Made available in DSpace on 2015-01-26T13:21:22Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-08-26Bitstream added on 2015-01-26T13:30:38Z : No. of bitstreams: 1 000798818.pdf: 341307 bytes, checksum: a33a2c9977f57c10c36e049053a2657c (MD5) / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) / Após uma agressão, o coração remodela-se para manter estável a sua função; entretanto, a remodelação cardíaca (RC) é tempo dependente e a longo prazo pode ser prejudicial. A estenose aórtica supravalvar (EAo) tem sido utilizado para promover o desenvolvimento gradual de hipertrofia ventricular esquerda. Constatouse que ratos desenvolvem hipertrofia ventricular esquerda, disfunção diastólica e melhoria da função sistólica após 2 e 6 semanas de EAo, manutenção da disfunção diastólica e deterioração do desempenho sistólico na 12ª semana e, na 18ª semana há acentuação da disfunção sistólica e aparecimento de insuficiência cardíaca. Diferentes fatores poderiam contribuir para a disfunção no modelo experimental de EAo como o déficit de oxigênio ou de substrato energético. Em condições aeróbicas normais, aproximadamente 70% da produção de energia miocárdica deriva do metabolismo de ácidos graxos, sendo a contribuição glicolítica em torno de 30%. Estudos mostram que o fator responsável pela escolha do substrato energético cardíaco são os níveis plasmáticos elevados de ácidos graxos e triglicérides. Estudos utilizando modelos experimentais de insuficiência cardíaca constataram que o aumento na oferta de energia por lipídeos, não alteraram ou promoveram melhoria da RC. O objetivo deste trabalho foi testar a hipótese que a maior disponibilidade de energia proveniente dos lipídeos ricos em ácidos graxos saturados restaura o equilíbrio energético miocárdico, atenuando o processo de remodelação patológica (RP). Com a finalidade de testar esta hipótese, foram avaliadas a estrutura, a função e o metabolismo miocárdico de ratos com EAo, tratados com dieta hiperlipídica saturada. Foram utilizados ratos Wistar machos, com 21 dias de idade, separados em grupo controle (Sham) e estenose aórtica supravalvar (EAo); após 6 semanas da cirurgia, os ratos foram redistribuídos em mais dois ... / After an aggression, the heart undergoes remodeling to maintain its function stable; however, cardiac remodeling (CR) is time dependent and, in long term, may be harmful. The supravalvular aortic stenosis (AS) has been used to promote gradual development of left ventricular hypertrophy. It was observed that rats develop left ventricular hypertrophy, diastolic dysfunction and improved systolic function after 2 and 6 weeks of AS. After 12 weeks, diastolic dysfunction is maintained and systolic performance deteriorates; around the 18th week, systolic dysfunction is accentuated and signs of heart failure appear. Different factors could contribute to the dysfunction in the experimental model of AS, such as oxygen or energy substrate deficit. Under normal aerobic conditions, approximately 70% of myocardial energy production comes from fatty acid metabolism, and glycolysis contribution is around 30%. Studies have showed that the responsible factor for the choice of cardiac energy substrate is the elevated plasma levels of fatty acids and triglycerides. Studies that used experimental models of heart failure found that the increase in energy supply by lipids did not change or improved RC. The aim of this study was to test the hypothesis that the increased energy availability derived from lipids rich in saturated fatty acids restores myocardial energy balance, attenuating the pathological remodeling process. In order to test this hypothesis, we have evaluated the myocardial structure, function and metabolism of rats with AS fed with saturated high-fat diet. Male Wistar rats, 21 days old, were distributed into control group (Sham) or supravalvular aortic stenosis (AS); 6 weeks after surgery, rats were redistributed into two groups: fed with saturated high-fat diet or normolipidic diet (AS-N, n=12; Sham-N, n=14; AS-H, n=14 and Sham-H, n=14). The nutritional profile was determined. RC was characterized by the ...

Orientador: Antonio Carlos Cicogna / Banca: André Soares Leopoldo / Banca: Silvio Assis de Oliveira Júnior / Banca: Marcos Ferreira Minicucci / Banca: Paula Schmidt Azevedo Gaiolla / Resumo: Após uma agressão, o coração remodela-se para manter estável a sua função; entretanto, a remodelação cardíaca (RC) é tempo dependente e a longo prazo pode ser prejudicial. A estenose aórtica supravalvar (EAo) tem sido utilizado para promover o desenvolvimento gradual de hipertrofia ventricular esquerda. Constatouse que ratos desenvolvem hipertrofia ventricular esquerda, disfunção diastólica e melhoria da função sistólica após 2 e 6 semanas de EAo, manutenção da disfunção diastólica e deterioração do desempenho sistólico na 12ª semana e, na 18ª semana há acentuação da disfunção sistólica e aparecimento de insuficiência cardíaca. Diferentes fatores poderiam contribuir para a disfunção no modelo experimental de EAo como o déficit de oxigênio ou de substrato energético. Em condições aeróbicas normais, aproximadamente 70% da produção de energia miocárdica deriva do metabolismo de ácidos graxos, sendo a contribuição glicolítica em torno de 30%. Estudos mostram que o fator responsável pela escolha do substrato energético cardíaco são os níveis plasmáticos elevados de ácidos graxos e triglicérides. Estudos utilizando modelos experimentais de insuficiência cardíaca constataram que o aumento na oferta de energia por lipídeos, não alteraram ou promoveram melhoria da RC. O objetivo deste trabalho foi testar a hipótese que a maior disponibilidade de energia proveniente dos lipídeos ricos em ácidos graxos saturados restaura o equilíbrio energético miocárdico, atenuando o processo de remodelação patológica (RP). Com a finalidade de testar esta hipótese, foram avaliadas a estrutura, a função e o metabolismo miocárdico de ratos com EAo, tratados com dieta hiperlipídica saturada. Foram utilizados ratos Wistar machos, com 21 dias de idade, separados em grupo controle (Sham) e estenose aórtica supravalvar (EAo); após 6 semanas da cirurgia, os ratos foram redistribuídos em mais dois ... / Abstract: After an aggression, the heart undergoes remodeling to maintain its function stable; however, cardiac remodeling (CR) is time dependent and, in long term, may be harmful. The supravalvular aortic stenosis (AS) has been used to promote gradual development of left ventricular hypertrophy. It was observed that rats develop left ventricular hypertrophy, diastolic dysfunction and improved systolic function after 2 and 6 weeks of AS. After 12 weeks, diastolic dysfunction is maintained and systolic performance deteriorates; around the 18th week, systolic dysfunction is accentuated and signs of heart failure appear. Different factors could contribute to the dysfunction in the experimental model of AS, such as oxygen or energy substrate deficit. Under normal aerobic conditions, approximately 70% of myocardial energy production comes from fatty acid metabolism, and glycolysis contribution is around 30%. Studies have showed that the responsible factor for the choice of cardiac energy substrate is the elevated plasma levels of fatty acids and triglycerides. Studies that used experimental models of heart failure found that the increase in energy supply by lipids did not change or improved RC. The aim of this study was to test the hypothesis that the increased energy availability derived from lipids rich in saturated fatty acids restores myocardial energy balance, attenuating the pathological remodeling process. In order to test this hypothesis, we have evaluated the myocardial structure, function and metabolism of rats with AS fed with saturated high-fat diet. Male Wistar rats, 21 days old, were distributed into control group (Sham) or supravalvular aortic stenosis (AS); 6 weeks after surgery, rats were redistributed into two groups: fed with saturated high-fat diet or normolipidic diet (AS-N, n=12; Sham-N, n=14; AS-H, n=14 and Sham-H, n=14). The nutritional profile was determined. RC was characterized by the ... / Mestre

Introdução: A deposição de cálcio junto aos folhetos valvares esta intimamente relacionada à fisiopatologia da estenose valvar aórtica degenerativa (EAD). A tomografia computadorizada com multidetectores (TCMD), além de possibilitar o delineamento tridimensional das estruturas cardíacas, permite a quantificação da intensidade da calcificação valvar. Atualmente, a relação entre a localização dos depósitos valvares de cálcio e a gravidade hemodinâmica na estenose aórtica permanece incerta. Objetivo: Avaliar se a topografia da calcificação valvar influencia a repercussão hemodinâmica na EAD. Métodos: Trata-se de estudo prospectivo, unicêntrico, incluindo 97 pacientes com EAD moderada ou importante. O escore de cálcio da valva aórtica foi calculado a partir da TCMD sem contraste. A topografia da calcificação valvar foi avaliada através de análise tomográfica específica com infusão de baixa dose de contraste endovenoso, objetivando uma detalhada segmentação anatômica dos planos valvares. A medida da atenuação, expressa em unidades Hounsfield (UH), foi utilizada para quantificar o conteúdo de cálcio na região central e periférica do plano valvar aórtico. Resultados: Pacientes com EAD importante apresentaram escore de cálcio valvar aórtico superior ao dos portadores de EAD moderada (3131 ± 1828 unidades Agatston [UA] e 1302 ± 846 UA, respectivamente; p < 0,001). Quanto à topografia da calcificação, pacientes com EAD importante exibiram atenuações significativamente maiores no centro do plano valvar do que em sua periferia (507,4 ± 181,7 UH vs. 449,8 ± 114,5 UH; p = 0,001). Inversamente, pacientes com EAD moderada apresentaram menor atenuação na região central do que na periferia valvar (308,7 ± 92,9 UH vs. 347,6 ± 84,2 UH, p < 0,001). A razão da atenuação centro/periferia também foi significativamente maior nos pacientes com EAD importante (1,14 ± 0,32 vs. 0,89 ± 0,13; p < 0,001), permanecendo significativamente associada à presença de EAD importante mesmo após ajuste para o grau subjacente de calcificação Resumo valvar. Conclusão: A gravidade da EAD parece resultar não apenas do grau de calcificação, mas também da localização dos depósitos valvares de cálcio / Introduction: The pathophysiology of degenerative aortic valve stenosis (AS) is intimately related to the development of calcific deposits in the valve structure. Multidetector computed tomography (MDCT), a reliable method to delineate the tridimensional heart geometry, has been shown to accurately quantify the global aortic valve calcium content. Currently, the relationship between calcium location and hemodynamic disease severity is poorly understood. Objective: The present prospective study was conducted to test the hypothesis of whether the location of valve calcification influences the functional severity of AS. Methods: Prospective, single-arm study including 97 patients with diagnosed moderate or severe AS. Aortic valve calcium score was calculated from nocontrast multidetector computed tomography (MDCT). \"Low-contrast- os \" MDCT images were acquired for segmentation of the cardiac anatomy, with the attenuation, expressed in Hounsfield units (HU), used to quantify the calcium content at the central and peripheral regions of the aortic valve zone. Results: The calcium score was higher among patients with severe AS compared to patients without severe AS (3131±1828 Agatston units [AU] vs. 1302±846 AU respectively; p < 0.001). Patients with severe AS had significantly higher attenuations at the center of the valve than at its periphery (507.4±181.7 HU vs. 449.8±114.5 HU; p=0.001). Conversely, patients without severe AS had lower attenuation at the center than at the periphery of the valve (308.7 ± 92.9 HU vs. 347.6±84.2 HU; p < 0.001). The center/periphery attenuation ratio was significantly higher for patients with severe AS than for those without severe disease (1.14±0.32 vs. 0.89 ± 0.13; p < 0.001), and remained significantly associated with the presence of severe AS even after adjusting for the underlying degree of valve calcification. Conclusion: The severity of degenerative aortic valve stenosis appears to result not only from the degree of calcification but also from the localization of the calcific deposits within the valve

Abstract The stem cell is a primitive cell that is capable of dividing to reproduce itself and can give rise to a selection of differentiated progeny. Stem cells are thought to be involved in or even main factors in many diseases. In postnatal humans, mesenchymal tissues have the capacity to regenerate from stem cells called mesenchymal stem cells (MSC). It is currently thought that these cells will become the basis of therapy for many diseases. In the present study, a novel in vitro method was developed to examine human bone marrow derived MSC differentiation into osteoblast lineage, and to study the role of MSC in a variety of mesenchymal diseases. The ability of MSCs to differentiate into osteoblasts was investigated during aging. In addition, the interindividual variability in the osteogenesis of MSCs and in the osteoblastic response of MSC to estrogen and testosterone was studied. Furthermore, an ex vivo model using a human aortic valve microenvironment was developed to explore whether the extracellular matrix influences the osteoblastic differentiation of the MSC. Finally, the role of MSC in neurofibromatosis type 1 (NF1) related congenital pseudarthrosis of the tibia (CPT) was studied. It was found that after menopause the osteogenic potential of MSCs does not decrease. It was also found that estrogen receptor (ER) alpha genotype confers interindividual variability of response to estrogen and testosterone in MSC derived osteoblasts. In addition, it was found that the non-calcified valves with living valve cells inhibited osteogenesis of co-cultured MSCs, whereas the calcified and devitalised valves promoted differentiation towards an osteoblastic lineage. Finally, MSCs from NF1-related pseudarthrosis showed altered NF1 gene expression, poor osteoblastic differentiation and bone formation. In conclusion, MSC can be easily isolated from the bone marrow and MSC has the capacity to regenerate tissue even at later stages of life. These results could help explain the contradictory effects of 17β-estradiol (E2) on osteoblasts in vitro and might also provide new insights into understanding the differences in responses to hormone replacement therapy. It seems that adult stem cells from bone marrow undergo milieu-dependent differentiation to express phenotypes that are similar to cells in the local microenvironment. Finally, the NF1 gene was shown to have a role in bone development and remodelling.

Abstract Calcified aortic valve disease represents a spectrum of disease spanning from mild aortic valve sclerosis to severe aortic valve stenosis (AS), being an actively regulated disease process and showing some hallmarks of atherosclerosis. The calcified aortic valve lesion develops endothelial injury and is characterized by inflammation, lipid accumulation, renin-angiotensin system activation and fibrosis. There is no approved pharmacological treatment available in AS. This study was aimed to characterize gene expression of endothelial factors in aortic valves in patients representing different stages of calcified aortic valve disease to reveal new targets for pharmacological interventions in AS. Aortic valves obtained from 75 patients undergoing valve replacement surgery were studied. Expression of natriuretic peptides (ANP, BNP and CNP), their processing enzymes (corin and furin), natriuretic receptors (NPR-A, NPR-B and NPR-C), endothelin-1 (ET-1), endothelin converting enzyme-1 (ECE-1), endothelin receptors A and B (ETA and ETB), and apelin pathway (apelin and its receptor APJ) was characterized by reverse-transcriptase polymerase chain reaction (RT-PCR) and immunohistochemistry. AS was characterized by distinct downregulation of gene expression of CNP, its processing enzyme furin and the target receptor NPR-B. Furthermore, increased amount of ET-1 and its target receptor ETA as well as imbalance between ETA and ETB receptors and downregulated endothelial nitric oxide synthase (eNOS) gene expression were observed. Finally, gene expression of apelin and APJ receptor were significantly upregulated in stenotic valves when compared to controls in combination with disequilibrium between expression of angiotensin II receptors AT1 and AT2. The study provides a better understanding of molecular mechanisms associated with calcific aortic valve disease and suggest potential targets for novel therapeutic interventions.

Para investigar se estresse oxidativo contribui para a progressão da calcificação/estenose valvar aórtica (VA), avaliamos a produção de espécies reativas de oxigênio (ERO) e efeitos dos antioxidantes tempol e ác. lipóico em modelo de calcificação VA em coelhos. Superóxido, H2O2 e 3-nitrotirosina aumentaram em células inflamatórias e principalmente nos núcleos de calcificação, juntamente com as subunidades p22phox, Nox2 da NADPH oxidase e da proteína dissulfeto isomerase, que co-localizam. PCR mostrou aumento da Nox4 em relação a Nox1. A calcificação foi menor com ác.lipóico e maior com tempol, coicidindo com resultados de modelo in vitro em células musculares lisas. VA humanas estenóticas tiveram aumento semelhante de ERO e da expressão protéica em torno da calcificação. Estresse oxidativo pode contribuir para a progressão da estenose aórtica. / To invetigate whether oxidative stress contributes to aortic valve (AV) calcification/stenosis progression, we assessed reactive oxygen species (ROS) production and effects of antioxidants tempol and lipoic acid in a rabbit AV calcification model. Superoxide, H2O2 and 3-nitrotyrosine increased in inflammatory cells and mainly in calcifying nuclei, coincident with NADPH oxidase subunits p22phox, Nox2 and protein disulfide isomerase, which co-localized. PCR showed switch from Nox1 to Nox4. Calcification was smaller with lipoic acid and greater with tempol, similar to an in vitro smooth muscle cell calcification model results. Human stenotic AV had analogous increase in ROS and protein expression around calcifying nuclei. Oxidative stress can contribute to AV stenosis progression.

No description available.

Thesis (MScEng (Mechanical and Mechatronic Engineering))--Stellenbosch University, 2008. / Aortic valve replacements are frequently performed during heart surgery. However, since this is quite a stressful procedure, many patients are turned down for medical reasons. Stented valves, designed and manufactured for percutaneous insertion, eliminate many of the risks involved in open-heart surgery, thus providing a solution to patients not deemed strong enough for open-chest aortic valve replacements. The aortic valve is a complex structure, and therefore numerical simulation is necessary to obtain flow and stress data to support the design of a prosthetic heart valve in the absence of viable physical measuring methods. To aid in the design of a prosthetic heart valve, various finite element valve models were created, and the fluid structure interaction (FSI) between the valves and the blood was simulated using commercial finite element software. The effect of the geometry of the leaflets on the haemodynamic behaviour over the cardiac cycle was investigated. It was found that leaflet dimensions should be chosen judiciously, because of their considerable effect on the stress distribution and performance of the valve. A simple leaflet geometry optimisation was done for a 20 mm and 26 mm valve, respectively, by means of existing geometry relationships found in the literature. Simulations were done to obtain the maximum leaflet attachment forces that can be used by a stent designer for fatigue loading, or to investigate the structural strength of the stent. These simulations were numerically validated. The effect of leaflet thickness and stiffness on resistance to opening, stress distribution and strain were investigated. Results showed that leaflet thickness has a greater effect on the performance of the valve than leaflet stiffness, and thereby validated the results of similar tests contained in the literature. After simulating over-, as well as under-dilation of a stented valve, it was found that problems associated with over-dilation can be minimised to a certain extent by increasing the coaptation1 region of the leaflets. A simple pulse duplicator was designed based on a four-element Windkessel model. The pulse duplicator was used to study the performance of the prototype valves by means of high-speed photography, the results of which were fed into one of the numerical finite element models and compared to real valve performance. Some of the prototype valves showed efficiencies of 88%.

La sténose valvulaire aortique (SVA) est une pathologie associée au vieillissement et aux facteurs de risque cardiovasculaire. Afin d’étudier la SVA et d’explorer de nouvelles thérapies, plusieurs modèles animaux ont été récemment développés, mais la plupart de ces modèles ciblent les mécanismes de développement de la SVA reliés à l’hypercholestérolémie. Le syndrome de Werner (WS) est une maladie caractérisée par un vieillissement prématuré. Récemment, il a été découvert que des souris mutantes ayant une délétion du domaine hélicase du gène Werner, responsable du WS, démontraient un profile hémodynamique typique de la SVA. De ce fait, nous avons émis l’hypothèse que ces souris pourraient développer une SVA plus rapidement que des souris de type sauvage. Nous avons donc étudié les effets cette mutation chez des souris WrnΔhel/Δhel, en comparant le taux de progression d’une SVA entre des souris WrnΔhel/Δhel (WrnΔhel) et des souris de type sauvage comme groupe contrôle. À la suite d’une diète riche en sucre et en gras sur une période de 24 semaines, les souris WrnΔhel ont démontré une diminution plus prononcée de leur aire de valve aortique (mesures échocardiographiques) que les souris contrôles, supportée par les analyses histologiques concernant la fibrose des valves aortiques. Les souris n’ont toutefois développé aucun signe évident d’athérosclérose comme l’infiltration de lipides ou l’inflammation, bien que certaines caractéristiques liées à la dysfonction endothéliale semblent être augmentées chez les souris WrnΔhel. D’autres mesures échocardiographiques indiquant une SVA, comme une hypertrophie du ventricule gauche dans le groupe WrnΔhel, ont été obtenues. Nous avons aussi observé des indices de vieillissement plus marqués quant aux analyses sanguines et de la moelle osseuse des souris WrnΔhel en comparaison avec les souris contrôles. Par conséquent, ce modèle expérimental de vieillissement pourrait être utilisé pour les études futures sur la SVA sans les principaux effets athérogéniques des autres modèles expérimentaux. / Aortic valve stenosis (AVS) is associated with aging and classical cardiovascular risk factors. Different animal models were recently developed to study AVS and explore new therapies, however, most of these models rely almost exclusively on hypercholesterolemia-related mechanisms for AVS development. Werner syndrome (WS) is a disorder characterized by premature aging. It was recently demonstrated that mutant mice with a deletion of the helicase domain of the Werner gene, the gene responsible for WS, showed hemodynamic profile typical of AVS. We therefore hypothesized that mice with the WrnΔhel deletion could develop AVS earlier than wild-type (WT) mice. We studied the effect of the WrnΔhel mutation by comparing the rate of progression of AVS in homozygous mutant versus WT mice. By twenty-four weeks on a high-fat/high-carbohydrate diet, WrnΔhel/Δhel (WrnΔhel) mice showed a stronger decrease of the aortic valve area measured by serial echocardiography than WT mice, supported by histological analyses of valve fibrosis but without developing major signs of atherosclerosis such as lipid infiltration or increased inflammation. Some features linked to endothelial dysfunction also appeared to be increased in WrnΔhel mice. Other echocardiographic measurements were typical of AVS, such as left ventricle hypertrophy in the WrnΔhel group. We also observed stronger aging properties from WrnΔhel mice bone marrow and blood analyses compared to the WT group. Consequently, this experimental aging model could be used for AVS research without the major confounding atherogenic effects of other experimental models.

Introdução: Uma nova alternativa de tratamento foi desenvolvida, o Implante por Cateter de Bioprótese Valvar Aórtica (TAVI, em inglês, Transcatheter Aortic Valve Implantation), indicado para os pacientes portadores de estenose aórtica grave com várias comorbidades, considerados inoperáveis pelo tratamento cirúrgico convencional. O TAVI ainda não foi incorporado ao rol de políticas de saúde do Brasil pelo Sistema Único de Saúde (SUS), tampouco pela Agência Nacional de Saúde Suplementar (ANS), pois há escassez de evidências científicas fundamentadas em análise econômica do procedimento que relatem os resultados e o custo a longo prazo em comparação à cirurgia convencional. Objetivo: Identificar o custo direto médio do implante por cateter de bioprótese valvar aórtica, verificar se há alteração significativa de custo nas diferentes vias de acesso utilizadas e identificar os fatores preditores que possam elevar o custo do procedimento. Método: Trata-se de uma pesquisa com abordagens quantitativa, exploratória, descritiva, transversal, retrospectiva e documental, realizada em um hospital da Secretaria de Estado de Saúde de São Paulo (SES-SP), da Administração Direta, especializado no tratamento de doenças cardiovasculares de alta complexidade. A população do estudo correspondeu aos procedimentos eletivos do TAVI, desde a inauguração da sala híbrida, em março de 2012, até agosto de 2015, totalizando 108 procedimentos, sendo 92 por via transfemoral, 8 por via transapical e 8 por via transaórtica. Resultados: O custo direto médio dos procedimentos TAVI nas três vias totalizou R$ 82.230,94. Por via transfemoral, esse custo médio foi de R$ 82.826,38; por via transaórtica, R$ 79.440,91; e por via transapical, R$ 78.173,41. O total de material e medicamento/solução representou, por via transfemoral, 91,89% do total do custo direto médio do procedimento TAVI; por via transapical, 91,81%; e por via transaórtica, 90,69%, e o custo fixo com a válvula transcateter, no valor de R$ 65 mil, representou 78,47% sobre o custo total do procedimento TAVI, por via transfemoral; 83,14%, por via transapical; e 81,82%, por via transaórtica. O Teste Kruskal-Wallis Teste das Variáveis Contínuas apresentou diferença estatisticamente significativa entre as vias de acesso. No custo total do procedimento TAVI, o Teste de Bonferroni mostrou diferença na associação entre as vias transfemoral e transapical. No entanto, na associação com a via transaórtica, não apresentou diferença estatisticamente significativa. Os fatores preditores que elevaram o custo do procedimento TAVI foram: vias de acesso, duração do procedimento, material de hemodinâmica, medicamento/solução, material de consumo, material de perfusão, total de material e medicamento/solução, recursos humanos, gases medicinais, depreciação e energia. A segunda válvula foi a única variável referente às intercorrências no Centro Cirúrgico que elevou o custo do procedimento. A média de idade dos pacientes com indicação ao TAVI foi de 81,50 ±6,96 anos. Conclusão: O TAVI é um avanço a ser discutido e acompanhado, havendo a necessidade de reforçar novas pesquisas que avaliem os benefícios do tratamento com base nos resultados e custos, a fim de auxiliar na tomada de decisão para incorporação desse tratamento para o público-alvo, melhorando a qualidade de vida dos pacientes e proporcionando a integração destes novamente às atividades diárias. / Introduction: A new treatment alternative has been developed, the Transcatheter Aortic Valve Implantation (TAVI), indicated for patients with severe aortic stenosis with various comorbidities deemed inoperable by conventional surgical treatment. TAVI has not yet been incorporated into the Brazilian health policies by the Public Health System (SUS), or by the National Supplementary Health Agency (ANS), because there is a shortage of scientific evidence based on an economic analysis of the procedure that reports the results and the long-term costs compared to conventional surgery. Objective: To identify the average direct cost of the transcatheter aortic valve implantation, to verify if there is significant change of cost in the different access routes used, and to identify predictive factors that could increase the cost of the procedure. Method: This is a study with quantitative, exploratory, descriptive, transversal, retrospective, and documentary approaches, carried out in a hospital of the State Department of Health of São Paulo (SES-SP), of the Direct Administration, specialized in the treatment of high-complexity cardiovascular diseases. The study population corresponded to TAVI elective procedures, from the inauguration of the hybrid room, in March 2012, up to August 2015, totaling 108 procedures, of which 92 were transfemoral, 8 were transapical, and 8 were transaortic. Results: The average direct cost of the TAVI procedures in the three routes totaled R$ 82,230.94. Transfemorally, this average cost was R$ 82,826.38; through the transaortic route, R$ 79,440.91; and through the transapical route, R$ 78,173.41. The total material and medication / solution represented 91.89% of the total average direct cost of the TAVI procedure through the transfemoral route; 91.81% through the transapical route; and 90.69% through the transaortic route, and the fixed cost with the transcatheter valve, in the amount of R$ 65,000.00, represented 78.47% of the total cost of the TAVI procedure through the transfemoral route; 83.14%, through the transapical route; and 81.82% through the transaortic route. The Kruskal-Wallis Test Continuous Variables Test showed a statistically significant difference among the access routes. In the total cost of the TAVI procedure, the Bonferroni Test showed a difference in the association between the transfemoral and transapical routes. However, in the association with the transaortic route, there was no statistically significant difference. Predictive factors that increased the cost of the TAVI procedure were: access routes, length of procedure, hemodynamic material, drug / solution, consumption material, infusion material, total material and medicine/solution, human resources, medical gas, depreciation and energy. The second valve was the only variable related to the complications in the or that increased the cost of the procedure. The mean age of patients with TAVI was 81.50 ± 6.96 years. Conclusion: TAVI is an advance to be discussed and monitored, and there is a need to encourage new studies that evaluate the benefits of treatment based on the results and costs, in order to assist in the decision making for the incorporation of this treatment into its population, improving the quality of life of patients and providing once again their integration into daily activities.