Relevant bibliographies by topics / Aortic aneurysms

Academic literature on the topic 'Aortic aneurysms'

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Published: 4 June 2021
Last updated: 3 March 2023

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Journal articles on the topic "Aortic aneurysms"

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von Kodolitsch, Aydin, Bernhardt, Habermann, Treede, Reichenspurner, Meinertz, and Dodge-Khatami. "Aortic aneurysms after correction of aortic coarctation: A systematic review." Vasa 39, no. 1 (February 1, 2010): 3–16. http://dx.doi.org/10.1024/0301-1526/a000001.

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Despite advanced techniques for surgical or percutaneous therapy coarctation of the aorta continues to carry a high risk of aneurysmal formation. Mortality of these aneurysms ranges between <1 and >90%, reflecting remarkable differences in surgical strategies and the follow-up management of coarctation. We review the frequency, anatomical types, risk factors and mechanisms of aortic aneurysm forming late after surgical or percutaneous therapy of aortic coarctation. We emphasize that aneurysms do not form exclusively at the site of previous intervention, but also at remote locations such as the ascending aorta. Moreover, aneurysm formation may only in part be attributed to a specific technique of coarctation therapy, and we emphasize the role of a bicuspid aortic valve and inherent weakness of the aortic wall as significant risk factors for aneurysm after aortic coarctation. We report the presenting symptoms, follow-up protocols, and imaging criteria for local and proximal aneurysms. Finally, we discuss criteria for prophylactic intervention at the site of such aneurysms, and present therapeutic options for different types of aneurysms. With this systematic review, we wish to provide data for establishing more uniform strategies for preventing, diagnosing and treating aneurysms associated with aortic coarctation.
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Federspiel, Jan M., Philipp A. Schnabel, Thomas Tschernig, Brittany Balint, Tanja Schwab, Matthias W. Laschke, and Hans-Joachim Schäfers. "Aortic aneurysms with tricuspid aortic valve have more degeneration than unicuspid aortic valve aneurysms." European Journal of Cardio-Thoracic Surgery 60, no. 2 (March 1, 2021): 333–40. http://dx.doi.org/10.1093/ejcts/ezab101.

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Abstract OBJECTIVES The unicuspid aortic valve (UAV) is a rare cardiac malformation and is associated with the formation of ascending aortic aneurysms. To characterize its associated aortic wall changes, normal and aneurysmatic ascending aortic wall specimens were analysed, focusing on the potential mechanisms of aneurysm formation. Patients with tricuspid aortic valve (TAV) served as controls. METHODS In a retrospective observational study, 74 specimens (dilated and non-dilated aortas; individuals with UAV and TAV) obtained intraoperatively were studied. Standard stains and immunohistochemical labelling of cleaved caspase-3, cluster of differentiation 31 and endothelial nitric oxide synthase (eNOS) were performed to assess the degree of apoptosis, distribution of eNOS within the aortic wall, smooth muscle cell (SMC) nuclei loss and mucoid extracellular matrix accumulation (MEMA). RESULTS Deeper ingrowth of vasa vasorum was found in dilated aortas. Interestingly, eNOS was expressed mostly in vasa vasorum. More apoptosis was seen in UAV aortas compared to TAV aortas (P &lt; 0.001). Both UAV and TAV aortas were comparable regarding SMC nuclei loss (P = 0.419). In dilated compared to non-dilated aortas regardless valve morphology SMC nuclei loss was increased (P = 0.005) and more pronounced translamellar MEMA was present (P = 0.011). The highest grade of distribution (P = 0.043) and the highest severity (P = 0.005) regarding MEMA were seen in TAV dilated specimens compared to UAV dilated specimens. CONCLUSIONS Aneurysms with UAV show increased apoptosis, the role of which is unclear. Strikingly, more severe MEMA was found in TAV aneurysms compared to UAV aneurysms. Thus, UAV-associated aortic wall changes and resulting aneurysm may be less aggressive than aneurysms with TAV.
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Kisis, Kaspars, Dainis Krievins, Marcis Gedins, Janis Savlovskis, Natalija Ezite, and Patricija Ivanova. "Patient with Syphilitic Thoracic and Abdominal Aortic Aneurysms." Acta Chirurgica Latviensis 10, no. 2 (January 1, 2010): 131–33. http://dx.doi.org/10.2478/v10163-011-0028-7.

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Patient with Syphilitic Thoracic and Abdominal Aortic AneurysmsWe are presenting a rare case of patient with two syphilitic aneurysms localized in thoracic and abdominal aorta. Routine lung computer tomography (CT) for the patient with complains about irritating and unclear ethiology cough revealed 10 cm diameter aneurysm of descending thoracic aorta (TAA) and additionally 4.8 cm aneurysm of abdominal aorta (AAA) just below the aortic hiatus. As there was no evidence of previous trauma, Marfan syndrome or connective tissue disease patient was screened for syphilis. Diagnosis of tertiary syphilis was confirmed and specific treatment started. As complains of irritating cough intensified - patients TAA was successfully treated endovascularly with thoracic stent graft (Valiant®Captivia, Medtronic Ltd.) on emergency basis. On control CT angiography 3 month after treatment there was no evidence of graft migration, endoleaks and aneurysmal sac was thrombosed. AAA has not increased in size, and open repair is planned.
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Joshi, Nikhil V., Maysoon Elkhawad, Rachael O. Forsythe, Olivia M. B. McBride, Nikil K. Rajani, Jason M. Tarkin, Mohammed M. Chowdhury, et al. "Greater aortic inflammation and calcification in abdominal aortic aneurysmal disease than atherosclerosis: a prospective matched cohort study." Open Heart 7, no. 1 (March 2020): e001141. http://dx.doi.org/10.1136/openhrt-2019-001141.

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ObjectiveUsing combined positron emission tomography and CT (PET-CT), we measured aortic inflammation and calcification in patients with abdominal aortic aneurysms (AAA), and compared them with matched controls with atherosclerosis.MethodsWe prospectively recruited 63 patients (mean age 76.1±6.8 years) with asymptomatic aneurysm disease (mean size 4.33±0.73 cm) and 19 age-and-sex-matched patients with confirmed atherosclerosis but no aneurysm. Inflammation and calcification were assessed using combined 18F-FDG PET-CT and quantified using tissue-to-background ratios (TBRs) and Agatston scores.ResultsIn patients with AAA, 18F-FDG uptake was higher within the aneurysm than in other regions of the aorta (mean TBRmax2.23±0.46 vs 2.12±0.46, p=0.02). Compared with atherosclerotic control subjects, both aneurysmal and non-aneurysmal aortae showed higher 18F-FDG accumulation (total aorta mean TBRmax2.16±0.51 vs 1.70±0.22, p=0.001; AAA mean TBRmax2.23±0.45 vs 1.68±0.21, p<0.0001). Aneurysms containing intraluminal thrombus demonstrated lower 18F-FDG uptake within their walls than those without (mean TBRmax2.14±0.43 vs 2.43±0.45, p=0.018), with thrombus itself showing low tracer uptake (mean TBRmax thrombus 1.30±0.48 vs aneurysm wall 2.23±0.46, p<0.0001). Calcification in the aneurysmal segment was higher than both non-aneurysmal segments in patients with aneurysm (Agatston 4918 (2901–8008) vs 1017 (139–2226), p<0.0001) and equivalent regions in control patients (442 (304-920) vs 166 (80-374) Agatston units per cm, p=0.0042).ConclusionsThe entire aorta is more inflamed in patients with aneurysm than in those with atherosclerosis, perhaps suggesting a generalised inflammatory aortopathy in patients with aneurysm. Calcification was prominent within the aneurysmal sac, with the remainder of the aorta being relatively spared. The presence of intraluminal thrombus, itself metabolically relatively inert, was associated with lower levels of inflammation in the adjacent aneurysmal wall.
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Kim, Ha Won, and Brian K. Stansfield. "Genetic and Epigenetic Regulation of Aortic Aneurysms." BioMed Research International 2017 (2017): 1–12. http://dx.doi.org/10.1155/2017/7268521.

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Aneurysms are characterized by structural deterioration of the vascular wall leading to progressive dilatation and, potentially, rupture of the aorta. While aortic aneurysms often remain clinically silent, the morbidity and mortality associated with aneurysm expansion and rupture are considerable. Over 13,000 deaths annually in the United States are attributable to aortic aneurysm rupture with less than 1 in 3 persons with aortic aneurysm rupture surviving to surgical intervention. Environmental and epidemiologic risk factors including smoking, male gender, hypertension, older age, dyslipidemia, atherosclerosis, and family history are highly associated with abdominal aortic aneurysms, while heritable genetic mutations are commonly associated with aneurysms of the thoracic aorta. Similar to other forms of cardiovascular disease, family history, genetic variation, and heritable mutations modify the risk of aortic aneurysm formation and provide mechanistic insight into the pathogenesis of human aortic aneurysms. This review will examine the relationship between heritable genetic and epigenetic influences on thoracic and abdominal aortic aneurysm formation and rupture.
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Onalan, Mehmet Akif, Omer Ali Sayin, and Emin Tireli. "Surgical Resection Of Thoracic Aortic Aneurysms In Wiskott–Aldrich Syndrome." Heart Surgery Forum 21, no. 4 (July 2, 2018): E305—E306. http://dx.doi.org/10.1532/hsf.1972.

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Aortic aneurysms are a rare condition in children. Wiskott-Aldrich syndrome is a primary immunodeficiency characterized by infections, thrombocytopenia, and eczema. Aortitis and aneurysm formation seem to be progressive in patients with Wiskott–Aldrich syndrome. The risk of death from aneurysmal rupture in patients with Wiskott–Aldrich syndrome is high and surgery is required for resection of aneurysms. We report a case where a successful resection of a descending thoracic aneurysm. We present a-12 year-old child with this syndrome who underwent a one-stage descending aortic aneurysm repair under continuous visceral perfusion.Histologic examination showed the presence of an aortitis withgranulomatous inflammatory response and multinucleated cells.
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Samura, Makoto, Nobuya Zempo, Yoshitaka Ikeda, Masaaki Hidaka, Yoshikazu Kaneda, Kazuhiro Suzuki, Hidetoshi Tsuboi, and Kimikazu Hamano. "Single-stage thoracic and abdominal endovascular aneurysm repair for multilevel aortic disease." Vascular 22, no. 1 (May 13, 2013): 55–60. http://dx.doi.org/10.1177/1708538112473965.

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This investigation evaluated the results of single-stage thoracic endovascular aneurysm repair (TEVAR) and endovascular aneurysm repair (EVAR) for multilevel aortic disease in a series of nine patients. The lesions repaired included thoracic and abdominal aortic aneurysms ( n = 7) and subacute type B dissections with abdominal aortic aneurysms ( n = 2). All procedures were successfully performed, and none of the patients experienced postoperative stroke or spinal cord ischemia. The median follow-up period for these patients was 18.9 months (range 1.7–31.4 months) and none of the patients exhibited any signs of type I endoleaks or aneurysmal diameter enlargements more than 5 mm. In conclusion, single-stage TEVAR and EVAR procedures for multilevel aortic disease were found to be safe and feasible modalities for high-risk patients.
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Dolmaci, Onur B., Sulayman El Mathari, Antoine H. G. Driessen, Robert J. M. Klautz, Robert E. Poelmann, Jan H. N. Lindeman, and Nimrat Grewal. "Are Thoracic Aortic Aneurysm Patients at Increased Risk for Cardiovascular Diseases?" Journal of Clinical Medicine 12, no. 1 (December 29, 2022): 272. http://dx.doi.org/10.3390/jcm12010272.

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Objectives: Abdominal aortic aneurysms are associated with a sharply increased cardiovascular risk. Cardiovascular risk management is therefore recommended in prevailing guidelines for abdominal aneurysm patients. It has been hypothesized that associated risk relates to loss of aortic compliance. If this hypothesis is correct, observations for abdominal aneurysms would also apply to thoracic aortic aneurysms. The objective of this study is to test whether thoracic aneurysms are also associated with an increased cardiovascular risk burden. Methods: Patients who underwent aortic valve or root surgery were included in the study (n = 239). Cardiovascular risk factors were studied and atherosclerosis was scored based on the preoperative coronary angiographies. Multivariate analyses were performed, controlling for cardiovascular risk factors and aortic valve morphology. Comparisons were made with the age- and gender-matched general population and non-aneurysm patients as control groups. A thoracic aortic aneurysm was defined as an aortic aneurysm of ≥45 mm. Results: Thoracic aortic aneurysm was not associated with an increased coronary atherosclerotic burden (p = 0.548). Comparison with the general population revealed a significantly higher prevalence of hypertension (61.4% vs. 32.2%, p < 0.001) and a lower prevalence of diabetes (1.4% vs. 13.1%, p = 0.001) in the thoracic aneurysm group. Conclusions: The extreme cardiovascular risk associated with abdominal aortic aneurysms is location-specific and not explained by loss of aortic compliance. Thoracic aortic aneurysm, in contrast to abdominal, is not part of the atherosclerotic disease spectrum and, therefore, cardiovascular risk management does not need to be implemented in treatment guidelines of isolated thoracic aneurysms. Hypertension should be treated.
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Cury, Marcelo, Fernanda Zeidan, and Armando C. Lobato. "Aortic Disease in the Young: Genetic Aneurysm Syndromes, Connective Tissue Disorders, and Familial Aortic Aneurysms and Dissections." International Journal of Vascular Medicine 2013 (2013): 1–7. http://dx.doi.org/10.1155/2013/267215.

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There are many genetic syndromes associated with the aortic aneurysmal disease which include Marfan syndrome (MFS), Ehlers-Danlos syndrome (EDS), Loeys-Dietz syndrome (LDS), familial thoracic aortic aneurysms and dissections (TAAD), bicuspid aortic valve disease (BAV), and autosomal dominant polycystic kidney disease (ADPKD). In the absence of familial history and other clinical findings, the proportion of thoracic and abdominal aortic aneurysms and dissections resulting from a genetic predisposition is still unknown. In this study, we propose the review of the current genetic knowledge in the aortic disease, observing, in the results that the causative genes and molecular pathways involved in the pathophysiology of aortic aneurysm disease remain undiscovered and continue to be an area of intensive research.
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Faries, Peter L., Luis A. Sanchez, Michael L. Marin, Richard E. Parsons, Ross T. Lyon, Steve Oliveri, and Frank J. Veith. "An Experimental Model for the Acute and Chronic Evaluation of Intra-Aneurysmal Pressure." Journal of Endovascular Therapy 4, no. 3 (August 1997): 290–97. http://dx.doi.org/10.1177/152660289700400310.

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Purpose: To develop an animal model for the acute and chronic monitoring of pressure within abdominal aortic aneurysms (AAAs) to be treated with endovascular grafts. Methods: A strain-gauge pressure transducer was placed within an AAA created from a prosthetic vascular graft. Prosthetic aneurysms were implanted into 17 canine infrarenal aortas. The intra-aneurysmal pressure was monitored and correlated with noninvasive forelimb sphygmomanometry for 2 weeks. After this time, an intravascular manometer catheter was passed into the aneurysm. Simultaneous pressure measurements were obtained using the implanted strain-gauge pressure transducer, the manometer catheter, and the forelimb sphygmomanometer. Angiography was performed to assess intraluminal morphology, aneurysm anastomoses, and adjoining aortic vessels. In addition, two control animals underwent intra-aneurysmal pressure monitoring after standard surgical aneurysm repair. Results: There was excellent correlation (r = 0.97) between the pressure measurements obtained with the implanted strain-gauge pressure transducer and the intravascular manometer. Close correlation was also observed between the implanted strain-gauge transducer and the forelimb sphygmomanometer (r = 0.88) during postprocedural monitoring. Intra-aneurysmal pressure was lowered dramatically by surgical exclusion (aneurysm: 15/5 ± 7/4 mmHg; systemic: 124/66 ± 34/17 mmHg; p < 0.001). The prosthetic aneurysms were successfully imaged with angiography. Conclusions: This animal model provides an accurate and reproducible means for measuring intra-aneurysmal pressure on an acute and chronic basis. It may be possible to use this model in the assessment of endovascular devices to determine their efficacy in reducing intra-aneurysmal pressure. Evaluation of complications associated with their use, such as patent aneurysm side branches, perigraft channels, and perianastomotic reflux, may also be possible.
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Dissertations / Theses on the topic "Aortic aneurysms"

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Rossaak, Jeremy Ian, and n/a. "The genetics of abdominal aortic aneurysms." University of Otago. Dunedin School of Medicine, 2004. http://adt.otago.ac.nz./public/adt-NZDU20070502.143818.

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Abdominal Aortic Aneurysms (AAA) are amongst the top ten most common cause of death in those over 55 years of age. The disease is usually asymptomatic, often being diagnosed incidentally. Once diagnosed, elective repair of an AAA results in excellent long-term survival with a 3-5% operative mortality. However, up to one half of patients present with ruptured aneurysms, a complication that carries an 80% mortality in the community, and of those reaching hospital, a 50% mortality. Clearly early diagnosis and treatment results in improved survival. Screening for AAA, with ultrasound, would detect aneurysms early, prior to rupture. However, debate continues over the cost effectiveness of population based screening programmes. The identification of a sub-population at a higher risk of developing AAA would increase the yield of a screening prograrmne. A number of populations have been examined, none of which have received international acceptance. About 20% of patients with an AAA have a family history of an aneurysm. The disease is also considered to be a disease of Caucasians, both facts suggesting a strong genetic component to the disease. Perhaps a genetically identified sub-population at a high risk of developing an AAA would prove to be an ideal population for screening. This thesis examines the incidence of aneurysms and the family histories of patients with AAA in the Otago region of New Zealand. Almost twenty percent of the population has a family history of AAA. DNA was collected from each of these patients for genetic analysis. The population was divided into familial AAA and non-familial AAA for the purpose of genetic analysis and compared to a control population. AAA is believed to be a disease of Caucasians; a non-Caucasian population with a low incidence of AAA may prove to be a good control population for genetic studies. A literature review demonstrated a higher incidence of AAA in Caucasians than other ethnic groups and within Caucasians a higher incidence in patients of Northern European origin. The incidence was low in Asian communities, even in studies involving of migrant Asian populations. The New Zealand Maori are believed to have originated from South East Asia, therefore could be expected to have a low incidence of AAA and would make an ideal control population for genetic studies. A pilot study was undertaken to examine the incidence of AAA in the New Zealand Maori. The age standardised incidence of AAA proved to be at least equal in Maori to non-Maori, with a more aggressive form of the disease in Maori, manifesting with a younger age at presentation and a higher incidence of ruptured aneurysms at diagnosis. It is well known that at the time of surgery, an AAA is at the end stage in its life. At this time, inflammation and matrix metalloproteinases (MMP) enzymes are prevalent within the aneurysm wall and have destroyed the wall of the aorta. One of the most important genetic pathways regulating these enzymes is the plasminogen activator inhibiter 1-Tissue plasminogen activator-plasmin pathway. Genetic analysis of this pathway demonstrated an association of the 4G5G polymorphism in the promoter of the PAl-1 gene with familial AAA. In this insertion:deletion polymorphism, the 5G variant binds an activator and repressor, resulting in reduced PAI-1 expression and ultimately increased MMP activation. This allele was associated with familial aneurysms, 47% versus 62% non-familial AAA and 61% controls (p=0.024). A polymorphism within the tissue plasminogen activator gene was also examined and no association was found with AAA. Another way the MMPs expression could be increased is from mutations or polymorphisms in their own genetic structure. Stromelysin 3 is itself a MMP capable of destroying the aortic wall and it has a role in activating other MMPs. A 5A6A insertion:deletion polymorphism exists in the promoter of this gene. The 5A allele variant results in increased stromelysin expression and is associated with AAA 46% versus 33% in controls p=0. 0006. The actions of the MMPs are themselves inhibited by the tissue inhibitors of matrix metalloproteinases. The TIMP genes have been sequenced; two polymorphisms have been identified in the non-coding promoter area of the TIMP 1 gene. Further studies are necessary to examine the effect of these polymorphisms. Inflammation has been implicated in aneurysm progression. One of the roles of the inflammatory cells found in an aneurysm is to deliver the MMP�s to the AAA. The HLA system is integral in controlling this inflammation and was therefore examined. From this series of studies it is concluded that there is a genetic component to AAA. This thesis presents the first genetic polymorphism associated with familial AAA and explores the role of a genetic pathway in the formation of AAA.
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Norrgård, Örjan. "Familial occurrence of abdominal aortic aneurysms." Doctoral thesis, Umeå universitet, Kirurgi, 1985. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-100555.

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The occurrence of clinically diagnosed and/or ruptured abdominal aortic aneurysms (AAAs) in the families of 220 patients with AAAs, treated at the Surgical Clinic, University Hospital of Umeå in the northern part of Sweden during the years 1965-82, was studied. A questionnaire concerning the blood relatives was answered by 87/89 patients. 16/87 patients (18%) had blood relatives with AAAs. In 14 families one blood relative was affected, and in 2 families two blood relatives were affected. First degree relatives were affected in 9/87 cases (10%), and second degree relatives in 7/87 cases (8%). 9/468 (1.9%) of the patients' brothers and sisters but only five of all their cousins had AAAs, and 7/204 (3.4%) of the dead brothers and sisters had died of ruptured AAAs. Concerning the patients who were not included in the letter survey at least 14/133had blood relatives with AAAs. However, the great majority of these patients were dead when the study was performed and could not be asked aboutthe occurrence of AAAs in their families. The patients with AAAs had significantly higher serum concentrations of triglyceride and (YLDL + LDL)-cholesterol and a significantly lower serum concentration of HDL-cholesterol than randomly selected healthy controls of the same sex and age as the patients. We also compared the distributions of genetic markers (HLA antigens, the blood group systems ABO, Rh, MNSs, P, Kell, Lewis and Duffy and the serum protein group systems haptoglobin, transferrin, group-specific component, complement C3, properdin factor and alpha-1-antitrypsin) in patients with AAAs with the distributions in controls and in some cases with the expected distributions according to the Hardy-Weinberg law. A significantly decreased frequency of Rh-negative individuals, and significantly increased frequencies of Kell-positi ve individuals, of MN heterozygotes and of heterozygotes concerning haptoglobin type was found. Furthermore, the aneurysm walls of patients with and without AAAs in the family were compared concerning the morphology, but no differences were found. We also studied the occurrence of collagen types I and III in the aneurysm walls, and the occurrence of vimentin and desmin in the smooth muscle cells of the aneurysm walls, but all these components were present in the aneurysm walls of both the patients with and those without AAAs in the family. To summarize the results, there seems to be an increased frequency of AAAs, and especially of ruptured AAAs, among the brothers and sisters of patients with AAAs. Elevated serum concentrations of triglyceride and (VLDL + LDL)- cholesterol and a lowered serum concentration of HDL-cholesterol seems to be common in patients with AAAs. There seems to be a hereditary predisposition to the development of AAAs, because we found associations with four different genetic markers (Rh, MN, Kell, haptoglobin group). However, there is probably no specific "familial" type of AAAs, because we found no differences between the patients with and those without AAAs in the family.Key words:

S. 1-42: sammanfattning, s. 43-103: 5 uppsatser


digitalisering@umu
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Polzer, Stanislav. "Stress-Strain Analysis of Aortic Aneurysms." Doctoral thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2012. http://www.nusl.cz/ntk/nusl-234135.

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Tato práce se zabývá problematikou aneurysmat břišní aorty a možností využít konečnoprvkovou deformačně-napěťovou analýzu těchto aneurysmat ke stanovení rizika ruptury. První část práce je věnována úvodu do problematiky, popisu kardiovaskulární soustavy člověka s důrazem na abdominální aortu, anatomii, fyziologii a patologii stěny tepny s důrazem na procesy vedoucí ke vzniku aneurysmatu. Dále se práce věnuje rizikovým faktorům přispívajících ke vzniku aneurysmat spolu s analýzou současných klinických postupů ke stanovení rizika ruptury spolu se srovnáním navrhovaného kritéria maximálního napětí. Dominantní část této disertace je věnována identifikaci faktorů ovlivňujících napjatost a deformaci stěny aneurysmatu spolu s návrhem nových postupů, prezentací vlastních poznatků vedoucích ke zpřesnění určení rizika ruptury pomocí deformačně- napěťové analýzy a metody konečných prvků. Nejprve je analyzován vliv geometrie, vedoucí k závěru, že je nezbytné používání individuálních geometrií pacienta. Dále je pozornost zaměřena na odbočující tepny, které ve stěně působí jako koncentrátor napětí a mohou tedy ovlivňovat napjatost v ní. Jako další podstatný faktor byl identifikován vliv nezatížené geometrie a bylo napsáno makro pro její nalezení, které bylo opět zahrnuto jako standardní součást do výpočtového modelu. Mechanické vlastnosti jak stěny aneurysmatu, tak intraluminálního trombu jsou experimentálně testovány pomocí dvouosých zkoušek. Také je zde analyzován vliv modelu materiálu, kde je ukázáno, že srovnávání maximálních napětí u jednotlivých modelů materiálu není vhodné díky zcela rozdílným gradientům napětí ve stěně aneurysmatu. Dále je zdůrazněna potřeba znalosti distribuce kolagenních vláken ve stěně a navržen program k jejímu získání. Intraluminální trombus je analyzován ve dvou souvislostech. Jednak je ukázán vliv jeho ruptury na napětí ve stěně a jednak je analyzován vliv jeho poroelastické struktury na totéž. Posledním identifikovaným podstatným faktorem je zbytková napjatost ve stěně. Její významnost je demonstrována na několika aneurysmatech a i tato je zahrnuta jako integrální součást do našeho výpočtového modelu.Na závěr jsou pak navrženy další možné směry výzkumu.
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Nordon, Ian Michael. "Mining the proteome of abdominal aortic aneurysms." Thesis, St George's, University of London, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.546777.

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Forester, Nerys Dawn. "Mechanisms of inflammation in abdominal aortic aneurysms." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.417894.

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Koenig, Sara Nichole. "Investigation of Notch1 Functions in Aortic Valve Disease and Ascending Aortic Aneurysms." The Ohio State University, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=osu1480641922918658.

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Malina, Martin. "Endovascular repair of abdominal aortic aneurysms aspects on a novel technique /." Lund : Dept. of Vascular and Renal Diseases, Lund University, Malmö University Hospital, 1998. http://books.google.com/books?id=hWBsAAAAMAAJ.

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Huusko, T. (Tuija). "Genetic and molecular background of ascending aortic aneurysms." Doctoral thesis, Oulun yliopisto, 2013. http://urn.fi/urn:isbn:9789526201269.

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Abstract Thoracic aortic aneurysms (TAAs) are a significant source of morbidity and mortality. Classical risk factors for TAAs are hypertension, atherosclerosis, male gender, smoking, age, high body mass index, family history and chronic obstructive pulmonary disease. In addition, in certain cases of TAAs, i.e., ascending aortic aneurysms (AscAA), genetic factors are highly prominent. Matrix metalloproteinases are in a major role in the destruction of the aortic wall and the imbalance between matrix metalloproteinases, and their inhibitors are involved in the formation of aneurysms. In addition, osteopontin is a potent regulator of matrix metalloproteinases and it is widely expressed in injured arteries. Recently, telomere shortening has been shown to be involved in the development of abdominal aortic aneurysms (AAA). In this aneurysm type, atherosclerosis has a major role. Since atherosclerosis is frequently absent in the case of TAAs, the length of telomeres was measured in the blood samples of TAA patients. The purpose of this thesis was to study the genetic background of TAAs of the ascending aorta and furthermore, the molecular background of this disease. The first study was done with families with TAAs, and dissections and one chromosomal locus (5q13-14) of the studied seven loci showed a significant genetic linkage for TAAs. Two other studies were done exploiting our TAA case-control material. Study II showed elevated levels of osteopontin, matrix metalloproteinase type 2 and 9 in the plasma and tissue samples of TAA patients compared with controls. In the third study, longer blood leukocyte telomeres were found in the DNA samples of TAA patients compared with controls; furthermore, the elevation of telomere lengthening protein telomerase expression was found in the tissue samples of TAA patients. This thesis presents region 5q13-14 as a potential genetic regulator for TAAs in Finnish families. In addition, elevated levels of osteopontin, matrix metalloproteinase type 2 and 9 can be considered as a plasma biomarker for aneurysmal disease. Furthermore, longer blood leukocytes were found to be a significant risk factor for developing TAAs
Tiivistelmä Rinta-aortan aneurysmat ovat merkittävä sairastumisiin ja kuolemiin johtava tekijä. Perinteisinä riskitekijöinä aneurysmille on pidetty korkeaa verenpainetta, ateroskleroosia, miessukupuolta, tupakointia, ikää, ylipainoa, suvussa esiintyneitä aneurysmatapauksia ja keuhkoahtaumatautia. Näiden lisäksi erityisesti nousevan rinta-aortan alueella esiintyvissä aneurysmissa myös perinnöllisillä tekijöillä on korostunut merkitys. Matriksimetalloproteinaaseilla ja niiden estäjillä on merkittävä rooli, kun aortan seinämää hajotetaan. Tasapainon järkkyminen kyseisten proteiinien keskinäisessä suhteessa voi johtaa aneurysman muodostumiseen. Myös osteopontiinin tiedetään olevan tehokas matriksimetalloproteinaasien säätelijä, ja sitä tuotetaankin yleisesti vahingoittuneessa verisuonessa. Telomeerien lyhentyminen on vastikään yhdistetty vatsa-aortan alueella esiintyviin aneurysmiin, joissa ateroskleroosilla on yleensä merkittävä rooli. Koska ateroskleroosi on vain harvoin nousevan rinta-aortan alueen aneurysmien taustalla, rinta-aortan aneurysmapotilaiden valkosolujen telomeerien suhteelliset pituudet määritettiin. Väitöskirjan ensimmäisessä osatyössä keskityttiin löytämään geneettinen kytkentä rinta-aortan aneurysmien ja jonkin seitsemän tutkitun kromosomialueen välille. Geneettinen kytkentä löydettiin kromosomialueelta 5q13-14. Osatöissä 2 ja 3 hyödynnettiin rinta-aortan aneurysmien potilas- ja verrokkiaineistoja. Osatyö 2 osoitti, että matriksimetalloproteinaasien (2 ja 9) määrät ovat kohonneet rinta-aortan aneurysmapotilaiden näytteissä verrokkeihin verrattuna. Osatyössä 3 telomeerien suhteelliset pituudet veren valkosoluissa olivat pidemmät nousevan rinta-aortan aneurysmapotilaiden näytteissä verrokkihenkilöiden näytteisiin verrattuna. Myös telomeraasin tuotto oli lisääntynyt rinta-aortan aneurysmapotilaiden aorttakudosnäytteissä. Väitöskirjassa esitetään tuloksena kromosomialue 5q13-14 geneettisenä säätelijänä suomalaisissa suvuittain esiintyvissä rinta-aortan aneurysmatapauksissa. Kohonneita matriksimetalloproteinaasien ja osteopontiinin tasoja voidaan lisäksi pitää biomarkkereina rinta-aortan aneurysmien sairastavuudelle. Veren valkosolujen pidemmät telomeerit näyttävät myös olevan yhteydessä rinta-aortan aneurysmien sairastavuuteen
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Nasim, Akhtar. "Evaluation of endovascular repair of abdominal aortic aneurysms." Thesis, University of Leicester, 1997. http://hdl.handle.net/2381/29600.

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Initially a retrospective study was undertaken to assess the current abdominal aortic aneurysm practice in terms of workload, mortality, complications and risk factors, to assess whether there is a role for endovascular AAA repair in Leicester. Then an experimental animal model was developed to investigate the necessity for anchoring the distal end of the graft with a second stent, the effect of placing stents across the renal ostia, and whether inferior mesenteric or lumbar artery backbleeding persists into the excluded aneurysm sac. A study has also been performed to assess the clinical application of this technique. A prospective study was undertaken in 82 consecutive patients referred for elective aneurysm repair to determine the best imaging modality for pre-operative assessment prior to endovascular AAA repair. A comparison was made between computed tomography (CT), magnetic resonance angiography (MRA), colour duplex and intra-arterial digital substraction angiography (IA-DSA). The morphology of the aneurysm in these patients was assessed to determine the proportion of patients that may benefit from this technique. Finally, the preliminary clinical experience with 3 different endoluminal grafts, one of which was developed in this study, was assessed. The results presented in this thesis show that work load of AAAs in Leicester has slowly increased over the past decade but there has been no significant improvement in the mortality figures for elective and emergency aneurysm surgery during this period. The results of the animal work show that a distal stent is necessary for complete exclusion of the aneurysm sac, but the safety of deploying stents across the renal arteries remains uncertain. This study also shows that MRA provides the best non-invasive assessment of aneurysm morphology prior to endovascular repair when compared to CT and IA-DA (p < 0.01).
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Xu, Dong. "Genetic factors and phenotypic variability in Marfan syndrome and abdominal aortic aneurysm /." [St. Lucia, Qld.], 1999. http://www.library.uq.edu.au/pdfserve.php?image=thesisabs/absthe16256.pdf.

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Books on the topic "Aortic aneurysms"

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Upchurch, Gilbert R., and Enrique Criado, eds. Aortic Aneurysms. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9.

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E, Pierce George, ed. Abdominal aortic aneurysms. Philadelphia: Saunders, 1989.

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Marianne, Kneipp, and Lawrence Evelyn P, eds. Surgical treatment of aortic aneurysms. Philadelphia: Saunders, 1986.

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1937-, Kawada S., Ueda T. 1951-, and Shimizu H. 1962-, eds. Cardio-aortic and aortic surgery. Tokyo: Springer, 2001.

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Borst, H. G. Surgical treatment of aortic dissection. New York: Churchill Livingstone International, 1996.

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Enrique, Criado, and SpringerLink (Online service), eds. Aortic Aneurysms: Pathogenesis and Treatment. Totowa, NJ: Humana Press, 2009.

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1956-, Calligaro Keith D., Dougherty Matthew J, and Hollier Larry H, eds. Diagnosis and treatment of aortic and peripheral arterial aneurysms. Philadelphia: W.B. Saunders, 1999.

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Tanabe, Tatsuzo. Aortic aneurysms: Pathophysiology, diagnosis, and treatment. Sapporo, Japan: Hokkaido University School of Medicine, 1993.

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Igakubu, Hokkaidō Daigaku, ed. Aortic aneurysms: Pathophysiology, diagnosis, and treatment. Sapporo, Japan: Hokkaido University School of Medicine, 1993.

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Hakaim, Albert G., ed. Current Endovascular Treatment of Abdominal Aortic Aneurysms. Oxford, UK: Blackwell Publishing, 2006. http://dx.doi.org/10.1002/9780470753156.

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Book chapters on the topic "Aortic aneurysms"

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Lillvis, John H., Guy M. Lenk, and Helena Kuivaniemi. "Genetics of Abdominal Aortic Aneurysms." In Aortic Aneurysms, 1–26. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_1.

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Stanley, James C. "Open Surgical Treatment of Pararenal Abdominal Aortic Aneurysms." In Aortic Aneurysms, 159–68. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_10.

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Fontcuberta, Juan, Manuel Doblas, Antonio Orgaz, Angel Flores, Jose Gil, Ignacio Leal, and Enrique Criado. "Pelvic Ischemia During Endovascular Abdominal Aortic Aneurysm Repair." In Aortic Aneurysms, 169–82. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_11.

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Kabbani, Loay S., and Gilbert R. Upchurch. "Open Operative Therapy for Ruptured Abdominal Aortic Aneurysm." In Aortic Aneurysms, 183–96. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_12.

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Riesenman, Paul J., and Mark A. Farber. "Endovascular Repair of Ruptured Abdominal Aortic Aneurysm." In Aortic Aneurysms, 197–206. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_13.

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Eliason, Jonathan L., and Todd E. Rasmussen. "Complications After Endovascular Ruptured Abdominal Aortic Aneurysm Repair." In Aortic Aneurysms, 207–16. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_14.

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Modrall, J. Gregory. "Treatment of Mycotic Abdominal Aortic Aneurysms and Infected Aortic Grafts." In Aortic Aneurysms, 217–35. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_15.

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Carignan, Martin J., and Marc A. Passman. "Evaluation and Management of Aortoenteric Fistula." In Aortic Aneurysms, 237–45. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_16.

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Tamaddon, Houman, Peter Ford, and Robert Mendes. "Management of Abdominal Aortic Aneurysm in the Setting of Coexistent Renal and Splanchnic Disease." In Aortic Aneurysms, 247–62. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_17.

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O'Hara, Patrick J. "Management of Abdominal Aortic Aneurysms in Patients with Renal Ectopia and Renal Fusion." In Aortic Aneurysms, 263–76. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60327-204-9_18.

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Conference papers on the topic "Aortic aneurysms"

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Fatima, Javairiah. "Thoracoabdominal Aortic Aneurysms Secondary to Aortic Dissection: Fenestrated Endovascular Aortic Aneurysm Repair." In PAIRS 2022 Annual Congress. Thieme Medical and Scientific Publishers Pvt. Ltd., 2022. http://dx.doi.org/10.1055/s-0042-1756263.

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Martufi, Giampaolo, Jose F. Rodriguez, and Ender A. Finol. "Anisotropic Wall Mechanics of Abdominal Aortic Aneurysms." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-192265.

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The prevalence of AAA is growing along with population age and according to different studies AAA rupture is the 13th most common cause of death in the U.S., causing an estimated 15,000 deaths per year. In biomechanical terms, AAA rupture is a phenomenon that occurs when the developing mechanical stresses within the aneurysm inner wall, as a result of the exerted intraluminal pressure, exceed the failure strength of the aortic tissue. To obtain a reliable estimation of wall stress, it is necessary to perform an accurate three-dimensional reconstruction of the AAA geometry and model an appropriate constitutive law for the aneurysmal tissue material characterization. In this regard, a recent study on the biaxial mechanical behavior of human AAA tissue specimens [1] demonstrates that aneurysmal arterial tissue behaves mechanically anisotropic. The objectives of the present work are to determine the effect of material anisotropy of the aneurysmal abdominal aorta on wall stress distribution and to establish a comparison of wall mechanics between ruptured and unruptured aneurysms.
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Sugita, Shukei, and Takeo Matsumoto. "Tensile Strength of the Aorta can be Estimated From Mechanical Parameters Which Depends on Degree of Intramural Collagen Fiber Alignment." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14247.

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Aortic aneurysms larger than a critical value, ∼50 mm for example, have high risk of rupture due to the Laplace’s law. However, aneurysms smaller than the critical diameter sometimes rupture (1, 2). Since intramural stress is relatively low in smaller aneurysms, their rupture indicates weakening of aneurysmal wall. For more reliable prediction of risk of aneurysm rupture, therefore, local strength of aneurysmal wall should be obtained.
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Trachet, Bram, Marjolijn Renard, Joris Bols, Steven Staelens, Bart Loeys, and Patrick Segers. "Hemodynamics in Ascending and Abdominal Aorta Aneurysm Formation in the ApoE−/− Angiotensin II Mouse Model." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80243.

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Aortic aneurysm is a pathological dilatation of the aorta that can be life-threatening when it ruptures. Aneurysms occur throughout the entire aorta but there is a predisposition for the ascending and the abdominal aorta, an observation that cannot be fully explained by the current knowledge of the disease pathophysiology. ApoE −/− mice infused with angiotensin II have recently been reported to develop not only abdominal [1], but also ascending aortic aneurysms [2]. These animals thus provide the perfect model to compare aneurysm progression in both aortic locations and to investigate whether disturbed hemodynamics play a role in the initial phase of aneurysm growth. In this study, both imaging and computational biomechanics techniques were used to elucidate the flow field at the location of the aneurysm prior to onset of the disease.
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Speelman, L., E. Moltzer, K. van der Heiden, P. van Heijningen, A. F. W. van der Steen, J. Essers, F. Gijsen, and J. Wentzel. "Biomechanical Characteristics of Aortic Aneurysms Generated in Fibulin-4 Deficient Mice." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80590.

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Aortic aneurysms affect approximately 5% of the elderly population and aneurysm rupture is responsible for a significant number of deaths in the western world. Risk factors for aortic aneurysm include high cholesterol, high blood pressure, and smoking. Fibulin-4 is a glycoprotein, which is expressed in medial layers of blood vessels and a critical component for the structural integrity and elasticity of the aortic wall [1]. Mice with reduced levels of Fibulin-4 develop aortic abnormalities similar to Fibulin-4 patients, such as dilation of the ascending aorta. A 4-fold reduction of Fibulin-4 expression (fib-4R/R) causes a severe dilation, while a mice with a 2-fold reduction (fib-4+/R) show an onset of aneurysm formation, comparable with the development of an aneurysm in aging humans [2].
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Swillens, Abigail, Lieve Lanoye, Julie De Backer, Nikos Stergiopulos, Frank Vermassen, Pascal Verdonck, and Patrick Segers. "The Impact of an Abdominal Aortic Aneurysm on Aortic Wave Reflection." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-175514.

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The economical growth and increased welfare in the Western world have a reverse side, with an increased death toll due to cardiovascular diseases. Among these, aortic aneurysms (a local dilation) are particularly lethal as they may grow unnoticed until rupture occurs. In this study, we assessed the impact of the presence of an abdominal aortic aneurysm on arterial hemodynamics and wave reflection in particular. Experimental and numerical methods were applied. Linear wave separation was used to quantify the reflections; wave intensity analysis was applied to assess the nature of the reflected waves. In both the experimental and numerical models, negative reflections were found in the upper aorta corresponding to a backward expansion wave caused by the sudden expansion of the aorta. A numerical parameter study demonstrated that larger diameters and more compliant aneurysms generate stronger negative reflections.
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Ene, Florentina, Carine Gachon, Patrick Delassus, and Liam Morris. "Investigating the Effect of Intraluminal Thrombus in Abdominal Aortic Aneurysm by Computational and Experimental Methods." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206636.

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Abdominal aortic aneurysm (AAA) represents an abnormal dilatation and weakening of the abdominal aorta with high risk of rupture. Most aneurysms of the infrarenal aorta possess an asymmetrical fusiform morphology.
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Washington, Christopher B., Judy Shum, Satish C. Muluk, and Ender A. Finol. "Abdominal Aortic Aneurysm Growth: The Association of Aortic Wall Mechanics and Geometry." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53977.

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In an effort to prevent rupture, patients with known AAA undergo periodic abdominal ultrasound or CT scan surveillance. When the aneurysm grows to a diameter of 5.0–5.5 cm or is shown to expand at a rate greater than 1 cm/yr, elective operative repair is undertaken. While this strategy certainly prevents a number of potentially catastrophic ruptures, AAA rupture can occur at sizes less than 5 cm. From a biomechanical standpoint, aneurysm rupture occurs when wall stress exceeds wall strength. By using non-invasive techniques, such as finite element analysis (FEA), wall stress can be estimated for patient specific AAA models, which can perhaps more carefully predict the rupture potential of a given aneurysm, regardless of size. FEA is a computational method that can be used to evaluate complicated structures such as aneurysms. To this end, it was reported earlier that AAA peak wall stress provides a better assessment of rupture risk than the commonly used maximum diameter criterion [1]. What has yet to be examined, however, is the relationship between wall stress and AAA geometry during aneurysm growth. Such finding has the potential for providing individualized predictions of AAA rupture potential during patient surveillance. The purpose of this study is to estimate peak wall stress for an AAA under surveillance and evaluate its potential correlation with geometric features characteristic of the aneurysm’s morphology.
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Morrison, Tina M., and Charles A. Taylor. "Circumferential Cyclic Strain in Patients With Descending Thoracic Aortic Aneurysms: Implications for Endovascular Device Design." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-204872.

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Endovascular graft (EVG) therapy has emerged as a promising alternative to open surgical repair of thoracic aortic aneurysms. However, the long-term durability of thoracic endovascular repair (TEVAR) remains uncertain due to complications such as incomplete aneurysm exclusion (endoleaks), migration, and stent fracture and collapse. These complications could likely be reduced if the biomechanical environment of the thoracic aorta was better understood. Currently, there are three FDA approved EVGs for treatment of descending thoracic aortic aneurysms (DTAA), but the range of bench-top testing mechanisms for these devices are limited.
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Ayyalasomayajula, Avinash, Bruce R. Simon, and Jonathan P. Vande Geest. "Porohyperelastic Simulation of Abdominal Aortic Aneurysms." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193147.

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Abdominal aortic aneurysm (AAA) is a progressive dilation of the infrarenal aorta and results in a significant alteration in local hemodynamic environment [1]. While an aneurysmal diameter of 5.5cm is typically classified as being of high risk, recent studies have demonstrated that maximum wall stress could be a better indicator of an AAA rupture than maximum diameter [2]. The wall stress is greatly influenced by the blood pressure, aneurysm diameter, shape, wall thickness and the presence of thrombus. The work done by Finol et al. suggested that hemodynamic pressure variations have an insignificant effect on AAA wall stress and that primarily the shape of the aneurysm determines the stress distribution. They noted that for peak wall stress studies the static pressure conditions would suffice as the in vivo conditions. Wang et al have developed an isotropic hyperelastic constitutive model for the intraluminal thrombus (ILT). Such models have been used to study the stress distributions in patient specific AAAs [3, 4].
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Reports on the topic "Aortic aneurysms"

1

Karmy-Jones, R. Abdominal Aortic Aneurysm and Pheochromocytoma. Science Repository, June 2019. http://dx.doi.org/10.31487/j.ijscr.2019.01.02.

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Jianqing, Deng, Jie Liu, Dan Rong, Yangyang Ge, Hongpeng Zhang, and Xiaoping Liu. Locoregional Anesthesia Versus General Anesthesia in Endovascular Repair of Ruptured Abdominal Aortic Aneurysm: A Meta-Analysis. INPLASY - International Platform of Registered Systematic Review Protocols, March 2020. http://dx.doi.org/10.37766/inplasy2020.3.0010.

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Newman-Toker, David E., Susan M. Peterson, Shervin Badihian, Ahmed Hassoon, Najlla Nassery, Donna Parizadeh, Lisa M. Wilson, et al. Diagnostic Errors in the Emergency Department: A Systematic Review. Agency for Healthcare Research and Quality (AHRQ), December 2022. http://dx.doi.org/10.23970/ahrqepccer258.

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Objectives. Diagnostic errors are a known patient safety concern across all clinical settings, including the emergency department (ED). We conducted a systematic review to determine the most frequent diseases and clinical presentations associated with diagnostic errors (and resulting harms) in the ED, measure error and harm frequency, as well as assess causal factors. Methods. We searched PubMed®, Cumulative Index to Nursing and Allied Health Literature (CINAHL®), and Embase® from January 2000 through September 2021. We included research studies and targeted grey literature reporting diagnostic errors or misdiagnosis-related harms in EDs in the United States or other developed countries with ED care deemed comparable by a technical expert panel. We applied standard definitions for diagnostic errors, misdiagnosis-related harms (adverse events), and serious harms (permanent disability or death). Preventability was determined by original study authors or differences in harms across groups. Two reviewers independently screened search results for eligibility; serially extracted data regarding common diseases, error/harm rates, and causes/risk factors; and independently assessed risk of bias of included studies. We synthesized results for each question and extrapolated U.S. estimates. We present 95 percent confidence intervals (CIs) or plausible range (PR) bounds, as appropriate. Results. We identified 19,127 citations and included 279 studies. The top 15 clinical conditions associated with serious misdiagnosis-related harms (accounting for 68% [95% CI 66 to 71] of serious harms) were (1) stroke, (2) myocardial infarction, (3) aortic aneurysm and dissection, (4) spinal cord compression and injury, (5) venous thromboembolism, (6/7 – tie) meningitis and encephalitis, (6/7 – tie) sepsis, (8) lung cancer, (9) traumatic brain injury and traumatic intracranial hemorrhage, (10) arterial thromboembolism, (11) spinal and intracranial abscess, (12) cardiac arrhythmia, (13) pneumonia, (14) gastrointestinal perforation and rupture, and (15) intestinal obstruction. Average disease-specific error rates ranged from 1.5 percent (myocardial infarction) to 56 percent (spinal abscess), with additional variation by clinical presentation (e.g., missed stroke average 17%, but 4% for weakness and 40% for dizziness/vertigo). There was also wide, superimposed variation by hospital (e.g., missed myocardial infarction 0% to 29% across hospitals within a single study). An estimated 5.7 percent (95% CI 4.4 to 7.1) of all ED visits had at least one diagnostic error. Estimated preventable adverse event rates were as follows: any harm severity (2.0%, 95% CI 1.0 to 3.6), any serious harms (0.3%, PR 0.1 to 0.7), and deaths (0.2%, PR 0.1 to 0.4). While most disease-specific error rates derived from mainly U.S.-based studies, overall error and harm rates were derived from three prospective studies conducted outside the United States (in Canada, Spain, and Switzerland, with combined n=1,758). If overall rates are generalizable to all U.S. ED visits (130 million, 95% CI 116 to 144), this would translate to 7.4 million (PR 5.1 to 10.2) ED diagnostic errors annually; 2.6 million (PR 1.1 to 5.2) diagnostic adverse events with preventable harms; and 371,000 (PR 142,000 to 909,000) serious misdiagnosis-related harms, including more than 100,000 permanent, high-severity disabilities and 250,000 deaths. Although errors were often multifactorial, 89 percent (95% CI 88 to 90) of diagnostic error malpractice claims involved failures of clinical decision-making or judgment, regardless of the underlying disease present. Key process failures were errors in diagnostic assessment, test ordering, and test interpretation. Most often these were attributed to inadequate knowledge, skills, or reasoning, particularly in “atypical” or otherwise subtle case presentations. Limitations included use of malpractice claims and incident reports for distribution of diseases leading to serious harms, reliance on a small number of non-U.S. studies for overall (disease-agnostic) diagnostic error and harm rates, and methodologic variability across studies in measuring disease-specific rates, determining preventability, and assessing causal factors. Conclusions. Although estimated ED error rates are low (and comparable to those found in other clinical settings), the number of patients potentially impacted is large. Not all diagnostic errors or harms are preventable, but wide variability in diagnostic error rates across diseases, symptoms, and hospitals suggests improvement is possible. With 130 million U.S. ED visits, estimated rates for diagnostic error (5.7%), misdiagnosis-related harms (2.0%), and serious misdiagnosis-related harms (0.3%) could translate to more than 7 million errors, 2.5 million harms, and 350,000 patients suffering potentially preventable permanent disability or death. Over two-thirds of serious harms are attributable to just 15 diseases and linked to cognitive errors, particularly in cases with “atypical” manifestations. Scalable solutions to enhance bedside diagnostic processes are needed, and these should target the most commonly misdiagnosed clinical presentations of key diseases causing serious harms. New studies should confirm overall rates are representative of current U.S.-based ED practice and focus on identified evidence gaps (errors among common diseases with lower-severity harms, pediatric ED errors and harms, dynamic systems factors such as overcrowding, and false positives). Policy changes to consider based on this review include: (1) standardizing measurement and research results reporting to maximize comparability of measures of diagnostic error and misdiagnosis-related harms; (2) creating a National Diagnostic Performance Dashboard to track performance; and (3) using multiple policy levers (e.g., research funding, public accountability, payment reforms) to facilitate the rapid development and deployment of solutions to address this critically important patient safety concern.
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4

Endovascular aortic repair (EVAR) surgery more beneficial for ruptured abdominal aortic aneurysms than open repair. National Institute for Health Research, August 2018. http://dx.doi.org/10.3310/signal-000638.

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No clear difference between open and keyhole surgery for the repair of ruptured abdominal aortic aneurysms. National Institute for Health Research, May 2016. http://dx.doi.org/10.3310/signal-000234.

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Fewer wound hernias occur if mesh is used to reinforce abdominal aortic aneurysm surgery. National Institute for Health Research, September 2018. http://dx.doi.org/10.3310/signal-000644.

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Abdominal aortic aneurysm screening for women is unlikely to be a fair use of NHS resources. National Institute for Health Research, November 2018. http://dx.doi.org/10.3310/signal-000676.

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