Objetivo: O principal propósito do estudo foi pesquisar a disfunção ventricular esquerda subclínica em pacientes com lúpus eritematoso sistêmico juvenil (LESJ) através da técnica de speckle-tracking bidimensional. Foi investigada ainda uma possível correlação entre o comprometimento da deformação miocárdica e o SLEDAI-2K (Systemic Lupus Erithematosus Disease Activity Index 2000), bem como a presença de fatores de risco cardiovascular, tanto tradicionais como ligados à doença. Métodos: 50 pacientes assintomáticos do ponto de vista cardiovascular e 50 controles saudáveis (14,74 vs. 14,82 anos, p=0.83) foram avaliados pelo ecocardiograma convencional e pelo speckle-tracking bidimensional. Resultados: Apesar da fração de ejeção normal, os pacientes apresentaram redução de todos os parâmetros de deformação miocárdica longitudinal e radial, quando comparados aos controles: strain de pico sistólico longitudinal [-20,3 (-11 a -26) vs. -22 (-17,8 a -30.4) %, p < 0,0001], strain rate de pico sistólico longitudinal [-1,19 ± 0,21 vs. -1,3 ± 0,25 s-1, p=0,0005], strain rate longitudinal na diástole precoce [1,7 (0,99 a 2,95) vs. 2 (1,08 a 3,00) s-1 , p=0,0034], strain de pico sistólico radial [33,09 ± 8,6 vs. 44,36 ± 8,72%, p < 0,0001], strain rate de pico sistólico radial [1,98 ± 0,53 vs. 2,49 ± 0,68 s-1, p < 0,0001] e strain rate radial na diástole precoce [-2,31 ± 0,88 vs. -2,75 ± 0,97 s-1, p=0,02]. O strain de pico sistólico circunferencial [-23,67 ± 3,46 vs. - 24,6 ± 2,86%, p=0,43] e o strain rate circunferencial na diástole precoce [2 (0,88 a 3,4) vs. 1,99 (1,19 a 3,7) s-1, p=0,88] foram semelhantes em pacientes e controles. Apenas o strain rate de pico sistólico circunferencial [-1,5 ± 0,3 vs. -1,6 ± 0,3 s-1, p=0,036] mostrou-se reduzido no LESJ. Uma correlação negativa foi identificada entre o strain de pico sistólico longitudinal e o SLEDAI-2K (r = - 0,52; p < 0,0001) e também o número de fatores de risco cardiovascular por paciente (r = -0,32, p=0,024). Conclusões: Foi evidenciada disfunção sistólica e diastólica subclínica de ventrículo esquerdo no LESJ através da técnica de speckle-tracking bidimensional. A atividade da doença e a exposição aos fatores de risco cardiovascular provavelmente contribuíram para o comprometimento da deformação miocárdica nesses pacientes / Objectives: The main purpose of the study was to investigate left ventricular (LV) subclinical systolic and diastolic dysfunction in childhood-onset systemic lupus erythematosus (c-SLE) patients using two-dimensional speckletracking (2DST) echocardiography. We also interrogated possible correlations between impairment of myocardial deformation and the SLE Disease Activity Index 2000 (SLEDAI-2K), as well as the presence of traditional and disease-related cardiovascular risk factors (CRFs). Method: A total of 50 asymptomatic patients and 50 controls (age 14.74 vs. 14.82 years, p = 0.83) were evaluated by standard and 2DST echocardiography. Results: Despite a normal ejection fraction (EF), there was reduction in all parameters of LV longitudinal and radial deformation in patients compared to controls: peak longitudinal systolic strain [-20.3 (-11 to -26) vs. -22 (-17.8 to -30.4)%, p < 0.0001], peak longitudinal systolic strain rate [-1.19 ± 0.21 vs. -1.3 ± 0.25 s-1, p = 0.0005], longitudinal strain rate in early diastole [1.7 (0.99-2.95) vs. 2 (1.08-3.00) s-1, p = 0.0034], peak radial systolic strain [33.09 ± 8.6 vs. 44.36 ± 8.72%, p < 0.0001], peak radial systolic strain rate [1.98 ± 0.53 vs. 2.49 ± 0.68 s-1, p < 0.0001], and radial strain rate in early diastole [-2.31 ± 0.88 vs. -2.75 ± 0.97 s-1, p = 0.02]. Peak circumferential systolic strain [- 23.67 ± 3.46 vs. -24.6 ± 2.86%, p=0.43] and circumferential strain in early diastole [2 (0,88 a 3,4) vs. 1,99 (1,19 a 3,7) s-1, p=0.88 ] were similar between patients and controls, although peak circumferential systolic strain rate [-1.5 ± 0.3 vs. -1.6 ± 0.3 s-1, p = 0.036] was reduced in c-SLE. Further analysis of patients revealed a negative correlation between LV peak longitudinal systolic strain and SLEDAI-2K(r= -0.52, p < 0.0001) and also between LV PLSS and the number of CRFs per patient (r = -0.32, p = 0.024). Conclusions: 2DST echocardiography has identified subclinical LV deformation impairment in c-SLE patients. Disease activity and cumulative exposure to CRFs contribute to myocardial compromise

University of Macau / Faculty of Science and Technology / Department of Electrical and Electronics Engineering

Recentment ha estat demostrada l’existència de cèl.lules progenitores en el greix que envolta el cor. Aquesta nova font cel!lular ha esdevingut una bona alternativa per a regenerar el miocardi infartat. Per aquest motiu, és possible que posant en contacte el teixit adipós cardíac en forma de biomembrana amb la zona infartada es pugui limitar l’extensió de l’infart de miocardi. Els objectius de la present tesi són: 1) Generar els perfils genètics de l’evolució de l’IM en el model porcí. 2) Determinar l’existència de cèl.lules mesenquimals al teixit adipós d’origen pericardíac i caracteritzar-les. 3) Avaluar l’efecte de la transposició d’un pedicle adipós pericardíac vascularitzat sobre: a. l’IAM en el model porcí per a valorar els possibles efectes beneficiosos sobre la mida de l’infart i la funció ventricular. b. l’ICM en el model porcí per a valorar els possibles efectes beneficiosos sobre la mida de l’infart i la funció ventricular.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Global and regional mechanics of the cardiac ventricles were investigated using an anatomicallyaccurate computational model formulated from concise mathematical descriptions ofthe left and right ventricular wall geometries and the non-homogeneous laminar microstructureof cardiac muscle. The finite element method for finite deformation elasticity was developedfor the analysis and included specialised coordinate systems, interpolation schemesand parallel processing techniques for greater computational efficiency.The ventricular mechanics model incorporated the fully orthotropic pole-zero constitutivelaw, based on the three-dimensional architecture of myocardium, to account for the nonlinearmaterial response of resting cardiac muscle, relative to the three anatomically relevant axes.A fibre distribution model was introduced to reconcile some of the pole-zero constitutiveparameters with direct mechanical properties of the tissue (such as the limiting strainsestimated from detailed physiological observations of the collagen helices that surroundmyofibres), whilst other parameters were estimated from in-vitro biaxial tension tests onthin sections of myocardium. A non-invasive approach to in-vivo myocardial materialparameter estimation was also developed, based on a magnetic resonance imaging techniqueto effectively tag ventricular wall tissue.The spatially non-homogeneous distribution of myocardial residual strain was accounted forin the ventricular mechanics model using a specialised growth tensor. A simple model of fluidshift was formulated to account for the changes in local tissue volume due to movement ofintramyocardial blood. Contractile properties of ventricular myofibres were approximatedusing a quasi-static relationship between the fibre extension ratio, intracellular calciumconcentration and active fibre stress, and the framework has been developed to include amore realistic model of active myocardial mechanics, which could be coupled to a realisticdescription of the time-varying spread of electrical excitation throughout the ventricularwalls. Simple volumetric cavity models were incorporated to investigate the effects of arterialimpedance on systolic wall mechanics.Ventricular mechanics model predictions of the cavity pressure versus volume relationships,longitudinal dimension changes, torsional wall deformations and regional distributions ofmyocardial strain during the diastolic filling, isovolumic contraction and ejection phasesof the cardiac cycle showed good overall agreement with reported observations derivedfrom experimental studies of isolated and in-vivo canine hearts. Predictions of the spatialdistributions of mechanical stress at end-diastole and end-systole are illustrated.

Coordenação de Aperfeiçoamento de Pessoal de Nível Superior - CAPES / Dexamethasone is a drug belonging to the class of corticosteroids, mostly used as an anti-inflammatory. In excess or in indiscriminate chronic use can lead to endocrine and / or cardiovascular complications. Physical exercise can act in the treatment of these diseases by acting as an attenuator or in some cases, reversing some of these complications, allied to traditional drug treatment. Thus, the purpose of this dissertation was: to evaluate the effect of a resistance exercise program on the heart and ventricles in animals submitted to dexamethasone treatment for four weeks. It was detected that aerobic or resistance training is capable of promoting improvements in patients in chronic use of glucocorticoids as a decrease in hyperglycemia, hypertension and improvements in cardiovascular indexes. For the experiments, forty male Wistar rats were selected and divided into four groups. The absolute heart and absolute and dry weight of the left and right ventricles were evaluated. It was verified that the strength exercise associated with dexamethasone (0.2 mg.kg-1.dia-1) did not significantly alter the absolute heart weight and absolute and dry weight of the right ventricle. There was a significant difference in the dry weight of the left ventricle that when normalized by the tibia length ceased to exist. This results suggest that exercise may be effective with some effects arising from the use of glucocorticoids and that four weeks of exercise associated with dexamethasone are not able to change the absolute and dry weight of the heart and ventricles. / A dexametasona é um fármaco pertencente à classe dos corticosteroides, majoritariamente utilizado como anti-inflamatório. Em excesso ou em uso crônico indiscriminado pode levar a complicações endócrinas e/ou cardiovasculares. O exercício físico pode atuar no tratamento dessas enfermidades atuando como um atenuador ou em alguns casos, reverter algumas dessas complicações, aliado sempre ao tratamento medicamentoso tradicional. Desta forma, o objetivo desta dissertação foi: avaliar o efeito de um programa de exercícios resistidos no coração e ventrículos em animais submetidos ao tratamento com dexametasona por quatro semanas. Foi detectado que o exercício físico aeróbio ou resistido é capaz de promover melhorias em pacientes em uso crônico de glicocorticoides como diminuição da hiperglicemia, hipertensão e melhorias nos índices cardiovasculares. Para os experimentos, quarenta ratos Wistar machos foram selecionados e divididos em quatro grupos. Foram avaliados o peso absoluto do coração e peso absoluto e seco dos ventrículos esquerdo e direito. Foi verificado que o exercício de força associado ao dexametasona (0,2 mg.kg-1.dia-1) não alterou significativamente o peso absoluto do coração e peso absoluto e seco do ventrículo direito. Houve uma diferença significativa no peso seco do ventrículo esquerdo que ao normalizar pelo comprimento da tíbia deixou de existir. Os resultados sugerem que o exercício pode ser eficaz com alguns acometimentos decorrentes do uso de glicocorticoides e que quatro semanas de exercício associado a dexametasona não são capazes de alterar o peso absoluto e seco do coração e ventrículos.

INTRODUÇÃO: O acesso cirúrgico ao corno temporal do ventrículo lateral (CTVL) é realizado para tratamento de lesões temporais mediais, dentre as quais se destaca a esclerose hipocampal que leva à epilepsia, e pode ser realizado através das superfícies lateral ou inferior do lobo temporal ou pelo sulco lateral do cérebro (fissura silviana). O parênquima cerebral subcortical localizado entre o sulco limitante inferior da ínsula (SLI) e o CTVL é composto por importantes feixes de fibras brancas, os quais podem eventualmente ser lesionados nos acessos cirúrgicos trans-silvianos. OBJETIVO: Descrever a localização dos principais feixes de fibras brancas na região entre o SLI e o CTVL. MÉTODOS: Os principais feixes de fibras brancas subcorticais foram examinados em 14 hemisférios cerebrais cadavéricos adultos utilizando a técnica de dissecção de Klingler, sendo possível descrever suas posições em relação à extremidade anterior do SLI (nomeado de Ponto Temporal do Límen - PTL). RESULTADOS: Os principais feixes de fibras identificados profundamente ao SLI formam um arranjo multilaminar e podem ser divididos de acordo com a profundidade em que são encontrados. As fibras de associação curta da cápsula extrema, que continuam em direção aos opérculos, formam a camada subcortical mais superficial e foram encontradas sob todo o SLI. As fibras da cápsula externa são encontradas mais profundamente, em uma camada formada por três principais feixes em uma disposição anteroposterior sequencial: o fascículo uncinado (encontrado desde o PTL até 10,0 ± 2.2 mm posteriormente), o fascículo fronto-occipital inferior (encontrado entre 10,0 ± 2,2 mm e 35,5 ± 2,7 mm posterior ao PTL) e fibras claustro-corticais (encontradas desde 35,5 ± 2,7 mm posterior ao PTL até o final desse sulco). A extensão lateral da comissura anterior está logo abaixo dessa camada e suas fibras foram encontradas entre 8,4 ± 1,8 mm e 22,0 ± 6,8 mm posterior ao PTL. A camada mais profunda é formada pelas fibras da cápsula interna/corona radiata, onde se destacam as radiações ópticas cujas fibras foram encontradas entre 10,6 ± 3,4 mm e 34,5 ± 3,5 mm posterior ao PTL. CONCLUSÕES: O fascículo uncinado é aproximadamente encontrado sob o terço anterior do segmento anterior do SLI (entre o PTL e o corpo geniculado lateral), enquanto o fascículo fronto-occipital inferior e as fibras da radiação óptica são encontrados sob os dois terços posteriores deste segmento. Os resultados sugerem que na abordagem trans-silviana transinsular, uma incisão através do SLI, começando no PTL e se estendendo até 6 mm posteriormente, irá atravessar o fascículo uncinado, mas não o fascículo fronto-occipital inferior e as radiações ópticas / INTRODUCTION: The surgical approach to the temporal horn of the lateral ventricle (CTVL) is performed for treatment of medial temporal lesions, among which hippocampal sclerosis leading to epilepsy is emphasized, and can be performed through the lateral or inferior surfaces of the temporal lobe or through the sylvian fissure. The subcortical cerebral parenchyma located between the inferior limiting sulcus of the insula (SLI) and the CTVL is composed of important white matter fiber bundles, which may eventually be injured in transsylvian surgical approaches. OBJECTIVES: To describe the location of the main white matter fiber bundles in the region between SLI and CTVL. METHODS: The main subcortical white matter fiber bundles were examined in 14 adult cadaveric cerebral hemispheres using the Klingler dissection technique, and it was possible to describe their positions in relation to the anterior end of the SLI (named Temporal Limen Point - PTL). RESULTS: The main white matter fiber bundles identified deeply to the SLI form a multi-laminar arrangement that can be understood according to the depth in which they are found. The short association fibers of the extreme capsule, which continue toward the opercula, form the most superficial subcortical layer and were found underneath all the SLI. The external capsule fibers were found more deeply, in a layer formed by three main fiber bundles organized in a sequential anterior-posterior disposition: the uncinate fascicle (found from the PTL to 10.0 ± 2.2 mm posteriorly), the inferior fronto-occipital fascicle (found between 10.0 ± 2.2 mm and 35.5 ± 2.7 mm posterior to the PTL) and claustrocortical fibers (found from 35.5 ± 2.7 mm posterior to PTL to the end of this sulcus). The lateral extension of the anterior commissure was below this layer and its fibers were found between 8.4 ± 1.8 mm and 22.0 ± 6.8 mm posterior to the PTL. The deepest layer is formed by the fibers of the internal capsule/corona radiata, where the optical radiation fibers were distinguished and found between 10.6 ± 3.4 mm and 34.5 ± 3.5 mm posterior to the PTL. CONCLUSIONS: The uncinate fascicle is approximately found under the anterior third of the anterior SLI segment (between the PTL and the lateral geniculate body), while the inferior fronto-occipital fascicle and fibers of the optical radiation are found under the posterior two thirds of this segment. The results suggest that at the transsylvian-transinsular approach, an incision at the SLI, from the PTL to 6 mm posteriorly, will cross the uncinate fascicle, but not the inferior fronto-occipital fascicle and optical radiation fibers