Relevant bibliographies by topics / Aneurysmal dilatation

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

Academic literature on the topic 'Aneurysmal dilatation'

Author: Grafiati
Published: 7 June 2025
Last updated: 16 July 2025

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Journal articles on the topic "Aneurysmal dilatation"

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Kim, Su Wan, Jonggeun Lee, Seogjae Lee, Jee Won Chang, and Chang Lim Hyun. "Pathologic change of an arterialized giant venous aneurysm of a brachiocephalic arteriovenous fistula." Journal of Medicine and Life Science 20, no. 4 (2023): 178–82. http://dx.doi.org/10.22730/jmls.2023.20.4.178.

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Aneurysmal venous dilatation is a frequent complication of arterio venous fistulas (AVFs) created for hemodialysis. Venous aneurysm rupture can lead to lethal hemorrhage. A 49-year-old male patient presented with a giant aneurysmal dilatation of his AVF 10 years after its creation. The patient had complaints of pulsating pain and discomfort due to swelling of the left forearm. We performed an aneurysm resection and revised the overlying dermal lesion through a brachial plexus block. Here, we describe the pathological features of the arterialized venous aneurysm compared to simple venous aneurysms.
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Tang, Kuan, Yuanyou Li, Shuang Luo, and Jin Chen. "The risk factors of chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage." Neurology Asia 28, no. 1 (2023): 105–11. http://dx.doi.org/10.54029/2023umv.

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Objectives: The purpose of this study was to explore the independent risk factors of chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage. Methods: A retrospective study was carried out in patients with aneurysmal subarachnoid haemorrhage and admitted to the Second Affiliated Hospital of Chongqing Medical University from July 2017 to February 2021. The patients were grouped according to whether they had chronic ventricular dilatation. The patients’ demographic, clinical, and imaging datas including gender, age, hypertension, Hunt and Hess grade, Fisher grade, intraventricular hemorrhage, acute ventricular dilatation, aneurysm location, cerebrospinal fluid drainage, surgical methods, and meningitis were recorded and analyzed. And binary multivariate logistic regression models were used to investigate the independent risks for the chronic ventricular dilatation. Results: A total of 70 patients were analyzed and 36 (51.4%) developed chronic ventricular dilatation. Univariate analysis showed that age, Hunt and Hess grade, Fisher grade, intraventricular hemorrhage, acute ventricular dilatation, subtentorial aneurysms, and cerebrospinal fluid drainage were significantly different between the two groups. And there was no significant difference between the two groups in gender, hypertension, surgical method, or meningitis. Multivariate logistic regression analysis showed that acute ventricular dilatation was the only independent risk factor for chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage (OR 92.1, 95% CI: 11.7–999.9, P < 0.001). Conclusions: Acute ventricular dilatation was an independent risk factor of chronic ventricular dilatation after aneurysmal subarachnoid haemorrhage. Future research is needed to assess whether early treatment of acute ventricular dilatation can reduce chronic ventricular dilatation.
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Shah, Ravish, Tushar J. Vachharajani, and Anil K. Agarwal. "Aneurysmal Dilatation of Dialysis Arteriovenous Access." Open Urology & Nephrology Journal 6, no. 1 (2013): 1–5. http://dx.doi.org/10.2174/1874303x01306010001.

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Arteriovenous fistula is considered the “ideal vascular access” in patients with end stage renal disease (ESRD); however, its creation is not without complications. Aneurysmal dilatation is a poorly defined complication which, can potentially lead to access loss and life threatening hemorrhage. Increased venous pressure due to proximal venous stenosis along with repeated cannulations at the same site, are thought to play a significant role in pathogenesis. Given risk of substantial bleeding, it is recommended to avoid cannulation of aneurysmal area; however, as seen in our patient significant numbers of ESRD patients are at risk of being cannulated in the aneurysmal area. Nephrologist taking care of ESRD patients should be aware of its wide clinical spectrum along with signs of “unstable aneurysms” that would mandate an emergent surgical referral. Fistulogram often identifies a high grade proximal stenosis which can be treated by percutaneous angioplasty and perhaps halt the aneurysm progression. Although, endovascular interventions with stent graft placement can be considered in those with pseudoaneurysms related to arteriovenous grafts, it is often an interim measure in an attempt to prolong access longevity. With new surgical techniques and enhanced expertise, it is now possible to salvage the current AV access while simultaneously preserving the precious venous capital for the future AV accesses.
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Lee, Hung‐Chang, Yhu‐Chering Yang, Shin‐Lin Shih, and Hsein‐Jar Chiang. "Aneurysmal Dilatation of the Portal Vein." Journal of Pediatric Gastroenterology and Nutrition 8, no. 3 (1989): 387–89. http://dx.doi.org/10.1002/j.1536-4801.1989.tb09772.x.

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SUMMARYIn the following study, a case involving an aneurysmal dilatation of the portal vein is reported. The 5‐year‐old boy had a 2 month history of intermittent abdominal pain. A segmental dilatation of the portal vein was noted in the sonographic examination. The portal vein aneurysm diagnosis was later confirmed by superior mesenteric angiography and computed tomography. In our review of the literature, less than 30 cases of portal venous aneurysm have been reported. To our knowledge, this is the youngest case with such an anomaly.
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Tomasi, Jacques, Reda Belhaj Soulami, Marion Rolland, and Jean-Philippe Verhoye. "Endovascular Repair of a Dacron Pseudoaneurysm in an Ascending-to-Descending Aortic Bypass." AORTA 08, no. 04 (2020): 104–6. http://dx.doi.org/10.1055/s-0040-1715087.

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AbstractIn the setting of postcoarctation aortic repair, Dacron graft dilatation and late aneurysms are not uncommon. Reintervention usually involves redo open surgery and replacement of the aneurysmal graft or the pseudoaneurysmal suture line. The present case describes the endovascular repair of a Dacron anastomotic false aneurysm in an extra-anatomic ascending-to-descending aortic bypass, 19 years after surgical correction of aortic recoarctation.
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Yu, Yong peng, Hong qin Zhao, Wei feng Ren, and Xiang lin Chi. "Giant aneurysm of the basilar artery in an 86 year old woman." F1000Research 2 (April 18, 2013): 112. http://dx.doi.org/10.12688/f1000research.2-112.v1.

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In this article we present an 80 year old female patient with an unruptured giant aneurysm of the basilar artery presenting with posterior circulation ischemic symptoms. Angiography and CT revealed giant basilar aneurysmal dilatation with severe and wide intracranial arteriosclerosis. We described the uniqueness of this case. Giant basilar aneurysm is associated with various complications particularly brain stem infarction. It is emphasized that arteriosclerosis plays an important role in the formation of giant basilar aneurysms.
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Hopsu, Erkki, Jussi Tarkkanen, Seija I. Vento, and Anne Pitkäranta. "Acquired Jugular Vein Aneurysm." International Journal of Otolaryngology 2009 (2009): 1–4. http://dx.doi.org/10.1155/2009/535617.

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Venous malformations of the jugular veins are rare findings. Aneurysms and phlebectasias are the lesions most often reported. We report on an adult patient with an abruptly appearing large tumorous mass on the left side of the neck identified as a jugular vein aneurysm. Upon clinical examination with ultrasound, a lateral neck cyst was primarily suspected. Surgery revealed a saccular aneurysm in intimate connection with the internal jugular vein. Histology showed an organized hematoma inside the aneurysmal sac, which had a focally thinned muscular layer. The terminology and the treatment guidelines of venous dilatation lesions are discussed. For phlebectasias, conservative treatment is usually recommended, whereas for saccular aneurysms, surgical resection is the treatment of choice. While an exact classification based on etiology and pathophysiology is not possible, a more uniform taxonomy would clarify the guidelines for different therapeutic modalities for venous dilatation lesions.
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Nunes, Magda Lahorgue, Ana Paula Silveira Pinho, and Ana Sfoggia. "Cerebral aneurysmal dilatation in an infant with perinatally acquired HIV infection and HSV encephalitis." Arquivos de Neuro-Psiquiatria 59, no. 1 (2001): 116–18. http://dx.doi.org/10.1590/s0004-282x2001000100024.

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Although most children with human immunodeficiency virus (HIV) infection have neurological dysfunction, in childhood the incidence of symptomatic cerebrovascular disease is low. Cerebral aneurysmal arteriopathy in childhood AIDS has been reported in the past and considered to have a relatively long latency following the primary infection. We report a 1 month-old infant with congenitally acquired HIV infection, and herpes encephalitis; she presented a sudden cardiorespiratory arrest followed by coma and was found to have a giant saccular aneurysm of the left basilar artery. Literature review showed that cerebral aneurysmal artheriopathy is an unusual manifestation in newborns and infants and this case is possibly the youngest patient reported with aneurysma, herpes encephalitis and AIDS. The role of HIV and herpes simplex infections in the pathogenesis of this lesion is discussed.
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Hirai, S., S. Mine, E. Kobayashi, I. Yamakami, and A. Yamaura. "Angioarchitecture Predicting Hemorrhage in Cerebral Arteriovenous Malformations." Interventional Neuroradiology 5, no. 1_suppl (1999): 157–60. http://dx.doi.org/10.1177/15910199990050s128.

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To find out lesions responsible for hemorrhage in arteriovenous malformations (AVMs), a retrospective study of angioarchitecture around the nidus was conducted in 27 patients who underwent conservative treatment. Comparison of angiograms revealed disappearance of an intranidal aneurysmal dilatation after the hemorrhagic events in two cases. The hematomas were adjacent to the dilatation, and no subarachnoid hemorrhage was evident. Obstruction of venous drainage, noticed in a case of spontaneous regression of AVM, was not demonstrated in the cases of hemorrhage. The intranidal aneurysmal dilatation is likely to have caused the hemorrhage in our cases. Careful endavascular embolization using proper materials should be indicated for an intranidal aneurysmal dilatation to prevent subsequent hemorrhage.
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Vieira, Eduardo, Igor V. Faquini, Jose L. Silva, et al. "Subarachnoid neurocysticercosis and an intracranial infectious aneurysm: case report." Neurosurgical Focus 47, no. 2 (2019): E16. http://dx.doi.org/10.3171/2019.5.focus19280.

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Infectious intracranial aneurysms (IIAs) represent 2%–6% of all intracranial aneurysms and, classically, have been associated with bacterial or fungal agents. The authors report the case of a 42-year-old woman who presented with a typical history of subarachnoid hemorrhage. Digital subtraction angiography (DSA) showed an aneurysmal dilatation on the frontal M2 segment of the left middle cerebral artery (MCA). The patient was treated surgically, and multiple cysts were found in the left carotid and sylvian cisterns, associated with a dense inflammatory exudate that involved the MCA. The cysts were removed, and a fusiform aneurysmal dilatation was identified. The lesion was not amenable to direct clipping, so the authors wrapped it. Histopathological analysis of the removed cysts revealed the typical pattern of subarachnoid neurocysticercosis. The patient received cysticidal therapy with albendazole and corticosteroids, and she recovered uneventfully. Follow-up DSA performed 6 months after surgery showed complete resolution of the aneurysm. The authors performed a review of the literature and believe that there is sufficient evidence to affirm that the subarachnoid form of neurocysticercosis may lead to the development of an IIA and that Taenia solium should be listed among the possible etiological agents of IIAs, along with bacterial and fungal agents.
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Dissertations / Theses on the topic "Aneurysmal dilatation"

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Hofmann, Sigrun R., Antje Heilmann, Hans J. Häusler, Ingo Dähnert, Gabriele Kamin, and Robert Lachmann. "Congenital Idiopathic Dilatation of the Right Atrium: Antenatal Appearance, Postnatal Management, Long-Term Follow-Up and Possible Pathomechanism." Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-137447.

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Introduction: Idiopathic dilatation of the right atrium (IDRA) is a rare abnormality usually detected by chance at any time between antenatal and adult life. It is defined as isolated enlargement of the right atrium in the absence of other cardiac lesions causing right atrial dilatation. IDRA can be associated with atrial arrhythmia and systemic embolism. The clinical presentation shows high variability ranging from the lack of any symptoms up to cardiac failure. Methods/Results: We describe 2 children with antenatally diagnosed IDRA, the intrauterine course in 1 case, the postnatal management and its long-term follow-up. There has been no need for surgical intervention so far because of the lack of arrhythmias and no further progression of right atrial diameters. Thrombus formation in the right atrium, which is a potential risk for pulmonary embolism, led us to initiate anticoagulation in our cases to prevent such complications. Furthermore, we suggest one possible pathomechanism of congenital right atrial dilatation. Conclusion: Optimal management of severe IDRA depends on the individual case. Long-term follow-up of these patients is necessary to monitor a possible further progression of right atrial size and occurrence of arrhythmias. As a possible pathomechanism, a functional partial anomalous pulmonary venous insertion may imitate a structural abnormal pulmonary vein connection in some idiopathic cases of congenital right atrial dilatation<br>Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich
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Hofmann, Sigrun R., Antje Heilmann, Hans J. Häusler, Ingo Dähnert, Gabriele Kamin, and Robert Lachmann. "Congenital Idiopathic Dilatation of the Right Atrium: Antenatal Appearance, Postnatal Management, Long-Term Follow-Up and Possible Pathomechanism." Karger, 2012. https://tud.qucosa.de/id/qucosa%3A27734.

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Introduction: Idiopathic dilatation of the right atrium (IDRA) is a rare abnormality usually detected by chance at any time between antenatal and adult life. It is defined as isolated enlargement of the right atrium in the absence of other cardiac lesions causing right atrial dilatation. IDRA can be associated with atrial arrhythmia and systemic embolism. The clinical presentation shows high variability ranging from the lack of any symptoms up to cardiac failure. Methods/Results: We describe 2 children with antenatally diagnosed IDRA, the intrauterine course in 1 case, the postnatal management and its long-term follow-up. There has been no need for surgical intervention so far because of the lack of arrhythmias and no further progression of right atrial diameters. Thrombus formation in the right atrium, which is a potential risk for pulmonary embolism, led us to initiate anticoagulation in our cases to prevent such complications. Furthermore, we suggest one possible pathomechanism of congenital right atrial dilatation. Conclusion: Optimal management of severe IDRA depends on the individual case. Long-term follow-up of these patients is necessary to monitor a possible further progression of right atrial size and occurrence of arrhythmias. As a possible pathomechanism, a functional partial anomalous pulmonary venous insertion may imitate a structural abnormal pulmonary vein connection in some idiopathic cases of congenital right atrial dilatation.<br>Dieser Beitrag ist mit Zustimmung des Rechteinhabers aufgrund einer (DFG-geförderten) Allianz- bzw. Nationallizenz frei zugänglich.
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Silva, Junior José Elias da [UNESP]. "Aneurisma de aorta infrarenal tratado por via endovascular em pacientes assintomáticos versus sintomáticos: avaliação da medida do saco aneurismático após um ano de seguimento." Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/152531.

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Submitted by José Elias da Silva Júnior null (02525590104) on 2017-10-16T00:48:00Z No. of bitstreams: 1 Jose Elias da Silva Júnior - MEPAREM.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Rejected by Monique Sasaki (sayumi_sasaki@hotmail.com), reason: Solicitamos que realize uma nova submissão seguindo as orientações abaixo: No campo “Versão a ser disponibilizada online imediatamente” foi informado que seria disponibilizado o texto completo porém no campo “Data para a disponibilização do texto completo” foi informado que o texto completo deverá ser disponibilizado apenas 6 meses após a defesa. Caso opte pela disponibilização do texto completo apenas 6 meses após a defesa selecione no campo “Versão a ser disponibilizada online imediatamente” a opção “Texto parcial”. Esta opção é utilizada caso você tenha planos de publicar seu trabalho em periódicos científicos ou em formato de livro, por exemplo e fará com que apenas as páginas pré-textuais, introdução, considerações e referências sejam disponibilizadas. Se optar por disponibilizar o texto completo de seu trabalho imediatamente selecione no campo “Data para a disponibilização do texto completo” a opção “Não se aplica (texto completo)”. Isso fará com que seu trabalho seja disponibilizado na íntegra no Repositório Institucional UNESP. Por favor, corrija esta informação realizando uma nova submissão. Agradecemos a compreensão. on 2017-10-18T17:31:18Z (GMT)<br>Submitted by José Elias da Silva Júnior null (02525590104) on 2017-10-30T14:35:44Z No. of bitstreams: 1 Jose Elias da Silva Júnior - MEPAREM.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Rejected by LUIZA DE MENEZES ROMANETTO (luizamenezes@reitoria.unesp.br), reason: Solicitamos que realize uma nova submissão seguindo as orientações abaixo: No campo “Versão a ser disponibilizada online imediatamente” foi informado que seria disponibilizado o texto completo porém no campo “Data para a disponibilização do texto completo” foi informado que o texto completo deverá ser disponibilizado apenas 6 meses após a defesa. Caso opte pela disponibilização do texto completo apenas 6 meses após a defesa selecione no campo “Versão a ser disponibilizada online imediatamente” a opção “Texto parcial”. Esta opção é utilizada caso você tenha planos de publicar seu trabalho em periódicos científicos ou em formato de livro, por exemplo e fará com que apenas as páginas pré-textuais, introdução, considerações e referências sejam disponibilizadas. Se optar por disponibilizar o texto completo de seu trabalho imediatamente selecione no campo “Data para a disponibilização do texto completo” a opção “Não se aplica (texto completo)”. Isso fará com que seu trabalho seja disponibilizado na íntegra no Repositório Institucional UNESP. Por favor, corrija esta informação realizando uma nova submissão. Agradecemos a compreensão. on 2017-11-09T17:08:36Z (GMT)<br>Submitted by José Elias da Silva Júnior null (02525590104) on 2017-12-15T18:28:41Z No. of bitstreams: 1 silvajunior_je_me_bot.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Submitted by José Elias da Silva Júnior null (02525590104) on 2017-12-21T12:31:26Z No. of bitstreams: 1 silvajunior_je_me_bot.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Approved for entry into archive by Vivian Rosa Storti null (vstorti@reitoria.unesp.br) on 2018-01-18T17:56:40Z (GMT) No. of bitstreams: 1 silvajunior_je_me_bot.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Made available in DSpace on 2018-01-18T17:56:40Z (GMT). No. of bitstreams: 1 silvajunior_je_me_bot.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5) Previous issue date: 2017-08-25<br>Não recebi financiamento<br>A correção endovascular do aneurisma de aorta abdominal (EVAR) modificou o tratamento desta patologia, reduzindo a mortalidade e as complicações, á curto prazo quando comparada à cirurgia aberta. Ainda assim, os pacientes necessitam de seguimento rigoroso a fim de reconhecer as possíveis complicações. O crescimento do diâmetro do saco aneurismático pós-EVAR está relacionado ao risco de rotura ou necessidade de reabordagem, sendo que alguns fatores pré-operatórios podem prever esse aumento. OBJETIVO:Identificar se os sintomas pré-tratamento EVAR podem ser um fator preditivo para a continuidade da expansão do saco aneurismático após tratamento, no seguimento em 12 meses. MATERIAL E MÉTODOS: Estudo retrospectivo realizado através da coleta de dados do prontuário dos pacientes em seguimento na Faculdade de Medicina de Botucatu e que preencheram critérios de inclusão. Os pacientes foram separados em dois grupos de estudos: G1- Pacientes assintomáticos quanto a presença do aneurisma de aorta infrarenal; G2- Pacientes sintomáticos quanto a presença do aneurisma de aorta infrarenal. Todos os grupos foram acompanhados por 12 meses e avaliados quanto ao crescimento do saco aneurismático após o procedimento endovascular, através de AngioTC e Duplex Scan e coleta do exame “proteína C Reativa” para avaliação inflamatória relacionada ao EVAR. RESULTADOS: Foram estudados 112 pacientes. A faixa etária apresentou uma média de 68,6 anos. 80% eram do sexo masculino e 95% brancos. A maioria dos pacientes eram hipertensos e fumantes, 74,1% e 67% respectivamente. No total houve 22,3% de endoleak e o aumento do saco aneurismático foi de 26,8%. Avaliando todos os pacientes, ocorreu diminuição do diâmetro do AAA em média de 0,8cm, entre o pré e pós-operatório. Observou se que 25,3% dos assintomáticos e 30% dos sintomáticos tiveram crescimento do saco aneurismáticos. A presença de endoleak ocorreu em 19% dos assintomáticos e 41,2% dos sintomáticos. No total, 40 % dos pacientes que evoluíram com aumento do saco aneurismático apresentavam endoleak. CONCLUSÃO: Os pacientes que tiveram dor no pré-operatório, portanto, sintomáticos, apresentaram uma taxa numérica maior do crescimento do saco aneurismático em relação ao grupo que não apresentava sintomas, mas este achado não foi estatisticamente significante. A presença do endoleak não foi a única causa do crescimento dos AAAs. Não houve diferença do PCR colhido no pré-operatório em relação ao crescimento do AAA em ambos os grupos. A hipertensão arterial foi a comorbidades mais frequente na nossa casuística.<br>The endovascular repair of abdominal aortic aneurysm (EVAR) modified its treatment, reducing the mortality and complications in short-term compared to open repair. Even though, patients need strict follow-up to identify possibly complications. The sac aneurysm enlargement after EVAR is related to the risk of rupture or reintervention, with some preoperative factors can predict this enlargement. OBJECTIVE: Identify if the AAA symptons, especially pain, are predictors of abdominal aortic aneurym sac enlargement after EVAR. METHODS: Retrospective study through the gathering of data about the patientes in follow-up in Botucatu School Medicine. The patients were separated in two groups: G1 – assymptomatics in the preoperative; G2 – syptomatic in the preoperative. Both groups were followed-up for 12 months to the sac enlargement through AngioCT, duplex scan and Reative-C-Protein. RESULTS: 112 patientes were analysed. The age average was 68,6 years. 80% were male and 95% white. Most of them were hypertensive and smoker, 74,1% and 67% respectively. There was 22,3% of endoleaks and 26,8% sac enlargement ratio. 25,3% of the assymptomatics and 30% of the symptomatics had sac enlargement. 19% of the assymptomatics compared with 41,2% of the symptomatics had endoleak. 40% of the patients with sac enlargement had endoleaks. CONCLUSION: The symptomatics preoperative patients has a higher risk compared with assymptomatic group. The endoleak is not the only reason for the AAA sac enlargement. There was no difference between the groups G1 and G2 related to AAA sac enlargement and Reative-CProtein. Hypertension was the most prevalent comorbidity in our study.
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Silva, Júnior José Elias da. "“Aneurisma de aorta infrarenal tratado por via endovascular em pacientes assintomáticos versus sintomáticos. Avaliação da medida do saco aneurismático após um ano de seguimento.”." Universidade Estadual Paulista (UNESP), 2017. http://hdl.handle.net/11449/152890.

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Submitted by José Elias da Silva Júnior null (jedsjunior@hotmail.com) on 2018-02-28T17:41:26Z No. of bitstreams: 1 TESE FINAL CORRIGIDA.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Approved for entry into archive by ROSANGELA APARECIDA LOBO null (rosangelalobo@btu.unesp.br) on 2018-03-05T17:48:49Z (GMT) No. of bitstreams: 1 silvajunior_je_me_bot.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5)<br>Made available in DSpace on 2018-03-05T17:48:49Z (GMT). No. of bitstreams: 1 silvajunior_je_me_bot.pdf: 992178 bytes, checksum: 6cf7663fc6a01c288850e2c6ea550472 (MD5) Previous issue date: 2017-08-25<br>INTRODUÇÃO: A correção endovascular do aneurisma de aorta abdominal (EVAR) modificou o tratamento desta patologia, reduzindo a mortalidade e as complicações, á curto prazo quando comparada à cirurgia aberta. Ainda assim, os pacientes necessitam de seguimento rigoroso a fim de reconhecer as possíveis complicações. O crescimento do diâmetro do saco aneurismático pós-EVAR está relacionado ao risco de rotura ou necessidade de reabordagem, sendo que alguns fatores pré-operatórios podem prever esse aumento. OBJETIVO:Identificar se os sintomas pré-tratamento EVAR podem ser um fator preditivo para a continuidade da expansão do saco aneurismático após tratamento, no seguimento em 12 meses. MATERIAL E MÉTODOS: Estudo retrospectivo realizado através da coleta de dados do prontuário dos pacientes em seguimento na Faculdade de Medicina de Botucatu e que preencheram critérios de inclusão. Os pacientes foram separados em dois grupos de estudos: G1- Pacientes assintomáticos quanto a presença do aneurisma de aorta infrarenal; G2- Pacientes sintomáticos quanto a presença do aneurisma de aorta infrarenal. Todos os grupos foram acompanhados por 12 meses e avaliados quanto ao crescimento do saco aneurismático após o procedimento endovascular, através de AngioTC e Duplex Scan e coleta do exame “proteína C Reativa” para avaliação inflamatória relacionada ao EVAR. RESULTADOS: Foram 9 estudados 112 pacientes. A faixa etária apresentou uma média de 68,6 anos. 80% eram do sexo masculino e 95% brancos. A maioria dos pacientes eram hipertensos e fumantes, 74,1% e 67% respectivamente. No total houve 22,3% de endoleak e o aumento do saco aneurismático foi de 26,8%. Avaliando todos os pacientes, ocorreu diminuição do diâmetro do AAA em média de 0,8cm, entre o pré e pós-operatório. Observou se que 25,3% dos assintomáticos e 30% dos sintomáticos tiveram crescimento do saco aneurismáticos. A presença de endoleak ocorreu em 19% dos assintomáticos e 41,2% dos sintomáticos. No total, 40 % dos pacientes que evoluíram com aumento do saco aneurismático apresentavam endoleak. CONCLUSÃO: Os pacientes que tiveram dor no pré-operatório, portanto, sintomáticos, apresentaram uma taxa numérica maior do crescimento do saco aneurismático em relação ao grupo que não apresentava sintomas, mas este achado não foi estatisticamente significante. A presença do endoleak não foi a única causa do crescimento dos AAAs. Não houve diferença do PCR colhido no pré-operatório em relação ao crescimento do AAA em ambos os grupos. A hipertensão arterial foi a comorbidades mais frequente na nossa casuística.<br>BACKGROUND: The endovascular repair of abdominal aortic aneurysm (EVAR) modified its treatment, reducing the mortality and complications in short-term compared to open repair. Even though, patients need strict follow-up to identify possibly complications. The sac aneurysm enlargement after EVAR is related to the risk of rupture or reintervention, with some preoperative factors can predict this enlargement. OBJECTIVE: Identify if the AAA symptons, especially pain, are predictors of abdominal aortic aneurym sac enlargement after EVAR. METHODS: Retrospective study through the gathering of data about the patientes in follow-up in Botucatu School Medicine. The patients were separated in two groups: G1 – assymptomatics in the preoperative; G2 – syptomatic in the preoperative. Both groups were followed-up for 12 months to the sac enlargement through AngioCT, duplex scan and Reative-C-Protein. RESULTS: 112 patientes were analysed. The age average was 68,6 years. 80% were male and 95% white. Most of them were hypertensive and smoker, 74,1% and 67% respectively. There was 22,3% of endoleaks and 26,8% sac enlargement ratio. 25,3% of the assymptomatics and 30% of the symptomatics had sac enlargement. 19% of the assymptomatics compared with 41,2% of the symptomatics had endoleak. 40% of the patients with sac enlargement had endoleaks. CONCLUSION: The symptomatics preoperative patients has a higher risk compared with assymptomatic group. The endoleak is not the only 11 reason for the AAA sac enlargement. There was no difference between the groups G1 and G2 related to AAA sac enlargement and Reative-CProtein. Hypertension was the most prevalent comorbidity in our study.
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Books on the topic "Aneurysmal dilatation"

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Perkins, Jeremy. Peripheral arterial disease. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0104.

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Peripheral arterial disease is defined as an alteration to the blood supply to a limb, caused by an occlusion or stenosis in the arteries supplying that limb. The acuteness of the arterial compromise, and its severity and extent, will determine the symptoms experienced by the patient. Aneurysmal disease is defined as a localized dilatation of an artery and is most commonly seen in the infrarenal abdominal aorta. An infrarenal abdominal aorta is defined as being aneurysmal if its maximum anteroposterior diameter is 3 cm or greater.
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Bahr, Sabine. Häufigkeit der Entstehung von Rezidiven und Aneurysmen nach Aortenisthmusstenosen: Dilatation bei Erwachsenen. 1994.

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Elliott, Perry, Kristina H. Haugaa, Pio Caso, and Maja Cikes. Restrictive cardiomyopathy and arrhythmogenic right ventricular cardiomyopathy. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198726012.003.0044.

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Restrictive cardiomyopathy is a heart muscle disorder characterized by increased myocardial stiffness that results in an abnormally steep rise in intraventricular pressure with small increases in volume in the presence of normal or decreased diastolic left ventricular volumes and normal ventricular wall thickness. The disease may be caused by mutations in a number of genes or myocardial infiltration. Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac muscle disease associated with sudden cardiac death, ventricular arrhythmias, and cardiac failure. It is most frequently caused by mutations in desmosomal protein genes that lead to fibrofatty replacement of cardiomyocytes, right ventricular dilatation, and aneurysm formation.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0045.

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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_001.

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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_002.

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Mechanical complications after an acute infarction include different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies but may occur in 2–3% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment. Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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López-Sendón, José, and Esteban López de Sá. Mechanical complications of myocardial infarction. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199687039.003.0045_update_003.

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Mechanical complications after an acute infarction involve different forms of heart rupture, including free wall rupture, interventricular septal rupture, and papillary muscle rupture. Its incidence decreased dramatically with the widespread use of reperfusion therapies occurring in &lt;1% of ST-elevation myocardial infarction patients, and mortality is very high if not properly diagnosed, as surgery is the only effective treatment (Ibanez et al, 2017). Echocardiography is the most important tool for diagnosis that should be suspected in patients with hypotension, heart failure, or recurrent chest pain. Awareness and well-established protocols are crucial for an early diagnosis. Modern imaging techniques permit a more reliable and direct identification of left ventricular free wall rupture, which is almost impossible to identify with conventional echocardiography. Mitral regurgitation, secondary to papillary muscle ischaemia or necrosis or left ventricular dilatation and remodelling, without papillary muscle rupture, is frequent after myocardial infarction and is considered as an independent risk factor for outcomes. Revascularization to control ischaemia and surgical repair should be considered in all patients with severe or symptomatic mitral regurgitation in the absence of severe left ventricular dysfunction. Other mechanical complications include true aneurysms and thrombus formation in the left ventricle. Again, these complications have decreased with the use of early reperfusion therapies and, for thrombus formation, with aggressive antithrombotic treatment. In a single large randomized trial (STICH), surgical remodelling of the left ventricle failed to demonstrate a significant improvement in outcomes, although it still may be an option in selected patients.
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Book chapters on the topic "Aneurysmal dilatation"

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Perloff, Joseph K., Charles W. Urschell, William C. Roberts, and Walter H. Caulfield. "Aneurysmal Dilatation of the Coronary Arteries in Cyanotic Congenital Cardiac Disease*." In Case Reports in Cardiology. CRC Press, 2023. http://dx.doi.org/10.1201/9781003409342-10.

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Zhang, Shaojie, Joan D. Laubrie, S. Jamaleddin Mousavi, Sabrina Ben Ahmed, and Stéphane Avril. "Patient-Specific Finite Element Modeling of Aneurysmal Dilatation After Chronic Type B Aortic Dissection." In Computational Biomechanics for Medicine. Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-09327-2_2.

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Zeitler, E., and F. H. W. Heuck. "Aneurysmen und dilatative Angiopathie." In Arterien und Venen. Springer Berlin Heidelberg, 1997. http://dx.doi.org/10.1007/978-3-642-60381-5_12.

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Ibrahim, Michael, and Nimesh D. Desai. "Thoracic Aortic Dilatation, Aneurysm and Dissection." In Cardiovascular Genetics and Genomics. Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-66114-8_21.

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Gupta, Vipul. "Very Small (Less Than 2 mm) Aneurysm with Severe Vasospasm: Pretreatment Dilatation." In 100 Interesting Case Studies in Neurointervention: Tips and Tricks. Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-1346-2_54.

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Lylyk, Ivan, Carlos Bleise, Rene Viso, Esteban Scrivano, and Pedro Lylyk. "Paraophthalmic Internal Carotid Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage Caused by the Rupture of a Paraophthalmic Aneurysm, Treated with Coils and Complicated by Severe Vasospasm, Treated with Pharmaceutical Vessel Dilatation and Proximal Balloon Angioplasty; Diffuse Distal Vasospasm Treated with the NeuroFlo Device with Good Clinical Outcome." In The Aneurysm Casebook. Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-77827-3_119.

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Lylyk, Ivan, Carlos Bleise, Rene Viso, Esteban Scrivano, and Pedro Lylyk. "Paraophthalmic Internal Carotid Artery Aneurysm: Spontaneous Subarachnoid Hemorrhage Caused by the Rupture of a Paraophthalmic Aneurysm, Treated with Coils and Complicated by Severe Vasospasm, Treated with Pharmaceutical Vessel Dilatation and Proximal Balloon Angioplasty; Diffuse Distal Vasospasm Treated with the NeuroFlo Device with Good Clinical Outcome." In The Aneurysm Casebook. Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-319-70267-4_119-1.

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Weir, Bryce. "Epidemiology and Associated Disease States." In Subarachnoid Hemorrhage: Causes And Cures. Oxford University PressNew York, NY, 1998. http://dx.doi.org/10.1093/oso/9780195128758.003.0003.

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Abstract An aneurysm is a dilatation on a blood vessel,1 usually an artery. Many different types of aneurysms affect the nervous system (Table 3-1). The most common type is a saccular or ovoid protrusion attached by a small neck to the artery of origin, historically called a “berry.” Ruptured aneurysms account for most cases of subarachnoid hemorrhage (SAH), and the incidence of aneurysmal SAH is directly related to age. Aneurysmal rupture is extremely uncommon in infancy, becoming steadily less so during aging. For this reason the term “congenital” applied to aneurysms is a misnomer.
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Lee, Christine U., and James F. Glockner. "Case 17.27." In Mayo Clinic Body MRI Case Review, edited by Christine U. Lee and James F. Glockner. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199915705.003.0445.

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60-year-old man with hypertension resistant to medical therapy MIP images from noncontrast 3D SSFP renal MRA (Figure 17.27.1) demonstrate poor visualization of the renal arteries, with low contrast and low SNR. VR images from CE 3D MRA (Figure 17.27.2) reveal 2 left renal arteries and aneurysmal dilatation of the distal right main renal artery....
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Li, Yanliang, Monique Munro, Gerardo Ledesma-Gil, and William F. Mieler. "Takayasu arteritis: Bilateral progressive loss of vision with aneurysmal dilatation." In Clinical Cases in Medical Retina. Elsevier, 2025. http://dx.doi.org/10.1016/b978-0-12-822720-6.00057-4.

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Conference papers on the topic "Aneurysmal dilatation"

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Guzmán, Amador M., Nelson O. Moraga, and Cristina H. Amon. "Pulsatile Non-Newtonian Flow in a Double Aneurysm." In ASME 1997 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 1997. http://dx.doi.org/10.1115/imece1997-0241.

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Abstract An aneurysm is a permanent balloon-like, blood-filled dilatation on an arterial vessel. In an abdominal aortic aneurysm (AAA), the growth and eventual rupture of aneurysmal lesions depends on the interaction between the aneurysm wall and the blood motion along it. Rupture of an aneurysm occurs when the shear stresses exceed the strength of the wall [1]. When an AAA ruptures, 50 percent of patients die before reaching the operating room and 54 percent of the remaining will die within 30 days [2]. Therefore, AAA represents a great danger to the patient [3]. The objective of this study is to investigate the shear stresses in an aneurysm composed by two deforned regions and to examine the effect of the blood non-Newtonian behavior on the flow dynamics.
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Ferruzzi, J., M. S. Enevoldsen, and J. D. Humphrey. "On the Mechanical Behavior of Healthy and Aneurysmal Abdominal Aorta." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53852.

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Abdominal aortic aneurysm (AAA) is a pathological condition of the infrarenal aorta characterized by a local dilatation of the arterial wall. The main histopathologic features of an AAA are smooth muscle cell death and loss of elastin. The biomechanical behavior of AAAs has been widely studied to determine the rupture potential according to the principles of material failure. However, most prior approaches are limited by the use of data from uniaxial tensile testing and by the assumption of material isotropy, leading to inaccurate characterization of the 3D multiaxial mechanical response of the aneurysmal tissue. To date, the best data available on the behavior of human abdominal aorta (AA) and AAA to planar biaxial testing are the ones reported by Vande Geest et al. [1,2]. In a recent work [3], we considered a structurally motivated four-fiber family strain energy function (SEF) [4] to capture the biaxial behavior of the human AA and AAA from Vande Geest et al. [1,2]. We showed that this constitutive relation fits human data better than prior models and most importantly it captures the stiffening of the arterial wall related to both aging and aneurysmal development. These changes in mechanical behavior are mirrored by changes in the best-fit values of the parameters, with a progressive decrease of the isotropic part attributed to elastin and a parallel increase in values associated with the families of collagen fibers.
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Fazel Bakhsheshi, Mohammad, Florian Vixege, and Dana Grecov. "Reduction of the Aortic Aneurysm Sac Pressure Using a Stent With Venturi Structure: A Numerical Study." In 2018 Design of Medical Devices Conference. American Society of Mechanical Engineers, 2018. http://dx.doi.org/10.1115/dmd2018-6919.

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Aortic aneurysm is a common disorder which is due to weakening of the aortic wall [1]. Aneurysm rupture is a potentially life threatening complication [2]. The stent graft implantation is one of the potential alternatives for treating patients at high risk for an open surgical procedure. The short-term outcome for stent implantation is promising; however, as with any medical procedure, this has potential limitations such as side branch occlusion, device malfunctions, dilatation at the proximal portion and the so called ‘endoleak’. An endoleak is the persistent blood flow into and within the aneurysmal sac after endovascular repair (i.e. the blood leaks around the endograft which is supposed to have sealed off the entry of blood around it and can be classified into 5 categories[3]). Type I (inadequate seal) and III (graft mechanical failure) endoleaks, characterized by direct communication between systemic and aneurysm sac compartments, pose higher risk of aneurysm rupture and are therefore aggressively treated [4]. Despite advances in the treatment of aneurysm, we believe that there is a still great need for a medical device that can improve patient outcomes.
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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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Zhao, Xuefeng, Madhavan L. Raghavan, and Jia Lu. "Identifying the Distribution of Heterogeneous Anisotropic Elastic Properties in Cerebral Aneurysms." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206659.

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Cerebral aneurysms are focal dilatations of the intracranial arterial wall, whose rupture risk is likely related to pressure induced wall stress. Fundamental to stress and strain prediction in aneurysms is the constitutive behavior of wall tissue. However, delineating the constitutive equation of aneurismal tissue, in particular, experimental determination of the material parameters, presents some significant challenges due to the nonlinear, anisotropic and heterogeneous nature of the aneurysmal tissue.
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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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Kroon, Martin, and Gerhard Holzapfel. "A Theoretical Model for Saccular Cerebral Aneurysm Growth: Deformation and Stress Analysis." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176857.

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Aneurysms are abnormal dilatations of arteries, and these lesions are found almost exclusively in humans. Saccular cerebral aneurysms occur most frequently in the Circle of Willis, which is a circuit of arteries supplying the brain with blood. Aneurysms of this kind appear in a few percent of the human population in the Western world. Only a few percent of these lesions do actually rupture, but once rupture occurs the consequences are severe, often with death as outcome. Once a cerebral aneurysm is detected, clinicians need to decide whether operation is required or not. These decisions are mainly based on the size of the aneurysm, where larger aneurysms are considered to be more critical than smaller ones. This size criterion is, however, not very reliable, and criteria based on mechanical fields (stress or strain) of the aneurysm should be taken into account in the decision. This, however, requires knowledge of the constitutive behavior of the aneurysm wall, together with patient-specific information regarding geometry and boundary conditions. In order to be able to model the constitutive behavior of an aneurysm, the structural features of the aneurysm wall need to be determined. Knowledge of the etiology of the aneurysm may here provide important insights.
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Ma, Jiayao, Zhong You, and James Byrne. "A Novel Flow Diverter for Direct Treatment of Cerebral Aneurysms." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14013.

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Cerebral aneurysm (CA) is a localised dilatation in the wall of the brain vasculature which can cause it to swell out like a balloon. If not treated, it will continue to grow and eventually tear or rupture, resulting in severe disability from stroke and, in around 25% of cases, death [1]. CAs affect up to 5% of the adult population with 1% of detected aneurysms rupture every year [2].
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Kwon, Chi-Ho, Ki-Won Lee, and Young-Ho Kim. "Fluid-Structure Interactions Abdominal Aortic Aneurysm Models Under the Pulsatile Flow Condition." In ASME 2000 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2000. http://dx.doi.org/10.1115/imece2000-2542.

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Abstract Fluid-structure interaction studies were performed on various abdominal aortic aneurysm (AAA) models under the pulsatile flow condition. Eight aneurysm models were made with four different dilatation sizes and two different wall thickness. Stresses and deformations of the aneurysm wall were significantly affected by the dilatation size as well as the wall thickness. The change in wall thickness increased with the more dilated aneurysm. In spite of considerable radial deformations, axial deformations of the aneurysm wall were dominant. The present study showed the strong possibility to understand fluid-structure interactions in the human cardiovascular system.
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Trachet, Bram, Daniel Devos, Julie De Backer, Anne De Paepe, Bart L. Loeys, and Patrick Segers. "Patient-Specific Modelling of Aortic Arch Wall Shear Stress Patterns in Patients With Marfan Syndrome." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-206340.

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Marfan syndrome (MFS) is a genetic connective tissue disorder with a high prevalence of aortic aneurysm formation (a pathological dilatation of the aorta), typically at the aortic root. The disorder is caused by mutations in the gene encoding fibrillin-1 [1]. Recently, it has been shown in mouse models that selected manifestations of MFS, such as aortic aneurysm formation, can be explained by excessive signaling by the transforming growth factor–beta (TGF-beta) family of cytokines [2]. Although the footprint of the disease is clearly genetic, there is still a role for (computational) biomechanics and hemodynamics to elucidate why aneurysms develop preferentially at the level of the aortic root, since the genetic defect affects the entire (arterial) system. One of the most obvious parameters to study is the arterial wall shear stress (WSS). WSS plays an important role in the regulation of the vascular system and is considered a significant factor in the development and progression of cardiovascular disease in humans. Low and/or oscillating values of WSS have been associated with the formation of atherosclerotic lesions [3] and with the growth of aneurysms [4]. It is, however, hard to show a link between low WSS and aneurysm initiation, since in most cases the geometrical and physiological data are lacking during the first and most important stages of the aneurysm development. Furthermore follow-up studies in human patients are difficult, since aneurysms grow very slowly (only 0.9 mm/year in MFS patients treated with beta-blockers) and it will take several years before significant changes will have taken place. Therefore, in this study, we have computed the aortic flow field and WSS patterns for 5 different MFS patients with ages varying from 14 to 54 years old, in order to get an idea about the effect of age on the development of the disease.
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