Relevant bibliographies by topics / Aneurysm Progression

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Aneurysm Progression'

Author: Grafiati
Published: 7 June 2025
Last updated: 26 June 2025

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Journal articles on the topic "Aneurysm Progression"

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Jeong, Woowon, and Kyehan Rhee. "Hemodynamics of Cerebral Aneurysms: Computational Analyses of Aneurysm Progress and Treatment." Computational and Mathematical Methods in Medicine 2012 (2012): 1–11. http://dx.doi.org/10.1155/2012/782801.

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The progression of a cerebral aneurysm involves degenerative arterial wall remodeling. Various hemodynamic parameters are suspected to be major mechanical factors related to the genesis and progression of vascular diseases. Flow alterations caused by the insertion of coils and stents for interventional aneurysm treatment may affect the aneurysm embolization process. Therefore, knowledge of hemodynamic parameters may provide physicians with an advanced understanding of aneurysm progression and rupture, as well as the effectiveness of endovascular treatments. Progress in medical imaging and information technology has enabled the prediction of flow fields in the patient-specific blood vessels using computational analysis. In this paper, recent computational hemodynamic studies on cerebral aneurysm initiation, progress, and rupture are reviewed. State-of-the-art computational aneurysmal flow analyses after coiling and stenting are also summarized. We expect the computational analysis of hemodynamics in cerebral aneurysms to provide valuable information for planning and follow-up decisions for treatment.
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Cojocari, Vladimir, Vasile Culiuc, Florin Bzovii, Dumitru Casian, and Eugen Gutu. "Giant thrombosed saphenofemoral junction aneurysm: A case report." SAGE Open Medical Case Reports 5 (January 1, 2017): 2050313X1774101. http://dx.doi.org/10.1177/2050313x17741012.

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Introduction: Although saphenofemoral junction aneurysms are not so rare, only scarce of the published cases reported thrombosis of the aneurysmal sac and saphenous trunk. Presentation of case: A 65-year-old male with varicose disease, developed acute ascending superficial vein thrombosis of the left greater saphenous vein, involving the 6-cm saphenofemoral junction aneurysm. The patient underwent common femoral vein thrombectomy, aneurysm removal, and greater saphenous vein excision with uneventful postoperative course. Conclusion: Thrombosed giant saphenofemoral junction aneurysms require emergent surgical intervention aimed at preventing potential progression to deep vein thrombosis and pulmonary embolism.
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Melin, Leander Gaarde, Julie Husted Dall, Jes S. Lindholt, et al. "Cycloastragenol Inhibits Experimental Abdominal Aortic Aneurysm Progression." Biomedicines 10, no. 2 (2022): 359. http://dx.doi.org/10.3390/biomedicines10020359.

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The pathogenesis of abdominal aortic aneurysm involves vascular inflammation and elastin degradation. Astragalusradix contains cycloastragenol, which is known to be anti-inflammatory and to protect against elastin degradation. We hypothesized that cycloastragenol supplementation inhibits abdominal aortic aneurysm progression. Abdominal aortic aneurysm was induced in male rats by intraluminal elastase infusion in the infrarenal aorta and treated daily with cycloastragenol (125 mg/kg/day). Aortic expansion was followed weekly by ultrasound for 28 days. Changes in aneurysmal wall composition were analyzed by mRNA levels, histology, zymography and explorative proteomic analyses. At day 28, mean aneurysm diameter was 37% lower in the cycloastragenol group (p < 0.0001). In aneurysm cross sections, elastin content was insignificantly higher in the cycloastragenol group (10.5% ± 5.9% vs. 19.9% ± 16.8%, p = 0.20), with more preserved elastin lamellae structures (p = 0.0003) and without microcalcifications. Aneurysmal matrix metalloprotease-2 activity was reduced by the treatment (p = 0.022). Messenger RNA levels of inflammatory- and anti-oxidative markers did not differ between groups. Explorative proteomic analysis showed no difference in protein levels when adjusting for multiple testing. Among proteins displaying nominal regulation were fibulin-5 (p = 0.02), aquaporin-1 (p = 0.02) and prostacyclin synthase (p = 0.007). Cycloastragenol inhibits experimental abdominal aortic aneurysm progression. The suggested underlying mechanisms involve decreased matrix metalloprotease-2 activity and preservation of elastin and reduced calcification, thus, cycloastragenol could be considered for trial in abdominal aortic aneurysm patients.
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Chalouhi, Nohra, Muhammad S. Ali, Pascal M. Jabbour, et al. "Biology of Intracranial Aneurysms: Role of Inflammation." Journal of Cerebral Blood Flow & Metabolism 32, no. 9 (2012): 1659–76. http://dx.doi.org/10.1038/jcbfm.2012.84.

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Intracranial aneurysms (IAs) linger as a potentially devastating clinical problem. Despite intense investigation, our understanding of the mechanisms leading to aneurysm development, progression and rupture remain incompletely defined. An accumulating body of evidence implicates inflammation as a critical contributor to aneurysm pathogenesis. Intracranial aneurysm formation and progression appear to result from endothelial dysfunction, a mounting inflammatory response, and vascular smooth muscle cell phenotypic modulation producing a pro-inflammatory phenotype. A later final common pathway appears to involve apoptosis of cellular constituents of the vessel wall. These changes result in degradation of the integrity of the vascular wall leading to aneurysmal dilation, progression and eventual rupture in certain aneurysms. Various aspects of the inflammatory response have been investigated as contributors to IA pathogenesis including leukocytes, complement, immunoglobulins, cytokines, and other humoral mediators. Furthermore, gene expression profiling of IA compared with control arteries has prominently featured differential expression of genes involved with immune response/inflammation. Preliminary data suggest that therapies targeting the inflammatory response may have efficacy in the future treatment of IA. Further investigation, however, is necessary to elucidate the precise role of inflammation in IA pathogenesis, which can be exploited to improve the prognosis of patients harboring IA.
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Jamous, Mohammad A., Shinji Nagahiro, Keiko T. Kitazato, Tetsuya Tamura, Kazuyuki Kuwayama, and Koichi Satoh. "Role of estrogen deficiency in the formation and progression of cerebral aneurysms. Part II: experimental study of the effects of hormone replacement therapy in rats." Journal of Neurosurgery 103, no. 6 (2005): 1052–57. http://dx.doi.org/10.3171/jns.2005.103.6.1052.

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Object. The increased incidence of cerebral aneurysms in postmenopausal women appears to be related to low levels of circulating estrogen. Using a rat model of aneurysm induction, the authors found that oophorectomy increased the incidence of experimental cerebral aneurysms (Part I in this issue). In the current study they examined the effects of hormone replacement therapy (HRT) on the formation of cerebral aneurysms in rats. Methods. Forty-five female Sprague—Dawley rats were divided into three equal groups. The animals in Groups A and B were subjected to a cerebral aneurysm induction procedure (renal hypertension and right common carotid artery ligation) followed 1 month later by bilateral oophorectomy. After an additional week the rats in Group A received 17β estradiol continuous-release pellets. The rats in Group C served as controls. Three months after the aneurysm induction procedure, all the rats were killed and vascular corrosion casts of their cerebral arteries were prepared and checked for aneurysmal changes. Using a scanning electron microscope, the authors recorded aneurysmal changes as endothelial changes alone (Stage I), endothelial changes with intimal pad elevation (Stage II), and saccular aneurysm formation (Stage III). Aneurysmal changes (Stages I, II, and III) occurred in one third of rats that had undergone oophorectomy and were receiving HRT (Group A), compared with 87% of the rats that had undergone oophorectomy but did not receive HRT (Group B). Although most of the aneurysmal changes identified in Group A rats were limited to Stage I or II, most changes in Group B animals were identified as saccular dilation (Stage III). Conclusions. The findings demonstrated the significant protective role of estrogen against the formation and progression of cerebral aneurysms. It appears to be related to the beneficial effects of estrogen on the function and growth of endothelial cells, which play a major role in preserving the integrity of the vascular wall.
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Abecassis, Isaac Josh, Rajeev D. Sen, Jason Barber, et al. "Predictors of Recurrence, Progression, and Retreatment in Basilar Tip Aneurysms: A Location-Controlled Analysis." Operative Neurosurgery 16, no. 4 (2018): 435–44. http://dx.doi.org/10.1093/ons/opy132.

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Abstract BACKGROUND Endovascular treatment of intracranial aneurysms is associated with higher rates of recurrence and retreatment, though contemporary rates and risk factors for basilar tip aneurysms (BTAs) are less well-described. OBJECTIVE To characterize progression, retreatement, and retreated progression of BTAs treated with microsurgical or endovascular interventions. METHODS We retrospectively reviewed records for 141 consecutive BTA patients. We included 158 anterior communicating artery (ACoA) and 118 middle cerebral artery (MCA) aneurysms as controls. Univariate and multivariate analyses were used to calculate rates of progression (recurrence of previously obliterated aneurysms and progression of known residual aneurysm dome or neck), retreatment, and retreated progression. Kaplan–Meier analysis was used to characterize 24-mo event rates for primary outcome prediction. RESULTS Of 141 BTA patients, 62.4% were ruptured and 37.6% were unruptured. Average radiographical follow-up was 33 mo. Among ruptured aneurysms treated with clipping, there were 2 rehemorrhages due to recurrence (6.1%), and none in any other cohorts. Overall rates of progression (28.9%), retreatment (28.9%), and retreated progression (24.7%) were not significantly different between surgical and endovascular subgroups, though ruptured aneurysms had higher event rates. Multivariate modeling confirmed rupture status (P = .003, hazard ratio = 0.14) and aneurysm dome width (P = .005, hazard ratio = 1.23) as independent predictors of progression requiring retreatment. In a separate multivariate analysis with ACoA and MCA aneurysms, basilar tip location was an independent predictor of progression, retreatment, and retreated progression. CONCLUSION BTAs have higher rates of progression and retreated progression than other aneurysm locations, independent of treatment modality. Rupture status and dome width are risk factors for progression requiring retreatment.
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Loste, Alexia, Marc Clément, Sandrine Delbosc, et al. "Involvement of an IgE/Mast cell/B cell amplification loop in abdominal aortic aneurysm progression." PLOS ONE 18, no. 12 (2023): e0295408. http://dx.doi.org/10.1371/journal.pone.0295408.

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Aims IgE type immunoglobulins and their specific effector cells, mast cells (MCs), are associated with abdominal aortic aneurysm (AAA) progression. In parallel, immunoglobulin-producing B cells, organised in tertiary lymphoid organs (TLOs) within the aortic wall, have also been linked to aneurysmal progression. We aimed at investigating the potential role and mechanism linking local MCs, TLO B cells, and IgE production in aneurysmal progression. Methods and results Through histological assays conducted on human surgical samples from AAA patients, we uncovered that activated MCs were enriched at sites of unhealed haematomas, due to subclinical aortic wall fissuring, in close proximity to adventitial IgE+ TLO B cells. Remarkably, in vitro the IgEs deriving from these samples enhanced MC production of IL-4, a cytokine which favors IgE class-switching and production by B cells. Finally, the role of MCs in aneurysmal progression was further analysed in vivo in ApoE-/- mice subjected to angiotensin II infusion aneurysm model, through MC-specific depletion after the establishment of dissecting aneurysms. MC-specific depletion improved intramural haematoma healing and reduced aneurysmal progression. Conclusions Our data suggest that MC located close to aortic wall fissures are activated by adventitial TLO B cell-produced IgEs and participate to their own activation by providing support for further IgE synthesis through IL-4 production. By preventing prompt repair of aortic subclinical fissures, such a runaway MC activation loop could precipitate aneurysmal progression, suggesting that MC-targeting treatments may represent an interesting adjunctive therapy for reducing AAA progression.
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Rayz, Vitaliy L., and Aaron A. Cohen-Gadol. "Hemodynamics of Cerebral Aneurysms: Connecting Medical Imaging and Biomechanical Analysis." Annual Review of Biomedical Engineering 22, no. 1 (2020): 231–56. http://dx.doi.org/10.1146/annurev-bioeng-092419-061429.

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In the last two decades, numerous studies have conducted patient-specific computations of blood flow dynamics in cerebral aneurysms and reported correlations between various hemodynamic metrics and aneurysmal disease progression or treatment outcomes. Nevertheless, intra-aneurysmal flow analysis has not been adopted in current clinical practice, and hemodynamic factors usually are not considered in clinical decision making. This review presents the state of the art in cerebral aneurysm imaging and image-based modeling, discussing the advantages and limitations of each approach and focusing on the translational value of hemodynamic analysis. Combining imaging and modeling data obtained from different flow modalities can improve the accuracy and fidelity of resulting velocity fields and flow-derived factors that are thought to affect aneurysmal disease progression. It is expected that predictive models utilizing hemodynamic factors in combination with patient medical history and morphological data will outperform current risk scores and treatment guidelines. Possible future directions include novel approaches enabling data assimilation and multimodality analysis of cerebral aneurysm hemodynamics.
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Lawson, Matthew F., William C. Newman, Yueh-Yun Chi, J. D. Mocco, and Brian L. Hoh. "Stent-Associated Flow Remodeling Causes Further Occlusion of Incompletely Coiled Aneurysms." Neurosurgery 69, no. 3 (2011): 598–604. http://dx.doi.org/10.1227/neu.0b013e3182181c2b.

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Abstract BACKGROUND: Incomplete coil occlusion is associated with increased risk of aneurysm recurrence. We hypothesize that intracranial stents can cause flow remodeling, which promotes further occlusion of an incompletely coiled aneurysm. OBJECTIVE: To study our hypothesis by comparing the follow-up angiographic outcomes of stented and nonstented incompletely coiled aneurysms. METHODS: From January 2006 through December 2009, the senior author performed 324 initial coilings of previously untreated aneurysms, 145 of which were Raymond classification 2 and 3. Follow-up angiographic studies were available for 109 of these aneurysms (75%). Angiographic outcomes for stented vs nonstented incompletely coiled aneurysms were compared. A multivariate analysis was performed to identify factors related to the progression of occlusion at follow-up, with adjustment for aneurysm location, size, neck size, Hunt-Hess grade, stent use, initial Raymond score, packing density, age, sex, and medical comorbidities. RESULTS: Of the 109 aneurysms, 37 were stented and 72 were not stented. With a median follow-up time of 15.4 months, 33 stented aneurysms (89%) progressed to complete occlusion compared with 29 nonstented aneurysms (40%). Recanalization rates were lower in the stented group (8.1%) compared with the nonstented group (37.5%; P < .001). On multivariate analysis, stent use (odds ratio, 18.5; 95% confidence interval, 4.3-76.9) and packing density (odds ratio, 1.093; 95% confidence interval, 1.021-1.170) were significant predictors of the progression of occlusion. Aneurysm size was negatively correlated with the progression of occlusion (odds ratio, 0.844; 95% confidence interval, 0.724-0.983). CONCLUSION: Stent-assisted coiling causes progression of occlusion, possibly by a flow remodeling effect. The odds of progression of occlusion of stent-coiled aneurysms were 18.5 times that of nonstented aneurysms.
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Sadamasa, Nobutake, Kazuhiko Nozaki, Yasushi Takagi, et al. "Cerebral aneurysm progression suppressed by blockage of endothelin B receptor." Journal of Neurosurgery 106, no. 2 (2007): 330–36. http://dx.doi.org/10.3171/jns.2007.106.2.330.

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Object Cerebral aneurysm is a major cause of subarachnoid hemorrhage, but the mechanisms of its development remain unclear. Mechanical stretch has been reported to induce vascular smooth-muscle cell apoptosis via endothelin B receptors (ETBRs). The objectives of this study were to clarify the expression and localization of ETBR in cerebral aneurysms and to examine the effect of ETBR blockage on the development of experimental cerebral aneurysms. Methods Seventy-two rats underwent a cerebral aneurysm induction procedure and were divided into four groups according to the duration of postoperative study periods. Expression of ETBR was confirmed by reverse transcription–polymerase chain reaction and immunohistochemical analysis. The authors also studied the effect of K-8794, an oral selective antagonist of ETBR, to see whether it would influence the formation of cerebral aneurysms. Two weeks after the aneurysm induction procedure, ETBR was rarely detected in anterior cerebral artery–olfactory artery bifurcations, but it was weakly expressed in experimental cerebral aneurysms at 1 month after the procedure, and markedly expressed at 3 months. The administration of K-8794 for 1 month after the procedure significantly reduced the number of advanced aneurysms and the number of apoptotic smooth-muscle cells. Conclusions These results suggest that ETBR might play a significant role in the progression of cerebral aneurysms and have the potential to improve prevention and treatment of cerebral aneurysms.
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Dissertations / Theses on the topic "Aneurysm Progression"

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Thompson, Andrew. "The aetiology behind AAA disease formation and progression." Thesis, University College London (University of London), 2009. http://discovery.ucl.ac.uk/17595/.

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AAA disease remains a common and life threatening condition, predominantly affecting men of retirement age. Whilst clinical studies have done much to predict the course of this disease, understanding the pathogenesis has been complicated by both a multi-factorial aetiology as well as several poorly defined stages to the disease (formation, growth and rupture). Evidence points to a considerable inheritable component to this condition, but as yet, associations with identified genetic variants are few and weak. This thesis describes the current understanding of the molecular mechanisms behind AAA pathogenesis, concentrating on aneurysm formation and growth. A meta-analysis of published candidate gene studies identified three genes with small but significant effects on risk of developing AAA (ACE, MTHFR and MMP9) and none with a significant effect on AAA growth. Further examination of five genes connected the Renin-Angiotensin System, using three distinct case control series, demonstrated the strongest reported association to date with AAA disease risk, with AGTR1+1166A>C. (OR 1.55 [1.30-1.83, p=5x10-7]). An interest in the role of the TGF-β pathway in AAA formation and growth has developed from the recent illumination of the mechanism behind aneurysm aetiology in Marfan syndrome. Haplotype analysis was used to investigate five genes coding for TGF-β and its binding protein (LTBP). Variants in TGFB3 and LTBP4 were significantly associated with altered AAA growth. The importance of inflammatory process was also supported by observations made in a very large longitudinal data set of AAA growth. Anti-inflammatory drugs, together with anti-platelet drugs and drugs used in diabetes, were significantly associated with decreased AAA growth independent of confounding factors. In conclusion, this thesis demonstrates; a role for the RAS in AAA formation; TGF-β in AAA growth; and anti-inflammatory drugs as potentially disease modifying. In addition, observations have also been made concerning a two tier effect illuding to the nature AAA progression.
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O'Connell, Mary Kathleen. "Understanding abdominal aortic aneurysm progression through three-dimensional microstructure imaging /." May be available electronically:, 2007. http://proquest.umi.com/login?COPT=REJTPTU1MTUmSU5UPTAmVkVSPTI=&clientId=12498.

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Haskett, Darren. "Toward a Method for Biomechanical Determination of Aneurysm Progression in Mouse Models." Thesis, The University of Arizona, 2011. http://hdl.handle.net/10150/144598.

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Aortic aneurysm is a complex disease manifesting in a localized dilation of the aorta developing over years and carries with it a significant chance of rupture resulting in death. As only surgical methods are currently available for treatment, there is a need to understand the underlying mechanisms of the disease and how they develop and lead to expansion and rupture. Thus, the study of the formation and progression of aneurysm has also focused on quantifying any changes observed in fiber realignment and altered mechanical properties leading to vascular disease. Animal models of aneurismal disease can be useful for studying alterations during disease development (e.g., in the tissue's mechanical response). Recent efforts have been aimed at determining both the biomechanical alterations that occur with aneurysm formation and their potential for rupture. However, previous animal model work is lacking quantitative descriptions of how biomechanical response and vessel remodeling change with time and lead to the diseased state. Thus, there is a need for determining an appropriate animal model for aneurysm and developing an adequate method for quantifying and determining disease progression through alterations in biomechanical response.
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Abekura, Yu. "Eicosapentaenoic acid prevents the progression of intracranial aneurysms in rats." Kyoto University, 2020. http://hdl.handle.net/2433/259723.

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Rodway, Alexander Dominic. "Progression of dilating disease in patients after open or endovascular abdominal aortic aneurysm repair." Thesis, Imperial College London, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501430.

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Ahmad, Mehtab. "Interleukin-1α as a biomarker of human abdominal aortic aneurysm (AAA) development and progression". Thesis, University of Birmingham, 2017. http://etheses.bham.ac.uk//id/eprint/7712/.

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This Thesis presents an analysis of the role of interleukin (IL)-1α (IL-1α) as a potential future surrogate biomarker for AAA. It is the only research work to date to have looked into the role of IL-1α as a biomarker in AAA disease, correlating titres with different anatomical, morphological and patient-related factors. It is the first piece, in over 20 years of published literature, to have performed a robust methodology study on the measurement of IL-1a in serum samples using different techniques. A comparison study of commercially available immunoassays in the context of IL-1α has never been undertaken before, and we are the first to undertake one. Additionally the work on the natural history of AAA is one of the largest single-centre cohort studies to analyse AAA growth in surveillance. The work covers three main areas: identifying why current strategies for monitoring AAA are ineffective, analysis of different serum processing methodologies and commercially available immunoassays used to measure IL-1α, and linking IL-1α to different anatomical, morphological and patient-related AAA factors.
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Miyata, Takeshi. "Osteoprotegerin Prevents Intracranial Aneurysm Progression by Promoting Collagen Biosynthesis and Vascular Smooth Muscle Cell Proliferation." Doctoral thesis, Kyoto University, 2021. http://hdl.handle.net/2433/264661.

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Setozaki, Shuji. "Prevention of abdominal aortic aneurysm progression by oral administration of green tea polyphenol in a rat model." 京都大学 (Kyoto University), 2017. http://hdl.handle.net/2433/225461.

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Lange, Christoph [Verfasser]. "Angiotensin AT2 receptor agonist, compound 21, prevents extracellular matrix degradation, maintains vascular integrity and prevents abdominal aortic aneurysm progression in the rat / Christoph Lange." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2019. http://d-nb.info/1202463851/34.

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Liu, Shengliang [Verfasser], Lars [Akademischer Betreuer] Mägdefessel, Tobias [Gutachter] Koppara, and Lars [Gutachter] Mägdefessel. "Role of Neutrophil Extracellular Traps and Necroptosis in Abdominal Aortic Aneurysm Disease Development and Progression / Shengliang Liu ; Gutachter: Tobias Koppara, Lars Mägdefessel ; Betreuer: Lars Mägdefessel." München : Universitätsbibliothek der TU München, 2020. http://d-nb.info/1205879900/34.

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Books on the topic "Aneurysm Progression"

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Tasse, Jordan C., and Bulent Arslan. Management of Acute Iliocaval Thrombosis. Edited by S. Lowell Kahn, Bulent Arslan, and Abdulrahman Masrani. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199986071.003.0035.

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Acute deep vein thrombosis (DVT) occurs in approximately 300,000 people per year in the United States. Iliocaval thrombosis is most commonly related to the progression of lower extremity DVT. Inferior vena cava (IVC) thrombosis occurs in approximately 4–15% of patients with acute DVT. Vena cava thrombosis is frequently associated with neoplastic disease. Foreign body placement such as an IVC filter or a venous catheter is a frequently reported cause of iliocaval thrombosis. External compression due to right common iliac artery mass effect (May–Thurner syndrome), tumor, lymphadenopathy, or aortic aneurysm are also commonly seen. This chapter discusses the interventional measures to manage acute iliocaval thrombosis.
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Michel, Jean-Baptiste. Biology of vascular wall dilation and rupture. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0016.

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Arterial pathologies, important causes of death and morbidity in humans, are closely related to modifications in the circulatory system during evolution. With increasing intraluminal pressure and arterial bifurcation density, the arterial wall becomes the target of interactions with blood components and outward convection of plasma solutes and particles, including plasma zymogens and leukocyte proteases. Abdominal aortic aneurysms of atherothrombotic origin are characterized by the presence of an intraluminal thrombus (ILT), a major source of proteases, including plasmin, MMP-9, and elastase. Saccular cerebral aneurysms are characterized by the interaction of haemodynamics and arterial bifurcation defects, of either genetic or congenital origin. They also develop an intrasaccular thrombus, implicated in rupture. Aneurysms of the ascending aorta (TAAs) are not linked to atherothrombotic disease, and do not develop an ILT. The most common denominator of TAAs, whatever their aetiology, is the presence of areas of mucoid degeneration, and increased convection and vSMC-dependent activation of plasma zymogens within the wall, causing extracellular matrix proteolysis. TAA development is also associated with an epigenetic phenomenon of SMAD2 overexpression and nuclear translocation, potentially linked to chronic changes in mechanotransduction. Aortic dissections share common aetiologies and pathology (areas of mucoid degeneration) with TAAs, but differ by the absence of any compensatory epigenetic response. There are main experimental animal models of aneurysms, all characterized by the cessation of aneurysmal progression after interruption of the exogenous stimuli used to induce it. These new pathophysiological approaches to aneurysms in humans pave the way for new diagnostic and therapeutic tools.
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Book chapters on the topic "Aneurysm Progression"

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Alblas, Dieuwertje, Marieke Hofman, Christoph Brune, Kak Khee Yeung, and Jelmer M. Wolterink. "Implicit Neural Representations for Modeling of Abdominal Aortic Aneurysm Progression." In Functional Imaging and Modeling of the Heart. Springer Nature Switzerland, 2023. http://dx.doi.org/10.1007/978-3-031-35302-4_37.

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Ivanov, Tihomir B., and Elena V. Nikolova. "Stability Analysis of an Inflation of Internally-Pressurized Hyperelastic Spherical Membranes Connected to Aneurysm Progression." In Advanced Computing in Industrial Mathematics. Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-49544-6_6.

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Gavish, Lilach, Louise S. Perez, Petachia Reissman, and S. David Gertz. "Irradiation with 780 nm Diode Laser Attenuates Inflammatory Cytokines While Upregulating Nitric Oxide in LPS-Stimulated Macrophages: Implications for the Prevention of Aneurysm Progression." In Lecture Notes in Electrical Engineering. Springer US, 2008. http://dx.doi.org/10.1007/978-0-387-71809-5_6.

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Yu, Yannan, and David Yen-Ting Chen. "Machine Learning for Cerebrovascular Disorders." In Machine Learning for Brain Disorders. Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3195-9_29.

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AbstractCerebrovascular disease refers to a group of conditions that affect blood flow and the blood vessels in the brain. It is one of the leading causes of mortality and disability worldwide, imposing a significant socioeconomic burden to society. Research on cerebrovascular diseases has been rapidly progressing leading to improvement in the diagnosis and management of patients nowadays. Machine learning holds many promises for further improving clinical care of these disorders. In this chapter, we will briefly introduce general information regarding cerebrovascular disorders and summarize some of the most promising fields in which machine learning shall be valuable to improve research and patient care. More specifically, we will cover the following cerebrovascular disorders: stroke (both ischemic and hemorrhagic), cerebral microbleeds, cerebral vascular malformations, intracranial aneurysms, and cerebral small vessel disease (white matter hyperintensities, lacunes, perivascular spaces).
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Dahl, Aaron B., and R. Eliot Fagley. "Thoracic Aortic Aneurysm." In Cardiac Anesthesia: A Problem-Based Learning Approach, edited by Mohammed M. Minhaj. Oxford University Press, 2019. http://dx.doi.org/10.1093/med/9780190884512.003.0028.

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Thoracic and thoracoabdominal aortic aneurysms often require surgical repair depending on the size of the aneurysm and the acuity of progression. The involvement of the aortic arch makes consideration of surgical approaches challenging, as it contains the vessels that provide cerebral perfusion. Risk factors for growth and rupture of thoracoabdominal aneurysms include aneurysm size, rapid aneurysm growth, aortic dissection, older age, female sex, chronic obstructive pulmonary disease, cigarette smoking, pain, and a positive family history. Without surgical repair, there is a risk of fatal rupture. Planning the appropriate surgical approach is complex, and protection of the spinal cord from ischemic complications is of paramount importance.
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Formanowicz, Piotr, Michał Nowicki, and Dorota Formanowicz. "Mathematical Modeling of Aortic Aneurysm Progression." In New Approaches to Aortic Diseases from Valve to Abdominal Bifurcation. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-809979-7.00007-9.

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Donegá Constantin, Bruno, and Erasmo Simão da Silva. "Abdominal Aortic Aneurysm Biomechanics." In Advances in Clinical Biomechanics [Working Title]. IntechOpen, 2025. https://doi.org/10.5772/intechopen.1010315.

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Abdominal aortic aneurysms (AAA) are localized dilations of the aorta that develop due to complex biomechanical and pathophysiological mechanisms. Aging and arterial remodeling contribute to the weakening of the aortic wall, increasing susceptibility to aneurysm formation and rupture. The primary risk factors include age, male sex, smoking, hypertension, and genetic predisposition. The most feared complication of AAA is rupture, which carries a high mortality rate, often exceeding 80%. Current clinical guidelines rely on aneurysm diameter and growth rate to indicate surgical repair; however, these criteria alone are insufficient to predict rupture risk accurately. Biomechanical analyses provide a deeper understanding of AAA progression. The arterial wall is a nonlinear, anisotropic, and viscoelastic structure, where collagen and elastin fibers play crucial roles in mechanical stability. Uniaxial tensile testing, finite element analysis, and computational fluid dynamics help assess wall stress distribution and predict failure points. The presence of intraluminal thrombus also influences aneurysm behavior, altering hemodynamics and mechanical resistance. Despite advancements, identifying reliable rupture predictors remains challenging. Integrating biomechanical models with clinical parameters could improve risk stratification and guide individualized treatment strategies. This chapter explores the biomechanics of AAA, highlighting the interplay between structural integrity, hemodynamics, and rupture risk assessment.
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Metsker, Oleg, Georgy Kopanitsa, Olga Irtyuga, and Vladimir Uspenskiy. "Dynamic Aortic Aneurism Risk Factors." In pHealth 2021. IOS Press, 2021. http://dx.doi.org/10.3233/shti210585.

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According to different systematic reviews incidence of thoracic aortic aneurysms (TAA) in the general population is increasing in frequency ranging from 5 to 10.4 per 100000 patients. However, only few studies have illustrated the role of different risk factors in the onset and progression of ascending aortic dilatation. Currently, noninvasive imaging techniques are used to assess the progression rate of aortic and aortic valve disease. Transthoracic (TT) Echocardiographic examination routinely includes evaluation of the aorta It is the most available screening method for diagnosis of proximal aortic dilatation. Since the predominant area of dilation is the proximal aorta, TT-echo is often sufficient for screening. We retrospectively analyzed the ECHO database with 78499 echocardiographic records in the Almazov National Medical Research Centre to identify patients with aneurysm. Detailed information including demographic characteristics, ECHO results and comorbidities were extracted from outpatient clinic and from hospital charts related to hospitalizations occurring within a year before index echocardiography was performed. Comorbid diseases were similarly extracted from outpatient clinic and/or hospital admissions. The classifier showed an AUC-ROC for predicting of aneurism detection after a repeated ECHO at 82%.
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Weir, Bryce. "Pathology of Saccular and Nonsaccular Aneurysms." In Subarachnoid Hemorrhage: Causes And Cures. Oxford University PressNew York, NY, 1998. http://dx.doi.org/10.1093/oso/9780195128758.003.0006.

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Abstract The critical change for saccular aneurysm formation is progressive fragmentation of the internal elastica. This usually develops during adulthood. Aneurysms develop relatively more frequently in cerebral arteries than in systemic muscular arteries, possibly because cerebral arteries have only one elastic lamina. The influence of defects in the muscularis layer, particularly at bifurcations, on the genesis of aneurysms is unclear. Such medial defects may be normal anatomic features. Aneurysms arise preferentially at the apex of a bifurcation, not because of congenital weakness but because this is the site of maximum hemodynamic stress. An “unbalanced” circle of Willis may increase the flow rate across a particular bifurcation, thereby subjecting it to increased stress and the likelihood of the development of an aneurysm. This is the only discernible inborn aspect of the pathogenesis of aneurysms. Once the internal elastic membrane is damaged, aneurysmal outpouching can begin in response to the pulsatile pressure head transmitted to the weakened apex by the impinging axial stream (Fig. 6-1).
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Iung, Bernard. "Genetic diseases of the aorta: aortic diseases related to Marfan syndrome and other genetic abnormalities." In ESC CardioMed, edited by Raimund Erbel. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0623.

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Bicuspid aortic valve affects 1–2% of babies at birth and is frequently associated with thoracic aortic aneurysm but the risk of aortic dissection is low. Indications for aortic surgery are based on studies on natural history. Aortic surgery is recommended when the maximum aortic diameter is greater than 55 mm in patients with a bicuspid aortic valve. Intervention is indicated at an earlier stage when there are associated risk factors, in particular familial history of aortic dissection or rapid progression, or if there is an indication for aortic valve replacement. The choice between partial or total replacement of the aorta should be based on anatomy, but also take into account the patient’s age and operative risk.
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Conference papers on the topic "Aneurysm Progression"

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Cebral, Juan R., Daniel Sforza, Satoshi Tateshima, Fernando Vinuela, and Christopher Putman. "Longitudinal Image Based Study of Cerebral Aneurysms: Growth, Contacts and Hemodynamics During Aneurysmal Progression." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53382.

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Improving current procedures for the evaluation and treatment of cerebral aneurysms requires a better understanding of the underlying mechanisms governing their formation, progression and rupture. It is generally accepted that these mechanisms are multi-factorial, involving: hemodynamics, wall biomechanics and mechano-biology, and contacts with peri-aneurysmal structures [1]. However, little is known about the relative importance and interactions of these factors. The broad objective of our research is to investigate the mechanisms of aneurysm progression by studying cerebral aneurysms that are followed longitudinally in time with non-invasive 3D imaging. In this context, the goal of this paper is to highlight the importance of considering possible contacts between the aneurysm and peri-aneurysmal structures and studying their effects on the aneurysm evolution. For this purpose, we present a computational analysis of a growing aneurysm in contact with bones at the base of the skull.
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Sforza, Daniel, Christopher Putman, Satoshi Tateshima, Fernando Vinuela, and Juan Cebral. "Hemodynamics and Growth of Intracranial Aneurysms." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19254.

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Understanding the underlying mechanisms responsible for the progression and rupture of cerebral aneurysms is important for improving their evaluation and treatment. Previous studies have identified the main factors involved in these processes: hemodynamics, vascular wall biomechanics and mechano-biology, and contacts with peri-aneurysmal structures [1]. However, little is known about their relative importance and interactions. The goal of our study is to shed light into the mechanisms of aneurysm progression by studying cerebral aneurysms that are followed longitudinally in time. This is a challenging problem because due to the poor prognosis of aneurysm ruptures preventive interventions are considered for most aneurysms. This paper presents preliminary results and observations made on a series of aneurysms followed with non-invasive imaging.
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Sforza, Daniel, Christopher Putman, Satoshi Tateshima, Fernando Viñuela, and Juan R. Cebral. "Hemodynamic Characteristics of Growing and Stable Aneurysms." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80178.

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The identification of cerebral aneurysm at high risk of immediate rupture requires determining the hemodynamic conditions that predispose aneurysms for rupture as well as understanding the underlying mechanisms responsible for aneurysm progression towards rupture. Towards this end, the purpose of this work was to compare the hemodynamics in growing and stable aneurysms as well as the local hemodynamic conditions in growing and stable regions of growing aneurysms.
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Gundert, Timothy J., and John F. LaDisa. "Evaluation of Cerebral Aneurysm Stent Performance in a Subject-Specific Computational Model." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19670.

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Rupture of cerebral aneurysms is the second leading cause of stroke in the United States [1]. Altered hemodynamics is thought to play a role in the progression and subsequent rupture of aneurysms. Blood flow into an aneurysm can be occluded by surgically clipping the aneurysm or using endovascular devices, such as stents or coils. In saccular aneurysms, coiling alone may be a sufficient method of inducing flow stagnation in the aneurysm, causing thrombosis and preventing rupture. When treating wide-necked aneurysms, stenting is often used in conjunction with coiling to prevent the migration of coils. Many investigators have studied the ability of a stent-only treatment to favorably alter flow in aneurysms [2, 3].
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Byrne, Greg, Fernando Mut, and Juan R. Cebral. "Using Vortex Coreline Detection to Characterize Aneurysmal Flow Activity." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80209.

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Assessing the risk of rupture of cerebral aneurysms is important for planning elective interventions. Since hemodynamics is thought to play a fundamental role in the mechanisms governing aneurysm progression and rupture, numerous investigations have tried to connect aneurysm hemodynamic conditions and rupture. In our previous work aneurysm flow patterns were qualitatively classified into simple / complex and stable / unstable categories by looking at the number of vortices within the aneurysm and their persistence during the cardiac cycle [1, 2]. The purpose of this work is to propose objective hemodynamic metrics that can capture these flow characteristics with the goal of relating them to aneurysm rupture.
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Embong, A. H., A. M. Al-Jumaily, G. Mahadevan, A. Lowe, and S. Sugita. "Development of an Abdominal Aortic Aneurysm Ruptures Mechanism Using a Geometric Analytical Technique." In ASME 2014 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2014. http://dx.doi.org/10.1115/imece2014-39823.

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Current ultrasound approaches practice probe for diagnosing instantaneous abdominal aortic aneurysms (AAA) based on arterial tissue deformation. However, tracking the progression of potential aneurysms, and predicting the risk of rupture is based on the diameter of the aneurysm and is still an insufficient method: Larger diameter aneurysms do not always lead to ruptures, and smaller diameter aneurysms unexpectedly rupture. In order to improve diagnostic accuracy of ultrasound imaging techniques, this paper presents geometric analyses of patient-specific instant deformations as a means to develop an aneurysm rupture mechanism. Segmented AAA images were used to analyze dependent elements that contribute to a three-dimensional (3-D) aneurysm reconstructive model using proposed Patient-Specific Aneurysm Rupture Predictor (P-SARP) method. The outcomes indicate that the proposed technique has the ability to associate the distortion of wall deformation with geometric analyses. This method can positively be integrated with established ultrasound techniques for improvements in the accuracy of future diagnoses of potential AAA ruptures.
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Tobe, Yasutaka, Takanobu Yagi, Yuki Iwabuchi, et al. "Combined Analysis of Pathology and Hemodynamics of Human Unruptured Cerebral Aneurysm With Thin-Walled Region." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14374.

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Cerebral aneurysms are known as the top reason of subarachnoid hemorrhage (SAH). They are studied in the medical and the engineering field to reveal their pathogenesis, progression, and rupture mechanisms1,2. The pathological studies revealed the site of predilection, rupture rate, the risk factors1, inflammation within the aneurysm, and conditions of endothelial cells (EC) in the aneurysms3. The current pathological analyses of the cerebral aneurysms are all phenomenological and it does not consider the cause-and-effect mechanisms between the mechanical stimulation and the physiological effect although hemodynamics is thought to play an important role in the mechanisms of aneurysms. One reason that the aneurysms’ mechanisms remain unsolved is because the pathology and hemodynamics are studied independently. Purpose of this study is to reveal the relationship of endothelial cell, thickness, and hemodynamics of the cerebral aneurysms by comparing the scanning electron microscope (SEM) analyses, μCT, and the computational fluid dynamics (CFD) analyses of the cerebral aneurysms.
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Zeinali-Davarani, S., A. Sheidaei, and S. Baek. "Towards Patient-Specific Modeling of an Enlarging Abdominal Aortic Aneurysm." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-205488.

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There has been a clear need for better understanding of the progression of abdominal aortic aneurysm (AAA) and obtaining reliable prediction of the AAA rupture. Finite element analysis (FEA) using non-axisymmetric models of AAAs provides better estimation of stress distribution in the aneurysmal wall with complex shapes [1]. However, FEA alone does not provide a mathematical description for the evolution of an AAA through growth and remodeling (G&R). A computational framework for modeling stress-mediated growth and structural remodeling of the arterial wall under physiological and pathological conditions has been suggested using a constrained mixture assumption [2]. Stress-mediated enlargement of intracranial aneurysms has been investigated using idealized axisymmetric geometries [3,4]. The kinetics of stress-mediated turnover of collagen fiber families and degradation of elastin were found to have particular importance in the G&R of aneurysmal wall.
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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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Dupay, A., P. Snyder, W. Lee, and S. Baek. "Surface Parameterization of an Abdominal Aortic Aneurysm to Characterize Geometrical Evolution During Longitudinal Study of Patients." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80737.

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For an abdominal aortic aneurysm (AAA) in vivo there are multiple tissues contacting its boundary, none of which have been fully considered for their effect throughout disease progression. Trends such as arterial asymmetry, surface curvature flattening, and arterial tortuosity could be significantly influenced by both surrounding tissue and hemodynamic factors. In order to quantify either the combined or separate influence of such factors during disease progression a precise characterization of aneurysm geometry evolution is needed. Multiple methods for geometrical parameterization of abdominal aortic aneurysms (AAAs) have been previously developed using isolated patient CT scan data but the focus has been mainly on the association of such geometrical parameters with the rupture risk and the efficacy of the parameterization is not fully investigated for a longitudinal study yet (multiple CT scans per patient at progressive intervals) [1]. For this study we have produced a series of 3D models for AAAs in longitudinal studies, developed an arterial centerline generation algorithm, and automated a geometric parameterization procedure for the arterial surfaces. It should be noted that the caliber of our collection of data is relatively rare as it is high resolution, features many patients, and on average has 4–5 images per patient.
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