in patients at low risk and hydronephrosis. OS is the "gold standard" for the definitive treatment of mycotic AAAs. In cases of complete thrombosis AAA is the only viable OS. OS is the method of choice in AAA with associated significant accessory renal arteries. OS is the method of choice for the treatment of AAA in patients with connective tissue disorders. Different types of endolic, infection, collapse and stent graft migration, or aneurysmal sac rupture, require late open surgical conversion after EVAR. OS is indicated if patients with RAAA are severely hemodynamically unstable, if they do not have a favorable anatomy, or if they have a large retroperitoneal hematoma. OS AAA can be performed only in centers with a large volume of work by experienced surgeons. The younger generation of vascular surgeons must be educated for both EVAR and OH AAA.
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Sevil, Fehim Can, Mehmet Tort, Çiğdem Özer Gökaslan, Hülya Sevil, and Necip Becit. "Incidence, follow-up and outcomes of incidental abdominal aortic aneurysms in computed tomography." Interactive CardioVascular and Thoracic Surgery 34, no. 4 (November 11, 2021): 645–51. http://dx.doi.org/10.1093/icvts/ivab319.
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Abstract OBJECTIVES The goal of our study was to determine the prevalence of abdominal aortic aneurysms (AAAs) that were incidentally diagnosed by computed tomography applied for different reasons and to discuss the risk factors that may cause AAA. METHODS A total of 5396 abdominal computed tomography examinations were performed, and the 103 incidentally detected AAAs were included in the study. Patients with and without AAA were compared in terms of age, gender, thoracic and abdominal aortic diameters and comorbid diseases. RESULTS The prevalence of the AAAs was 1.9%. Old age and male gender were significantly different between the groups (P < 0.001). The reason for applying computed tomography in 52 (50.5%) patients with AAA was associated with malignancy. In the evaluation of all patients in the study, the aortic diameter was determined to be larger in patients with malignancy than in patients without malignancy (18.07 ± 4.1 mm vs 17.7 ± 3.9 mm, respectively; P < 0.001). The thoracic aortic diameter was wider in patients with AAA compared to that in patients without AAA (37.2 ± 3.9 mm vs 33.9 ± 5.2 mm, respectively; P < 0.001). The presence of coronary artery disease, diabetes mellitus, hypertension and a history of smoking in patients with AAA was significantly different from that of patients without AAA (P < 0.001). There was no significant difference between the groups in terms of hyperlipidaemia and chronic obstructive pulmonary disease (P = 0.52 and P = 0.15, respectively). CONCLUSIONS Screening of older men with diseases such as malignancy, hypertension, diabetes mellitus and coronary artery disease for AAA is important for the early diagnosis and treatment of this disease.
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Jim, Jeffrey, Andres Fajardo, Patrick J. Geraghty, and Luis A. Sanchez. "Use of Zenith TX2 endografts in endovascular abdominal aortic aneurysm repair for large-diameter aortic necks." Vascular 20, no. 2 (March 22, 2012): 113–17. http://dx.doi.org/10.1258/vasc.2011.cr0289.
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The purpose of this case report is to describe the use of thoracic endografts in endovascular repair of abdominal aortic aneurysms (AAAs) with large-diameter aortic necks. We present four patients who underwent elective repair of AAAs. Preoperative imaging demonstrated all to have large aortic necks (35–37 mm) precluding treatment with standard abdominal aortic devices. All underwent endovascular treatment, which included the use of a Zenith TX2 endograft (Cook Medical Incorporated, Bloomington, IN, USA) as a proximal aortic cuff. There was 100% technical success. One patient developed gastrointestinal bleeding and a myocardial infarction. All were subsequently discharged home. On follow-up, there was one aneurysm-related death at three months. The remaining three patients are alive at a mean of 25.7 months after their operation. In conclusion, large proximal aortic necks preclude endovascular treatment with standard abdominal endograft components. The use of a thoracic endograft as a proximal aortic cuff is a feasible technique for patients unable to tolerate open aortic reconstruction.
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Vuruşkan, Ertan, Erhan Saraçoğlu, and İrfan Veysel Düzen. "Serum Bilirubin Levels and the Presence and Progression of Abdominal Aortic Aneurysms." Angiology 68, no. 5 (July 29, 2016): 428–32. http://dx.doi.org/10.1177/0003319716660240.
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The relationship between bilirubin levels and peripheral artery disease has been documented. Our aim was to demonstrate the possible relationship between serum bilirubin levels and abdominal aortic aneurysms (AAAs). The study included 219 patients, 110 had a previous diagnosis of AAA and 109 patients were normal controls. Only patients with AAAs which had a size of 40 to 54 mm were included in the study. Baseline laboratory values and 2 computerized tomographic measurements 12 months apart were recorded. Patients with AAA had significantly higher white blood cell (WBC) counts and neutrophil–lymphocyte ratio (NLR) but lower total and direct bilirubin levels compared with the control patients ( P < .05). Multivariate logistic regression analysis showed that WBC, NLR, and total and direct bilirubin levels were independent predictors of the presence of an AAA ( P = .03, P = .001, P = .001, and P = .001, respectively). White blood cells and total bilirubin level were independent predictors of a rapidly enlarging AAA (>10 mm/y, P = .002 and P < .001, respectively). This study demonstrated that increased WBC and decreased total bilirubin levels were independent predictors of an AAA, especially the subgroup in which the AAA was rapidly expanding.
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Braet, Drew J., Jonathan Eliason, Yunus Ahmed, Pieter A. J. van Bakel, Jiayang Zhong, Zhangxing Bian, Carlos Alberto Figueroa, and Nicholas S. Burris. "Vascular Deformation Mapping of Abdominal Aortic Aneurysm." Tomography 7, no. 2 (May 13, 2021): 189–201. http://dx.doi.org/10.3390/tomography7020017.
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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.
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Chaer, Rabih A., Brian G. DeRubertis, Robert Hynecek, K. Craig Kent, and Peter L. Faries. "Models of Abdominal Aortic Aneurysm: Characterization and Clinical Applications." Vascular 14, no. 6 (November 2006): 343–52. http://dx.doi.org/10.2310/6670.2006.00059.
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Abdominal aortic aneurysms (AAAs) are responsible for considerable morbidity, mortality, and cost to society. The pathogenesis of AAA formation, however, remains poorly understood. Animal models have been used in a range of experiments designed to provide further objective scientific assessment of the pathogenesis as well as the treatment of AAA. The purpose of this manuscript is to review the current models of AAA and their potential clinical implications.
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Leemans, Eva L., Tineke P. Willems, Maarten J. van der Laan, Cornelis H. Slump, and Clark J. Zeebregts. "Biomechanical Indices for Rupture Risk Estimation in Abdominal Aortic Aneurysms." Journal of Endovascular Therapy 24, no. 2 (November 21, 2016): 254–61. http://dx.doi.org/10.1177/1526602816680088.
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Purpose: To review the use of biomechanical indices for the estimation of abdominal aortic aneurysm (AAA) rupture risk, emphasizing their potential use in a clinical setting. Methods: A search of the PubMed, Embase, Scopus, and Compendex databases was made up to June 2015 to identify articles involving biomechanical analysis of AAA rupture risk. Outcome variables [aneurysm diameter, peak wall stress (PWS), peak wall shear stress (PWSS), wall strain, peak wall rupture index (PWRI), and wall stiffness] were compared for asymptomatic intact AAAs vs symptomatic or ruptured AAAs. For quantitative analysis of the pooled data, a random effects model was used to calculate the standard mean differences (SMDs) with the 95% confidence interval (CI) for the biomechanical indices. Results: The initial database searches yielded 1894 independent articles of which 19 were included in the analysis. The PWS was significantly higher in the symptomatic/ruptured group, with a SMD of 1.11 (95% CI 0.93 to 1.26, p<0.001). Likewise, the PWRI was significantly higher in the ruptured or symptomatic group, with a SMD of 1.15 (95% CI 0.30 to 2.01, p=0.008). After adjustment for the aneurysm diameter, the PWS remained higher in the ruptured or symptomatic group, with a SMD of 0.85 (95% CI 0.46 to 1.23, p<0.001). Less is known of the wall shear stress and wall strain indices, as too few studies were available for analysis. Conclusion: Biomechanical indices are a promising tool in the assessment of AAA rupture risk as they incorporate several factors, including geometry, tissue properties, and patient-specific risk factors. However, clinical implementation of biomechanical AAA assessment remains a challenge owing to a lack of standardization.
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Cassis, Lisa A., Manisha Gupte, Sarah Thayer, Xuan Zhang, Richard Charnigo, Deborah A. Howatt, Debra L. Rateri, and Alan Daugherty. "ANG II infusion promotes abdominal aortic aneurysms independent of increased blood pressure in hypercholesterolemic mice." American Journal of Physiology-Heart and Circulatory Physiology 296, no. 5 (May 2009): H1660—H1665. http://dx.doi.org/10.1152/ajpheart.00028.2009.
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Infusion of ANG II in hyperlipidemic mice augments atherosclerosis and causes formation of abdominal aortic aneurysms (AAAs). The purpose of this study was to define the contribution of ANG II-induced hypertension to these vascular pathologies. Male apolipoprotein E (apoE)- and LDL receptor (LDLr)-deficient mice were infused with ANG II (1,000 ng·kg−1·min−1) or norepinephrine (NE; 5.6 mg·kg−1·day−1) for 28 days. Infusion of ANG II or NE increased mean arterial pressure (MAP; ANG II, 133 ± 2.8; NE, 129 ± 13 mmHg) to a similar extent compared with baseline blood pressures (MAP, 107 ± 2 mmHg). Abdominal aortic width increased in both apoE-deficient (apoE−/−) or LDLr-deficient (LDLr−/−) mice infused with ANG II (apoE−/−: 1.4 ± 0.1; LDLr−/−: 1.6 ± 0.2 mm). In contrast, NE did not change diameters of abdominal aortas (apoE−/−: 0.91 ± 0.03; LDLr−/−: 0.87 ± 0.02 mm). Similarly, atherosclerotic lesions in aortic arches were much greater in mice infused with ANG II compared with NE. At a subpressor infusion rate of ANG II (500 ng·kg−1·min−1), AAAs developed in 50% of apoE−/− mice. Alternatively, administration of hydralazine (250 mg/l) to ANG II-infused apoE−/− mice (1,000 ng·kg−1·min−1) lowered systolic blood pressure ( day 28: ANG II, 157 ± 6; ANG II/hydralazine, 135 ± 6 mmHg) but did not prevent AAA formation or atherosclerosis. These results demonstrate that infusion of ANG II to hyperlipidemic mice induces AAAs and augments atherosclerosis independent of increased blood pressure.
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Miyama, Noriyuki, Monica M. Dua, Geoffrey M. Schultz, Hisanori Kosuge, Masahiro Terashima, Laura J. Pisani, Ronald L. Dalman, and Michael V. McConnell. "Bioluminescence and Magnetic Resonance Imaging of Macrophage Homing to Experimental Abdominal Aortic Aneurysms." Molecular Imaging 11, no. 2 (March 1, 2012): 7290.2011.00033. http://dx.doi.org/10.2310/7290.2011.00033.
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Macrophage infiltration is a prominent feature of abdominal aortic aneurysm (AAA) progression. We used a combined imaging approach with bioluminescence (BLI) and magnetic resonance imaging (MRI) to study macrophage homing and accumulation in experimental AAA disease. Murine AAAs were created via intra-aortic infusion of porcine pancreatic elastase. Mice were imaged over 14 days after injection of prepared peritoneal macrophages. For BLI, macrophages were from transgenic mice expressing luciferase. For MRI, macrophages were labeled with iron oxide particles. Macrophage accumulation during aneurysm progression was observed by in situ BLI and by in vivo 7T MRI. Mice were sacrificed after imaging for histologic analysis. In situ BLI ( n = 32) demonstrated high signal in the AAA by days 7 and 14, which correlated significantly with macrophage number and aortic diameter. In vivo 7T MRI ( n = 13) at day 14 demonstrated T2* signal loss in the AAA and not in sham mice. Immunohistochemistry and Prussian blue staining confirmed the presence of injected macrophages in the AAA. BLI and MRI provide complementary approaches to track macrophage homing and accumulation in experimental AAAs. Similar dual imaging strategies may aid the study of AAA biology and the evaluation of novel therapies.
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Uchida, Haruhito A., Tetsuharu Takatsuka, Yoshiko Hada, Ryoko Umebayashi, Hidemi Takeuchi, Kenichi Shikata, Venkateswaran Subramanian, Alan Daugherty, and Jun Wada. "Edaravone Attenuated Angiotensin II-Induced Atherosclerosis and Abdominal Aortic Aneurysms in Apolipoprotein E-Deficient Mice." Biomolecules 12, no. 8 (August 14, 2022): 1117. http://dx.doi.org/10.3390/biom12081117.
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Background: The aim of the study was to define whether edaravone, a free-radical scavenger, influenced angiotensin II (AngII)-induced atherosclerosis and abdominal aortic aneurysms (AAAs) formation. Methods: Male apolipoprotein E-deficient mice (8–12 weeks old) were fed with a normal diet for 5 weeks. Either edaravone (10 mg/kg/day) or vehicle was injected intraperitoneally for 5 weeks. After 1 week of injections, mice were infused subcutaneously with either AngII (1000 ng/kg/min, n = 16–17 per group) or saline (n = 5 per group) by osmotic minipumps for 4 weeks. Results: AngII increased systolic blood pressure equivalently in mice administered with either edaravone or saline. Edaravone had no effect on plasma total cholesterol concentrations and body weights. AngII infusion significantly increased ex vivo maximal diameters of abdominal aortas and en face atherosclerosis but was significantly attenuated by edaravone administration. Edaravone also reduced the incidence of AngII-induced AAAs. In addition, edaravone diminished AngII-induced aortic MMP-2 activation. Quantitative RT-PCR revealed that edaravone ameliorated mRNA abundance of aortic MCP-1 and IL-1β. Immunostaining demonstrated that edaravone attenuated oxidative stress and macrophage accumulation in the aorta. Furthermore, edaravone administration suppressed thioglycolate-induced mice peritoneal macrophages (MPMs) accumulation and mRNA abundance of MCP-1 in MPMs in male apolipoprotein E-deficient mice. In vitro, edaravone reduced LPS-induced mRNA abundance of MCP-1 in MPMs. Conclusions: Edaravone attenuated AngII-induced AAAs and atherosclerosis in male apolipoprotein E-deficient mice via anti-oxidative action and anti-inflammatory effect.
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May, James, Geoffrey H. White, Weiyun Yu, Richard C. Waugh, Michael S. Stephen, and John P. Harris. "A Prospective Study of Changes in Morphology and Dimensions of Abdominal Aortic Aneurysms following Endoluminal Repair: A Preliminary Report." Journal of Endovascular Therapy 2, no. 4 (November 1995): 343–47. http://dx.doi.org/10.1177/152660289500200406.
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Purpose: The aim of this prospective study was to analyze early changes in morphology and dimensions of abdominal aortic aneurysms (AAA) following endoluminal repair. Methods: Forty-two of 62 patients undergoing endoluminal repair of AAAs between May 1992 and November 1994 were potentially available for follow-up at 6 months or longer after operation. After excluding patients with failed endoluminal repairs, patients who died within 6 months of operation, and patients with anastomotic aneurysms, a study group of 30 patients remained. Contrast-enhanced computed tomography (CE-CT) was performed preoperatively, within 10 days of operation, and at 6 and 12 months postprocedure. Based on the postoperative CE-CT findings, patients were divided into two groups: those with no extravasation of contrast into the aneurysmal sac (group I; n = 26), and those in which there was contrast extravasation (“leak”) into the aneurysmal sac (group II; n = 4). Results: The mean maximum diameters of AAAs in group I diminished progressively at 6 and 12 months, while those in group II increased. Twenty-three (88%) patients in group I had decreased diameter of AAA, while all patients in group II had progressive increase in AAA diameter. Patients who had an increase in AAA diameter had a significantly higher incidence of leak compared with those who had a decrease in diameter (p = 0.001). Conclusions: The majority of AAAs in which the sac has been excluded from the general circulation diminish in size following successful endoluminal repair. An increase in size occurs in those AAAs in which a communication exists between the aortic lumen and the sac. These results suggest that successfully excluded AAAs that continue to increase in size should be suspected of having an undetected leak.
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Scharrer-Pamler, Reinhard, Thomas Kotsis, Xaver Kapfer, Johannes Görich, and Ludger Sunder-Plassmann. "Endovascular Stent-Graft Repair of Ruptured Aortic Aneurysms." Journal of Endovascular Therapy 10, no. 3 (June 2003): 447–52. http://dx.doi.org/10.1177/152660280301000308.
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Purpose: To demonstrate the endovascular approach to the management of ruptured abdominal aortic aneurysms (AAA). Methods: From 1995 to 2001, 24 patients (21 men; mean age 69 years, range 26–92) underwent emergency endovascular treatment for ruptured AAA. The average interval between onset of symptoms and admission to the hospital was 8.0 hours; the mean time between admission and the operation was 2.3 hours. No suprarenal occluding catheter was used. The stent-graft configurations were 19 bifurcated, 4 tube, and 1 aortomonoiliac. Results: Stent-graft placement was successful in 23 (96%) cases. Failed limb extension deployment prompted conversion to open surgery in the remaining patient. One case was converted to open surgery. Mean duration of treatment was 122 minutes. Three (12.5%) patients died in-hospital. The median hospital stay was 12 days. The rate of endoleaks (all type I) was 16.7%. The overall technical success rate was 77%. The 3-year actuarial survival rate was 75%. Conclusions: Our experience shows excellent results in emergency patients with ruptured AAAs treated with endovascular surgery. In order to verify these promising results, a broader-scale clinical study must be conducted.
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Patel, Ajay P., Eugene M. Langan, Spence M. Taylor, Bruce H. Gray, Christopher G. Carsten, David L. Cull, Bruce A. Snyder, Marcus D. Stanbro, Jerry R. Youkey, and Timothy M. Sullivan. "An Analysis of Standard Open and Endovascular Surgical Repair of Abdominal Aortic Aneurysms in Octogenarians." American Surgeon 69, no. 9 (September 2003): 744–48. http://dx.doi.org/10.1177/000313480306900903.
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While elective open abdominal aortic aneurysm (AAA) repair has been shown to be safe in selected octogenarians, very little is known about the role of endovascular AAA exclusion in this high-risk cohort. A retrospective review of our vascular surgical registry from January 1996 to December 2001 revealed 51 octogenarians that underwent infrarenal AAA repair. Since 1999 all octogenarians who presented for AAA repair were evaluated for preferential endovascular stent graft placement. Over the 6-year period, 35 patients underwent standard open repair while 16 patients were found to be anatomic candidates for and were treated with an endovascular stent graft. Hospital and office charts were reviewed to compare the endovascular cohort to the standard open cohort. Factors considered included patient comorbidities, perioperative data, and operative outcomes. Statistical analysis was done using Wilcoxon rank sum test and Fisher exact test. The median age for the entire group was 83 years. There were 11 females in the open group and 1 female in the endovascular group. There were no statistically significant differences in preoperative patient comorbidities between groups. Total mortality for the entire series was 11.8 per cent but this included 5 ruptured AAAs, all of which patients died, and 11 additional AAAs that were symptomatic, of which 1 patient died. Total nonruptured mortality for the entire series was 2.2 per cent (0% for the endo-group and 3.3% for the open group). There were statistically significant differences between the endovascular versus the open groups when comparing aneurysm diameter (5.6 cm vs. 6.2 cm; P = 0.016), estimated blood loss (225 cc vs. 2100 cc; P < 0.001), ICU days (0 vs. 3; P < 0.001), length of hospital stay (2 days vs. 12 days; P < 0.001), and patients with blood transfusions (1 vs. 27; P < 0.001). When comparing postoperative morbidities, 4 of the endovascular patients (25%) and 25 of the open patients (68.6%) had a complication ( P = 0.006). In conclusion, endovascular stent graft treatment of nonruptured infrarenal AAAs in octogenarians led to significantly better outcomes and should probably be considered the preferred treatment whenever anatomically appropriate. Endovascular exclusion of ruptured AAAs may potentially improve future outcomes in this high-risk group.
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Polzer, Stanislav, and T. Christian Gasser. "Biomechanical rupture risk assessment of abdominal aortic aneurysms based on a novel probabilistic rupture risk index." Journal of The Royal Society Interface 12, no. 113 (December 2015): 20150852. http://dx.doi.org/10.1098/rsif.2015.0852.
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A rupture risk assessment is critical to the clinical treatment of abdominal aortic aneurysm (AAA) patients. The biomechanical AAA rupture risk assessment quantitatively integrates many known AAA rupture risk factors but the variability of risk predictions due to model input uncertainties remains a challenging limitation. This study derives a probabilistic rupture risk index (PRRI). Specifically, the uncertainties in AAA wall thickness and wall strength were considered, and wall stress was predicted with a state-of-the-art deterministic biomechanical model. The discriminative power of PRRI was tested in a diameter-matched cohort of ruptured ( n = 7) and intact ( n = 7) AAAs and compared to alternative risk assessment methods. Computed PRRI at 1.5 mean arterial pressure was significantly ( p = 0.041) higher in ruptured AAAs (20.21(s.d. 14.15%)) than in intact AAAs (3.71(s.d. 5.77)%). PRRI showed a high sensitivity and specificity (discriminative power of 0.837) to discriminate between ruptured and intact AAA cases. The underlying statistical representation of stochastic data of wall thickness, wall strength and peak wall stress had only negligible effects on PRRI computations. Uncertainties in AAA wall stress predictions, the wide range of reported wall strength and the stochastic nature of failure motivate a probabilistic rupture risk assessment. Advanced AAA biomechanical modelling paired with a probabilistic rupture index definition as known from engineering risk assessment seems to be superior to a purely deterministic approach.
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Diehm, Schmidli, Dai-Do, and Baumgartner. "Current evidence and prospects for medical treatment of abdominal aortic aneurysms." Vasa 34, no. 4 (November 1, 2005): 217–23. http://dx.doi.org/10.1024/0301-1526.34.4.217.
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Abdominal aortic aneurysm (AAA) is a potentially fatal condition with risk of rupture increasing as maximum AAA diameter increases. It is agreed upon that open surgical or endovascular treatment is indicated if maximum AAA diameter exceeds 5 to 5.5cm. Continuing aneurysmal degeneration of aortoiliac arteries accounts for significant morbidity, especially in patients undergoing endovascular AAA repair. Purpose of this review is to give an overview of the current evidence of medical treatment of AAA and describe prospects of potential pharmacological approaches towards prevention of aneurysmal degeneration of small AAAs and to highlight possible adjunctive medical treatment approaches after open surgical or endovascular AAA therapy.
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Tshomba, Yamume, Simona Sica, Fabrizio Minelli, Marco Ferraresi, Chiara de Waure, Tommaso Donati, Francesca De Nigris, Claudio Vincenzoni, Francesco Snider, and Giovanni Tinelli. "Long-Term Results of Complex Abdominal Aortic Aneurysm Open Repair." Journal of Personalized Medicine 12, no. 10 (October 1, 2022): 1630. http://dx.doi.org/10.3390/jpm12101630.
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This study investigated the long-term outcomes of patients treated with open surgical repair for complex abdominal aortic aneurysms (c-AAAs). A total of 119 patients with c-AAAs undergoing repair between January 2010 and June 2016 in a high-volume aortic center were included. The long-term imaging follow-up consisted of yearly abdominal ultrasound examinations and 5-year computed tomography angiography. At a median follow-up of 76 months (IQR 38 months), forty-three deaths (37%) and three (2.5%) aortic-related deaths were observed. Long-term chronic renal decline was observed in fifty (43.8%) patients, significantly correlated with post-operative acute kidney injury. During the follow-up, five reinterventions (4.3%) were performed. The present study suggests that open c-AAA repair can be performed with acceptable operative risk with durable results. To achieve the best possible long-term outcome, the open surgery repair of complex AAA should be performed in high-volume aortic centers and tailored to the patient.
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Thompson, Matthew M., Robert D. Sayers, Ahktar Nasim, Jonathan R. Boyle, Guy Fishwick, and Peter R. F. Bell. "Aortomonoiliac Endovascular Grafting: Difficult Solutions to Difficult Aneurysms." Journal of Endovascular Therapy 4, no. 2 (May 1997): 174–81. http://dx.doi.org/10.1177/152660289700400209.
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Purpose: To describe a refined technique for aortomonoiliac endograft exclusion of abdominal aortic aneurysms (AAAs). Methods: A tapered aortomonoiliac graft was prepared from an 8-mm thin-walled expanded polytetrafluoroethylene tube graft predilated proximally to 35 mm and tapered distally to 15 mm. The proximal graft was sutured to a 5-cm-long, predilated Palmaz stent, which was mounted on a 30-mm balloon and backloaded into a 21F packaging sheath. With the patient under general anesthesia and both common femoral arteries exposed, the endograft was anchored in the infrarenal aorta and subsequently passed into one iliac system, where it was anastomosed to the iliac or femoral vessels. The contralateral common iliac artery was occluded, and an extra-anatomic, femorofemoral, or iliofemoral bypass grafting was performed. Results: Twenty of the 25 AAAs treated to date with this technique have been successful, with aneurysm exclusion achieved in 18 (2 minor distal endoleaks are scheduled for endovascular repair). The technical failures were analyzed, resulting in enhancements to the technique. Complications included 2 early (< 30 days) deaths, 1 case of minor embolization, 1 transient renal failure, 1 pulmonary embolus, and 1 wound infection. The only late complication was a graft infection localized to the groin. Conclusions: Aortomonoiliac endovascular aneurysm repair is effective in patients with AAAs involving the iliac arteries. Short-term results are acceptable, but long-term efficacy must be addressed before this procedure is widely adopted. Technical changes made in response to early learning curve problems have led to a safer, more reliable procedure.
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Remus, Ebony Washington, Robert E. O'Donnell, Kathryn Rafferty, Daiana Weiss, Giji Joseph, Katalin Csiszar, Sheri F. T. Fong, and W. Robert Taylor. "The role of lysyl oxidase family members in the stabilization of abdominal aortic aneurysms." American Journal of Physiology-Heart and Circulatory Physiology 303, no. 8 (October 15, 2012): H1067—H1075. http://dx.doi.org/10.1152/ajpheart.00217.2012.
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Abdominal aortic aneurysms (AAAs) are a major cause of morbidity and mortality in the United States today. We employed a model for AAA development using apolipoprotein E knock out mice fed a high-fat diet and treated with ANG II and β-aminopropionitrile (β-APN) for 4 wk. ANG II induces hypertension and atherosclerotic disease, whereas β-APN inhibits the activity of the lysyl oxidase/ lysyl oxidase-like protein (LOX/LOXL) family members. LOX/LOXL family members crosslink collagen and elastin in the extracellular matrix and therefore contribute to the integrity and stabilization of a healthy vessel wall. In this model, cotreatment with ANG II and β-APN caused a 90% AAA incidence and increased atherosclerotic lesion formation from less than 5% to greater than 25% after 4 wk. In more atheroprotected mouse strains (C57BL/6 and BalbC), cotreatment with ANG II and β-APN caused 50% and 40% AAA incidence, respectively. These data demonstrate the importance of LOX/LOXL to the stability of the vessel wall. Therapeutic strategies to overexpress LOX/LOXL enzymes or to support the crosslinking of soluble matrix proteins in a polymeric scaffold are a promising opportunity to achieve stabilization of AAAs.