In this work, we have developed user interactive capabilities that allow us to perform segmentation and manipulation of patient-specific geometries required for Computational Fluid Dynamics (CFD) studies, entirely in image domain and within a single platform of ‘IAFEMesh'. Within this toolkit we have added commonly required manipulation capabilities for performing CFD on segmented objects by utilizing libraries like ITK, VTK and KWWidgets. With the advent of these capabilities we can now manipulate a single patient specific image into a set of possible cases we seek to study; which is difficult to do in commercially available software like VMTK, Slicer, MITK etc. due to their limited manipulation capabilities. Levelset representation of the manipulated geometries can be simulated in our flow solver (SCIMITAR-3D) without creating any surface or volumetric mesh. This image-levelset-flow framework offers few advantages. 1) We don't need to deal with the problems associated with mesh quality, edge connectivity related to mesh models, 2) and manipulations like boolean operation result in smooth, physically realizable entities which is challanging in mesh domain. We have validated our image-levelset-flow setup with the known results from previous studies. We have modified the algorithm by Krissian et al. and implemented it for the segmentation of Type-A aortic dissection. Finally, we implemented these capabilities to study the hemodynamics in Type-A aortic dissection. Our image based framework is a first of its kind and the hemodynamic study of Type-A dissection too is first study onto the best of our knowledge.

<p><i>Chlamydophila pneumoniae</i> (<i>C. pneumoniae</i>) has been suggested as a stimulator of chronic inflammation in atherosclerosis. <i>C. pneumoniae</i> DNA was demonstrated in aortic biopsies in 50% of patients with stable angina pectoris or acute coronary syndrome undergoing coronary artery bypass grafting. <i>C. pneumoniae</i> mRNA, a marker of replicating bacteria, was demonstrated in 18% of the aortic biopsies. </p><p>Inflammation may have a role in the pathogenesis of thoracic aortic aneurysm, aortic dissection and aortic valve stenosis. <i>C. pneumoniae </i>DNA was demonstrated in aortic biopsies in 26% of thoracic aortic aneurysm patients and in 11% of aortic dissection patients undergoing thoracic surgery and in 22% of stenotic aortic heart valves from patients undergoing aortic valve replacement. No bacterial mRNA was demonstrated in these aortic biopsies, nor in the valves, suggesting that the infection has passed into a persistent state. <i>C. pneumoniae</i> DNA was demonstrated in peripheral blood mononuclear cells in only 5% of aortic valve stenosis patients and not in thoracic aortic aneurysm or aortic dissection patients, suggesting that the bacterium disseminated to the cardiovascular tissue long before the patient required surgery. The copper/zinc ratio in serum, a marker of infection/inflammation, was significantly elevated in thoracic aortic aneurysm patients, supporting an inflammatory pathogenesis. Patients positive for <i>C. pneumoniae</i> in the aortic valve had more advanced coronary atherosclerosis, further supporting a possible role for <i>C. pneumoniae</i> in atherosclerosis. </p><p>Mice were infected with <i>C. pneumoniae</i> that disseminated to all organs investigated (i.e. lungs, heart, aorta, liver and spleen). Trace element concentrations were altered in infected animals with an increased copper/zinc ratio in serum, a progressively increased iron concentration in the liver and a progressively decreased iron concentration in serum. Iron is important for <i>C. pneumoniae</i> metabolism, and a changed iron homeostasis was noted in infected mice by alterations in iron-regulating proteins, such as DMT1 and hepcidin.</p>

Background: Thoracic aortic aneurysms and dissections (TAAD) have a genetic component with an estimated 20-25% of the patients having a positive family history. An aneurysm often precedes a dissection. Acute aortic dissections are associated with high mortality and morbidity, even when operated on. Complications due to prophylactic surgery are considerably fewer. Therefore, patients at risk for dissection should be identified, followed-up and evaluated for prophylactic intervention. Aims: 1. To establish reference values for ascending (AoA) and descending aortic (AoD) diameters measured by computed tomography. 2. To study the effectiveness of phenotypic cascade screening in families with an inherited form of thoracic aortic aneurysms and dissections (FTAAD) and to address questions that arise when screening for a genetic disorder is applied. 3. To study the agreement of aortic diameters obtained by TTE and MRI and to study aortic stiffness in individuals from families with FTAAD. 4. To perform exome sequencing in order to identify pathogenic sequence variants causing FTAAD, to characterize the phenotype, and to compare thoracic aortic diameter and stiffness in mutation carriers and non-carriers. Results: Paper I: The diameter of the thoracic aorta increased by 0.17 mm (0.12 – 0.20 mm) per year. The mean sex-related difference in diameter was 1.99 mm (1.28 – 2.60 mm) with men having larger aortas than women. The mean difference in aortic diameter per unit BMI was 0.27 mm (0.14 – 0.44 mm). Upper normal limits for the AoA can be calculated by the formula D (mm)=31+0.16*age and for the AoD by D (mm)=21+0.16*age. Paper II: Of 106 individuals from families with FTAAD but without known thoracic aortic disease, 19 individuals (18%) were identified to have a dilated AoA. The expected number of individuals in this group with an autosomal dominant disease would have been 40 (p&lt;0.0001). In first-degree relatives younger than 40, we found only one individual with a dilated aorta although the expected number of individuals with disease causing mutation would have been 10. Paper III: Of 116 individuals investigated, 21 were identified with thoracic aortic dilatation and 95 individuals with normal thoracic aortic diameter. Aortic stiffness increased with age and diameter. The individuals with aortic dilatation were older than those without (49 vs. 37 years, p=0.001) and showed lower aortic elastic properties. The diameters measured by TTE and MRI correlated strongly (r2=0.93). The mean difference in diameters between the two methods was 0.72 mm (95% CI 0.41-1.02) with TTE giving larger diameters than MRI. Paper IV: From exome sequencing and segregation analysis, a 2-bp deletion in the MYLK gene (c.3272_3273del) was identified to cause FTAAD. The age and the aortic diameter at dissection or rupture varied in the family members. We did not find any differences in aortic diameter, aortic stiffness, or pulse wave velocity between carriers and non-carriers. Conclusions: Thoracic aortic diameter increases with age, and sex and body size are also associated with the diameter. In FTAAD, screening identifies family members with a previously unknown aortic dilatation. However, a normal aortic diameter does not exclude an individual from being a carrier of FTAAD. TTE can be used in follow-up for the ascending aorta. Individuals identified to have a dilated thoracic aorta have increased aortic stiffness compared to individuals with normal thoracic aortic diameter. The MYLK mutation (c.3272_3273del) causes thoracic aortic dissections with variable clinical expression. No differences in aortic stiffness were identified between MYLK mutation carriers and non-carriers.

Chlamydophila pneumoniae (C. pneumoniae) has been suggested as a stimulator of chronic inflammation in atherosclerosis. C. pneumoniae DNA was demonstrated in aortic biopsies in 50% of patients with stable angina pectoris or acute coronary syndrome undergoing coronary artery bypass grafting. C. pneumoniae mRNA, a marker of replicating bacteria, was demonstrated in 18% of the aortic biopsies. Inflammation may have a role in the pathogenesis of thoracic aortic aneurysm, aortic dissection and aortic valve stenosis. C. pneumoniae DNA was demonstrated in aortic biopsies in 26% of thoracic aortic aneurysm patients and in 11% of aortic dissection patients undergoing thoracic surgery and in 22% of stenotic aortic heart valves from patients undergoing aortic valve replacement. No bacterial mRNA was demonstrated in these aortic biopsies, nor in the valves, suggesting that the infection has passed into a persistent state. C. pneumoniae DNA was demonstrated in peripheral blood mononuclear cells in only 5% of aortic valve stenosis patients and not in thoracic aortic aneurysm or aortic dissection patients, suggesting that the bacterium disseminated to the cardiovascular tissue long before the patient required surgery. The copper/zinc ratio in serum, a marker of infection/inflammation, was significantly elevated in thoracic aortic aneurysm patients, supporting an inflammatory pathogenesis. Patients positive for C. pneumoniae in the aortic valve had more advanced coronary atherosclerosis, further supporting a possible role for C. pneumoniae in atherosclerosis. Mice were infected with C. pneumoniae that disseminated to all organs investigated (i.e. lungs, heart, aorta, liver and spleen). Trace element concentrations were altered in infected animals with an increased copper/zinc ratio in serum, a progressively increased iron concentration in the liver and a progressively decreased iron concentration in serum. Iron is important for C. pneumoniae metabolism, and a changed iron homeostasis was noted in infected mice by alterations in iron-regulating proteins, such as DMT1 and hepcidin.

Amyloid is a form of abnormal protein aggregation within the living body. Massive deposits can lead to organ failure. There is also increasing evidence that smaller pre-amyloid aggregates exert direct toxic effects to cells. To date 25 different proteins are known to occur as amyloid deposition in human tissues, although not all of these conditions are known to be associated with clinical diseases. This thesis deals with the very common form of amyloid localized to the arterial media. The fibril protein called ‘medin’ was identified in 1999. Medin is a 50 amino acid residue internal fragment of the precursor protein lactadherin. Lactadherin, first found in human milk, is expressed in various tissues such as breast epithelium (including carcinomas), macrophages and aorta. The function of the protein is not known but it has several functional domains. There is an EFG like domain, including an RGD-sequence, in the N-terminal part of the molecule. The C-terminal part consists of C1 and C2 coagulation factor V and VIII like domains. Medin is from within the C2 domain. This region is suggested to be involved in phosphatidyl serine binding, important in phagocytosis of apoptotic cells. Medin amyloid was originally described from studies of the aorta. It is shown here that deposits are more widely spread and can be found in many large arteries, particularly within the upper part of the body. The prevalence of medin amyloid increases with age and deposits are found, to a certain degree, in virtually everyone above the age of 60 years. The amyloid is not only found extracellularly but intracellular deposits may also occur. Amyloid is usually associated with elastic lamina or lamellae which often show signs of fragmentation. Given the localization of amyloid to elastic structures of the arterial media, three different vascular diseases were studied: temporal (giant cell) arteritis, thoracic aortic aneurysm and thoracic aortic dissection. Medin amyloid was found in temporal arteries with and without inflammation. In inflamed arteries, amyloid was mainly located along the broken internal elastic lamina. Medin was also demonstrated within giant cells. It is suggested that medin may be an antigen triggering autoimmune giant cell arteritis. In the study of thoracic aortic aneurysms and dissections, we found significant less medin amyloid in diseased aortic tissues compared with a control material. On the other hand, immunoreactive medin, probably in the state of oligomeric aggregates, was regularly found in association with aneurysms and dissections but not in the control material. It is suggested that medin oligomers exert toxic effects on smooth muscle cells which may lead to weakening of the arterial wall with aneurysm or dissection as a consequence.

Objetivo: Avaliar a presença de malformações cardiovasculares em 33 pacientes com síndrome de Turner acompanhadas no Hospital de Clinicas de Porto Alegre. Métodos: Estudo transversal no qual foi realizada ressonância magnética cardíaca (RMC) e torácica com ênfase na avaliação da aorta (RMA) em 33 pacientes. Resultados: As pacientes tinham idade media de 20 anos e 10 meses e altura de 138,7 cm. Aproximadamente 42,42% das pacientes apresentavam cariótipo 45,X e 33,33% pescoço alado. À RMC, 54,54% das pacientes apresentaram alteração, sendo válvula aórtica bicúspide o achado mais frequente, presente em 24,24%. À RMA, malformações cardiovasculares foram encontradas em 42,42%, sendo o alongamento do arco transverso presente em 27,27% das pacientes. Dilatação da aorta estava presente em 66,66% das pacientes, considerada severa em 12,12%. O local mais frequente de dilatação foi na raiz da aorta e na porção tubular da aorta ascendente. Conclusões: Os resultados do presente estudo corroboram achados preliminares da literatura que demonstram que anomalias cardiovasculares são comuns na síndrome de Turner, especialmente diagnosticadas pela ressonância magnética. Dilatação da aorta, principalmente na aorta ascendente, e extremamente frequente na síndrome de Turner e proporciona elevado risco de evento aórtico agudo como a dissecção, potencialmente fatal. / Objective: To evaluate the incidence of cardiovascular malformations in 33 patients with Turner's syndrome followed up in the Hospital de Clinicas of Porto Alegre. Methodology: A transversal study in which a Cardiac and Thoracic Magnetic Resonance Imaging (MRI ) with focus on the evaluation of the aorta was performed in 33 patients. Results: The patients had average age of 20 years and 10 months and height of 138,7 cm. Approximately 42,42% of the patients presented karyotype 45,X and 33,33% webbed neck. Through MRI 54,54% of patients showed anomalies; the bicuspid aortic valve was the most frequent found present in 24,24% of patients. Through MRI, cardiovascular malformations were found in 42,42%, and elongation of the transverse arch was present in 27,27% of patients. Aortic dilatation was found in 66,66% of patients, and it was considered severe in 12,12%. The most frequent place of dilatation was in the aortic root and in the tubular portion of the ascending thoracic aorta. Conclusion: The results of present study corroborate with the literature that says cardiovascular anomalies are common in Turner's syndrome, especially diagnosed through magnetic resonance imaging. Aortic dilatation, most prominent in the ascending aorta, is very frequent in Turner's syndrome and that predicts high risk for acute aortic events such as dissection, potencially fatal.

Objetivo: Avaliar a presença de malformações cardiovasculares em 33 pacientes com síndrome de Turner acompanhadas no Hospital de Clinicas de Porto Alegre. Métodos: Estudo transversal no qual foi realizada ressonância magnética cardíaca (RMC) e torácica com ênfase na avaliação da aorta (RMA) em 33 pacientes. Resultados: As pacientes tinham idade media de 20 anos e 10 meses e altura de 138,7 cm. Aproximadamente 42,42% das pacientes apresentavam cariótipo 45,X e 33,33% pescoço alado. À RMC, 54,54% das pacientes apresentaram alteração, sendo válvula aórtica bicúspide o achado mais frequente, presente em 24,24%. À RMA, malformações cardiovasculares foram encontradas em 42,42%, sendo o alongamento do arco transverso presente em 27,27% das pacientes. Dilatação da aorta estava presente em 66,66% das pacientes, considerada severa em 12,12%. O local mais frequente de dilatação foi na raiz da aorta e na porção tubular da aorta ascendente. Conclusões: Os resultados do presente estudo corroboram achados preliminares da literatura que demonstram que anomalias cardiovasculares são comuns na síndrome de Turner, especialmente diagnosticadas pela ressonância magnética. Dilatação da aorta, principalmente na aorta ascendente, e extremamente frequente na síndrome de Turner e proporciona elevado risco de evento aórtico agudo como a dissecção, potencialmente fatal. / Objective: To evaluate the incidence of cardiovascular malformations in 33 patients with Turner's syndrome followed up in the Hospital de Clinicas of Porto Alegre. Methodology: A transversal study in which a Cardiac and Thoracic Magnetic Resonance Imaging (MRI ) with focus on the evaluation of the aorta was performed in 33 patients. Results: The patients had average age of 20 years and 10 months and height of 138,7 cm. Approximately 42,42% of the patients presented karyotype 45,X and 33,33% webbed neck. Through MRI 54,54% of patients showed anomalies; the bicuspid aortic valve was the most frequent found present in 24,24% of patients. Through MRI, cardiovascular malformations were found in 42,42%, and elongation of the transverse arch was present in 27,27% of patients. Aortic dilatation was found in 66,66% of patients, and it was considered severe in 12,12%. The most frequent place of dilatation was in the aortic root and in the tubular portion of the ascending thoracic aorta. Conclusion: The results of present study corroborate with the literature that says cardiovascular anomalies are common in Turner's syndrome, especially diagnosed through magnetic resonance imaging. Aortic dilatation, most prominent in the ascending aorta, is very frequent in Turner's syndrome and that predicts high risk for acute aortic events such as dissection, potencially fatal.

Objetivo: Avaliar a presença de malformações cardiovasculares em 33 pacientes com síndrome de Turner acompanhadas no Hospital de Clinicas de Porto Alegre. Métodos: Estudo transversal no qual foi realizada ressonância magnética cardíaca (RMC) e torácica com ênfase na avaliação da aorta (RMA) em 33 pacientes. Resultados: As pacientes tinham idade media de 20 anos e 10 meses e altura de 138,7 cm. Aproximadamente 42,42% das pacientes apresentavam cariótipo 45,X e 33,33% pescoço alado. À RMC, 54,54% das pacientes apresentaram alteração, sendo válvula aórtica bicúspide o achado mais frequente, presente em 24,24%. À RMA, malformações cardiovasculares foram encontradas em 42,42%, sendo o alongamento do arco transverso presente em 27,27% das pacientes. Dilatação da aorta estava presente em 66,66% das pacientes, considerada severa em 12,12%. O local mais frequente de dilatação foi na raiz da aorta e na porção tubular da aorta ascendente. Conclusões: Os resultados do presente estudo corroboram achados preliminares da literatura que demonstram que anomalias cardiovasculares são comuns na síndrome de Turner, especialmente diagnosticadas pela ressonância magnética. Dilatação da aorta, principalmente na aorta ascendente, e extremamente frequente na síndrome de Turner e proporciona elevado risco de evento aórtico agudo como a dissecção, potencialmente fatal. / Objective: To evaluate the incidence of cardiovascular malformations in 33 patients with Turner's syndrome followed up in the Hospital de Clinicas of Porto Alegre. Methodology: A transversal study in which a Cardiac and Thoracic Magnetic Resonance Imaging (MRI ) with focus on the evaluation of the aorta was performed in 33 patients. Results: The patients had average age of 20 years and 10 months and height of 138,7 cm. Approximately 42,42% of the patients presented karyotype 45,X and 33,33% webbed neck. Through MRI 54,54% of patients showed anomalies; the bicuspid aortic valve was the most frequent found present in 24,24% of patients. Through MRI, cardiovascular malformations were found in 42,42%, and elongation of the transverse arch was present in 27,27% of patients. Aortic dilatation was found in 66,66% of patients, and it was considered severe in 12,12%. The most frequent place of dilatation was in the aortic root and in the tubular portion of the ascending thoracic aorta. Conclusion: The results of present study corroborate with the literature that says cardiovascular anomalies are common in Turner's syndrome, especially diagnosed through magnetic resonance imaging. Aortic dilatation, most prominent in the ascending aorta, is very frequent in Turner's syndrome and that predicts high risk for acute aortic events such as dissection, potencially fatal.

Le Syndrome d’Ehlers-Danlos vasculaire (SEDv) est une pathologie génétique rare à transmission autosomique dominante. Les patients sont prédisposés à la survenue de ruptures vasculaires, digestives et utérines induisant une létalité précoce. Cette pathologie est due à des mutations du gène COL3A1 (codant le collagène de type III), majoritairement de type faux-sens, agissant via un mécanisme dominant négatif. Plus rarement, de larges délétions ou des mutations non-sens induisent une haplo-insuffisance. In fine, les conséquences de ces mutations portent essentiellement sur la synthèse du collagène de type III, aboutissant à une fragilité artérielle importante. A ce jour, aucun traitement curatif n’est disponible. L’inactivation du gène Col3a1 chez la souris entraine une mortalité in utero et néonatale quasi-systématique en cas d’homozygotie, mais les souris Col3a1+/- sont exemptes de phénotype vasculaire évident. Afin d’obtenir un modèle de dissection artérielle liée à un défaut de collagène de type III, une perfusion chronique d’Angiotensine II (Ang II) à dose pressive a été utilisée. Nos résultats montrent que l’haplo-insuffisance en collagène de type III confère une sensibilité artérielle majeure à l’Ang II. Cette fragilité est caractérisée par le développement de dissections/ruptures de l’aorte ascendante et induit des décès prématurés de ces animaux. Ce phénotype est lié non seulement à l’élévation de pression artérielle mais aussi à l’activation des voies de signalisation de l’Ang II. Enfin, nous montrons qu’un traitement associant un bêtabloquant (propranolol) et un vasodilatateur artériel (hydralazine) permet de réduire la mortalité induite par l’Ang II. Ces résultats suggèrent l’intérêt de l’ajout d’un traitement préventif par inhibiteur de l’Ang II au traitement bêtabloquant (Celiprolol) recommandé dans la pathologie humaine.Parallèlement, nous avons généré un modèle murin knock-in génétiquement plus proche des patients SEDv, par l’introduction d’une mutation ponctuelle faux-sens (Gly183Ser) observée chez un patient. L’analyse préliminaire de ce modèle montre que les souris Col3a1+/G183S décèdent spontanément, dès 4 semaines, de ruptures/dissections de l’aorte ascendante. Cependant, ces souris ne présentent de modification ni de leurs paramètres hémodynamiques, ni de leurs diamètres aortiques. En revanche, environ 20 % des souris Col3a1+/G183S présentent des plaies au niveau du dos et des pattes. Ce nouveau modèle de souris est actuellement le seul à récapituler aussi fidèlement le phénotype des patients SEDv. Il devrait donc permettre de tester différentes approches thérapeutiques. / Vascular Ehlers-Danlos (vEDS) syndrome is a rare, inherited, autosomal dominant disease that results from mutations in the COL3A1 gene, encoding type III collagen. Patients are mostly affected by missense mutations probably acting through a dominant negative mechanism. A few patients present large deletions or nonsense mutations leading to a haploinsufficient mechanism. These mutations are supposed to lead to a defect in the synthesis and secretion of collagen type III, resulting in arterial wall fragility. Consequently, vEDS is mostly characterized by ruptures/dissections in arteries at a young age, which ultimately lead to premature death. While there is currently no surgical or therapeutic treatments available, a recent study reported the beneficial effect of the beta-blocker celiprolol, which prevents vascular complications in patients.To investigate the vascular phenotype of vEDS, a mouse model of this disease has been generated by the complete and ubiquitous inactivation of the COL3A1 gene. Col3a1-/- mice exhibit severe perinatal mortality and die prematurely from spontaneous vascular rupture. However, Col3a1+/- mice are viable and exhibit no obvious vascular phenotype. To determine the susceptibility of Col3a1+/- mice to develop vascular rupture/dissection, an experimental model of aneurysm induction was used, through the chronic infusion of Angiotensin II (Ang II). Our results showed that Ang II infusion led to severe premature mortality in Col3a1+/- compared to wild type. This fragility was characterized by the development of rupture/dissection in the ascending aorta. These lesions could be caused by the elevation of blood pressure and/or the activation of Ang II signaling pathways. We showed that treatment with a beta-blocker (propranolol) and an arterial vasodilator (hydralazine) reduced the mortality induced by Ang II in Col3a1+/- mice. These results suggest the beneficial effect of adding a preventive treatment inhibitor of Ang II to the beta-blocker treatment recommended in human pathology.Meanwhile, given that a majority of human vEDS cases is caused by missense mutations in the COL3A1 gene, we established a knock-in mouse model bearing a point mutation (Gly183Ser) found in vEDS patients. The preliminary characterization of this model showed that Col3a1+/G183S mice die spontaneously as early as 4 weeks of age from a dissection or rupture of the ascending aorta. However, these mice do not showed any changes of their hemodynamic parameters or aortic diameter. Furthermore, about 20 % of mouse Col3a1+/G183S display wounds in the back and legs. This new mouse model is currently the only that mimic more closely the human disease and could therefore be used to test different therapeutic strategies.

Les nouvelles technologies d'imagerie basées sur la tomodensitométrie en coupe permettent l'évaluation de très haute qualité de la structure 3D de l'aorte thoracique. La reconstruction virtuelle et les modèles géométriques de l'aorte sont indispensables à l'exploitation des images dont le temps de traitement manuel reste cependant considérable et les outils numériques insuffisants ou inadaptés pour mesurer correctement sa morphologie. L'aorte n'est pas un simple tube de conduction du sang mais un organe de régulation de la pulsatilité des ondes de pression provoquées par l'éjection cardiaque. Ses désordres biomécaniques peuvent accélérer la formation de calcifications dans sa paroi et entrainer des risques de graves complications, comme les anévrismes et les dissections. La réparation aortique basée sur l'implantation d'endoprothèses est en pleine évolution et requiert des renseignements morphologiques précis pour en améliorer le taux de succès. Notre objectif a été d'étudier la géométrie tridimensionnelle de l'aorte en développant des algorithmes appropriés. Une plateforme informatique a été conçue et testée pour étudier trois pathologies de l'aorte: l'athérosclérose calcifiée, l'anévrisme et la dissection. L'hypothèse du travail a été que la géométrie spécifique des artères de chaque individu joue un rôle complémentaire à celui des facteurs de risque traditionnels dans le développement de ces pathologies. Notre premier travail a montré que trois facteurs résument 80% de la variabilité géométrique de l'aorte thoracique: le volume aortique, le déroulement et la symétrie de l'arche aortique, avec des taux de variabilité respectifs de 46%, 22% et 12%. Dans deux travaux suivants, nous avons montré que les calcifications de l'aorte thoracique se concentrent principalement dans la crosse et dans le segment descendant proximal, et que cette distribution était associée à la morphologie de l'aorte indépendamment de l'âge, du sexe, de la surface corporelle et des facteurs de risque traditionnels. Le quatrième travail a montré que le score de dépôt calcique dans toute l'aorte thoracique incluant la crosse était plus étroitement associé aux complications non-cardiaques, vasculaires périphériques et cérébrales, que le score traditionnel de calcium coronaire. Il faut noter que la crosse aortique n'est pas visualisée dans les études de routine de calcium coronaire sans injection. Le cinquième travail décrit un modèle déformable capable de segmenter la lumière aortique dans un contexte pathologique. Il a été appliqué pour étudier de façon automatisée la taille d'un anévrisme abdominal avant et après la pose d'une endoprothèse. Dans le dernier travail, la méthode précédente a été adaptée pour étudier la géométrie aortique des patients atteints de dissection comparativement à un groupe témoin de patients qui en étaient indemnes. Trois variables géométriques ont été identifiées dans le modèle de prédiction du risque de dissection: le diamètre de la crosse, la longueur de l'aorte thoracique et l'âge. En conclusion, nos résultats montrent que les maladies aortiques sont étroitement associées à la géométrie de l'aorte indépendamment des facteurs de risque traditionnels. Les algorithmes que nous avons développés ouvrent la voie à l'automatisation et à une réduction de la variabilité des mesures. / New imaging technologies, including those associated with multislice computed tomography, allow to evaluate the structure of the thoracic aorta in 3D with an impressive resolution. Aortic virtual reconstruction and geometric modeling are essential for imaging evaluation because manual measurements are time-consuming, and the available tools still need to be adapted to complex aortic morphologies. The aorta is more than a simple tubular conduit vessel for blood. It also regulates the pulsatile pressure waves that are injected into the arterial system by the left ventricle. The biomechanical disorders produced by these waves can accelerate the formation of calcium deposits within the arterial wall. Furthermore, they are thought to be responsible for severe aortic complications, including aneurysms and dissections. Endovascular aortic repair is a modern technique based on the implantation of an endograft to restore the normal blood flow. Precise morphological measurements are required to improve this technique, for both surgery planning and patient follow up. Our objective was to develop original algorithms to study the aortic geometry in 3D. A computing platform was designed and tested to analyze three main aortic pathologies: calcified atherosclerosis, aneurysms and dissections. The hypothesis of our study was that the individual arterial geometry of a subject plays a complementary role in the development of vascular pathologies beyond traditional risk factors. Our first work revealed that 80% of the total geometric variability in the thoracic aorta might be explained using 3 factors: the aortic volume, the aortic arc unfolding and its asymmetry. Variability percentages accounted for 46%, 22% and 12%, respectively. The next 2 works, showed that calcifications in the thoracic aorta were concentrated in the aortic arch and in the proximal descending segment. This spatial distribution was associated with aortic morphology, independently of age, sex, body surface area and traditional risk factors. Our fourth article revealed that calcium deposits in the entire thoracic aorta (including the aortic arch) was associated with non-cardiac events, beyond the standard coronary artery calcium score. It is noteworthy that the aortic arch region is systematically excluded from standard scans. Our fifth manuscript described a novel deformable model applied to the aortic segmentation under pathological contexts. It was used to estimate the size and shape of abdominal aneurysms before and after endograft implantation. In the last work, this method was adapted to study the geometry of the thoracic aorta of patients with an aortic dissection with respect to a control group. Three anatomic variables were identified for the risk prediction model: the aortic arch diameter, the thoracic aortic length and the age of the patient. In conclusion, our results show that aortic diseases are closely associated with aortic geometry, independently from traditional risk factors. The developed algorithms improved the automation of measurements and reduced the variability of the estimations.