Cardiac remodeling after acute myocardial infarction (MI) is an important process that leads to progressive ventricular enlargement and heart failure. Several variables have been identified to predict an increase in left ventricular (LV) volume and a decrease of LV ejection fraction (LVEF) after an acute MI including infarct size, anterior location, cardiac enzyme level, transmurality of the infarct, patency of the infarct-related artery, end systolic volume (ESV) and mitral deceleration time, etc. / Regional disturbances of LV wall motion have long been recognized to occur in patients with cardiac diseases, such as hypertrophic cardiomyopathy, unstable angina, acute ischemia, and MI. Tissue Doppler imaging (TDI) is recently established for detecting regional contractile abnormalities and asynchrony, and can predict reverse remodeling and improved synchronicity after biventricular pacing therapy in heart failure patients. However, it is unclear whether LV asynchrony plays an important role in the evolutionary changes of LV remodeling after an acute infarction and whether it can predict the changes independently. / The identification of transmural extent of myocardial necrosis and degree of non-viability after acute MI is clinically important. TDI-derived strain rate imaging (SRI) quantifies local rate of myocardial deformation and has the potential to differentiate viable from infarcted myocardium. / Therefore, in this study we aimed to investigate: (1) Whether SRI may differentiate transmural from non-transmural MI as assessed by ce-MRI in routine patients post acute infarction, and establish practical cutoff values for identifying transmural scar tissue from non-transmural or subendocardial infarction with viable myocardium. (2) Whether LV systolic and diastolic asynchrony measured by TDI occurs early after acute MI even in the absence of widening of QRS complexes, and determine if this is explained by the site and extent of the infarction measured by ce-MRI. (3) The relationships between serial measurements of infarct size on ce-MRI and LV remodeling process after an acute infarction, and determine whether early assessment of infarct size predicts progressive ventricular enlargement and cardiac dysfunction, and whether it differs with infarct location. (4) The relationships between LV asynchrony, infarct size and LV remodeling, and determine whether early assessment of LV asynchrony by TDI compared with standard clinical correlates of LV remodeling and infarct size predicts progressive ventricular enlargement and cardiac dysfunction. (Abstract shortened by UMI.) / Zhang Yan. / "April 2005." / Adviser: John E. Sanderson. / Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0175. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 161-192). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.

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.