In order to identify patients with severe coronary artery disease (CAD) and at a higher risk of future cardiac events after uncomplicated myocardial infarction, 105 consecutive patients were studied prospectively. There were 93 men and 12 women with a mean age of 56 +/- 8.2 years. Treadmill testing, exercise radionuclide ventriculography, thallium-201 myocardial imaging and selective coronary arteriography were performed 6-8 weeks after infarction. Patients were grouped into those who had single and multiple vessel disease. Multiple regression analysis of 18 noninvasive indices was carried out using generalized linear interactive modelling (GLIM) and the results were compared with the severity of underlying CAD and the clinical outcome after a mean follow-up period of 18.8 +/- 3. 4 months. At the end of the follow-up period, patients were categorized into those who had no cardiac events, minor and major cardiac events. Multivariate analysis produced an algorithm from three factors found to be most predictive of the severity of CAD. These included ST-segment depression on exercise, total score of rest and exercise regional wall motion and the presence of significant redistribution on thallium-201 imaging. The sensitivity of this algorithm for predicting multiple vessel disease was 42%, with a specificity of 94%, and a predictive accuracy of 69%. However, the total score of regional wall motion abnormalities was the single most predictive factor of major cardiac events with a sensitivity of 94%, a specificity of 57%, and predictive accuracy of 63%. None of the other factors produced additional prognostic information. Therefore, exercise radionuclide ventriculography appears to be the investigation of choice in assessing prognosis after myocardial infarction.

by Frankie Kar-Ming Wong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1997. / Includes bibliographical references (leaves 101-107). / Acknowledgements --- p.IV / Abstract --- p.V / Abbreviations --- p.VI / Chapter Chapter 1 --- Introduction to Lipoprotein and Apolipoprotein --- p.1 / Chapter 1.1 --- Lipoprotein structure and classification --- p.1 / Chapter 1.2 --- Apolipoprotein A-I and B100 --- p.1 / Chapter 1.2.1 --- Apolipoprotein A-I (apoA-I) --- p.1 / Chapter 1.2.2 --- Apolipoprotein B100 (apoB100) --- p.3 / Chapter 1.2.3 --- Biological functions of apolipoprotein --- p.4 / Chapter 1.3 --- Evidence linking apoA-I and B100 with atherosclerosis --- p.4 / Chapter 1.4 --- The roles of apoA-I and B100 in the development of atherosclerosis --- p.6 / Chapter 1.5 --- Measurement of human serum lipoproteins as an assessment of risk for coronary heart disease (CHD) --- p.8 / Chapter 1.6 --- Aims of this study --- p.10 / Chapter Chapter 2 --- Purification of ApoA-I and B100 and Production of Polyclonal Antibodies --- p.12 / Chapter 2.1 --- Introduction --- p.12 / Chapter 2.1.1 --- Purification of apoA-I and B100 from human serum --- p.12 / Chapter 2.1.2 --- Immunization for polyclonal antibodies production against apoA-I and B100 --- p.14 / Chapter 2.1.3 --- Antibody purification --- p.15 / Chapter 2.1.3.1 --- Ammonium sulfate precipitation --- p.17 / Chapter 2.1.3.2 --- DEAE and QEAE Sepharose --- p.17 / Chapter 2.1.3.3 --- Protein A and Protein G --- p.17 / Chapter 2.1.3.4 --- Affinity chromatography --- p.18 / Chapter 2.2 --- Methods --- p.20 / Chapter 2.2.1 --- Purification of HDL and LDL --- p.20 / Chapter 2.2.2 --- Purification of apolipoproteins --- p.22 / Chapter 2.2.3 --- Immunization of rabbit with apoA-I and B100 --- p.23 / Chapter 2.2.4 --- Enzyme-linked immunosorbent assay (ELISA) --- p.24 / Chapter 2.2.5 --- Purification of lipoprotein specific immunoglobulin from antisera --- p.25 / Chapter 2.2.5.1 --- Salt fractionation --- p.25 / Chapter 2.2.5.2 --- Purification of immunoglobulin by Protein A affinity chromatography --- p.25 / Chapter 2.2.5.3 --- Isolation of specific antibody by lipoprotein-coupled affinity chromatography --- p.26 / Chapter 2.3 --- Results --- p.27 / Chapter 2.3.1 --- Purification of apoA-I and B100 --- p.27 / Chapter 2.3.2 --- Purification of immunoglobulins from rabbit anti-apolipoprotein sera --- p.32 / Chapter 2.4 --- Discussion --- p.38 / Chapter Chapter 3 --- Production of monoclonal antibodies against apoA-I and B100 --- p.48 / Chapter 3.1 --- Introduction --- p.48 / Chapter 3.1.1 --- What is monoclonal antibody? --- p.48 / Chapter 3.1.2 --- The basic methodology --- p.49 / Chapter 3.1.2.1 --- Immunization of host --- p.49 / Chapter 3.1.2.2 --- Cell lines required for fusion --- p.49 / Chapter 3.1.2.3 --- Fusion --- p.51 / Chapter 3.1.2.4 --- Selection of hybrids --- p.52 / Chapter 3.1.2.5 --- Screening assay --- p.54 / Chapter 3.1.2.6 --- Cloning --- p.54 / Chapter 3.1.2.7 --- Bulk production of monoclonal antibody --- p.55 / Chapter 3.1.2.8 --- Monoclonal antibody purification --- p.55 / Chapter 3.2 --- Methods --- p.55 / Chapter 3.2.1 --- Immunization of mice with apoA-I and apoB100 --- p.55 / Chapter 3.2.2 --- Preparation before fusion --- p.58 / Chapter 3.2.2.1 --- Preparation of tissue culture working solutions --- p.58 / Chapter 3.2.2.2 --- Preparation of spleen cells --- p.59 / Chapter 3.2.2.3 --- Preparation of myeloma cells --- p.60 / Chapter 3.2.3 --- Fusion --- p.60 / Chapter 3.2.4 --- Screening assay for positive clones --- p.61 / Chapter 3.2.5 --- Limiting dilution cloning --- p.61 / Chapter 3.2.6 --- Determination of isotype --- p.62 / Chapter 3.2.7 --- Cryopreservation of myeloma and established hybridoma cell lines --- p.62 / Chapter 3.2.7.1 --- Freezing cells --- p.62 / Chapter 3.2.7.2 --- Thawing cells --- p.63 / Chapter 3.2.8 --- Bulk production of monoclonal antibodies from ascites --- p.63 / Chapter 3.2.9 --- Purification of monoclonal antibodies from ascites --- p.63 / Chapter 3.2.10 --- Western blot analyses of the monoclonal antibodies --- p.64 / Chapter 3.2.11 --- Iodination of apolipoproteins --- p.64 / Chapter 3.2.12 --- Binding of the monoclonal antibody to iodinated apolipoprotein --- p.65 / Chapter 3.2.13 --- Competitive displacement analyses --- p.65 / Chapter 3.3 --- Results --- p.66 / Chapter 3.3.1 --- Development of monoclonal antibodies --- p.66 / Chapter 3.3.2 --- Purification of monoclonal antibody from ascites --- p.69 / Chapter 3.3.3 --- Western blotting analyses of AB6 and BE8 --- p.69 / Chapter 3.3.4 --- Monoclonal antibody titration curve for apolipoproteins by radioimmunoassays --- p.75 / Chapter 3.3.5 --- Competitive displacement analysis of AB6 and BE8 --- p.75 / Chapter 3.4 --- Discussion --- p.79 / Chapter Chapter 4 --- Enzyme-linked immunosorbent assay (ELISA) for ApoA-I --- p.84 / Chapter 4.1 --- Introduction --- p.84 / Chapter 4.1.1 --- Alkaline phosphatase (ALP) --- p.84 / Chapter 4.1.2 --- Conjugation methods --- p.85 / Chapter 4.1.3 --- Design of the immunoassay format --- p.87 / Chapter 4.1.4 --- Modified solid-phase: Protein A antibody-capture ELISA (PACE) --- p.87 / Chapter 4.2 --- Materials and Methods --- p.90 / Chapter 4.2.1 --- Conjugation of AB6 with maleimide activated alkaline phosphatase --- p.90 / Chapter 4.2.2 --- Titration curve of AB6-ALP conjugate --- p.90 / Chapter 4.2.3 --- Calibration curve of apoA-I sandwich ELISA --- p.91 / Chapter 4.2.4 --- Measurement of apoA-I by Protein A antibody-capture ELISA --- p.91 / Chapter 4.3 --- Results --- p.92 / Chapter 4.3.1 --- Characterization of AB6-ALP conjugate --- p.92 / Chapter 4.3.2 --- Calibration curve for the measurement of apoA-I --- p.92 / Chapter 4.4 --- Discussion --- p.95 / Chapter Chapter 5 --- General Conclusions --- p.99 / References --- p.101

A doença arterial coronária (DAC) avançada caracteriza-se pela presença de vasos calcificados e difusamente estenosados, o que reduz a acurácia da angiografia coronária não-invasiva por meio dos atuais aparelhos de tomografia computadorizada (CT) com 16 colunas de detectores (16-MDCTA). O principal objetivo deste estudo foi tentar demonstrar uma acurácia diagnóstica global de pelo menos 90% para a detecção de estenoses coronárias >= 50% em pacientes com DAC avançada e alta probabilidade de possuírem escores de cálcio coronário elevados, mediante a utilização de um sistema de CT com 32 colunas de detectores, todas capazes de adquirir simultaneamente cortes com 0,5 mm de espessura (32x0,5-MDCTA). Angiografias coronárias sincronizadas ao traçado de ECG foram obtidas por meio da 32x0,5-MDCTA (32 cortes de 0,5 mm, voxels isotrópicos de 0,35x0,35x0,35 mm³, rotação do gantry a 400 ms) em 30 pacientes consecutivos (25 do sexo masculino, com idade média igual a 59±13 anos e índice de massa corpórea médio de 26,2±4,9 Kg/m²) e portadores de DAC avançada. As principais artérias nativas, incluindo seus ramos de primeira ordem com diâmetro >= 1,5 mm bem como os enxertos coronários existentes, foram avaliados de forma independente quanto à presença de estenoses >= 50%. Os stents foram excluídos. As angiografias coronarianas convencionais (realizadas em média 18±12 dias antes das respectivas 32x0,5-MDCTAs) foram analisadas de maneira quantitativa (angiografia coronária quantitativa). A mediana do escore de cálcio de Agatston foi igual a 510 (variação entre 3 e 5066). A sensibilidade, a especificidade e os valores preditivos positivo e negativo para a detecção de estenoses >= 50% nas artérias coronárias nativas foram seguintes: 76% (29/38), 94% (190/202), 71% (29/41), e 96% (190/199), respectivamente. A acurácia diagnóstica global foi de 91% (219/240). Do total de vasos analisados, 20% (69/352) foram excluídos devido à existência de um dos seguintes artefatos: movimento, ruído e baixo realce do contraste radiológico isoladamente ou em conjunto (45/69 ou 65%), distorção da imagem secundária à presença de eletrodo de desfibrilador ou marcapasso (18/69 ou26%), e calcificação arterial excessiva (6/69 ou 9%). Conclui-se que a 32x0,5-MDCTA exclui com precisão as estenoses coronarianas >= 50% em pacientes com DAC avançada e escore de cálcio coronário elevado, com acurácia diagnóstica global de 91% / Advanced coronary artery disease (CAD) is characterized by calcified and diffusely stenotic vessels, hampering accuracy of noninvasive coronary angiography with current 16-detector computed tomography (CT) scanners. The main purpose of this study was to try to demonstrate an overall diagnostic accuracy of at least 90% for detection of coronary stenoses >= 50% by half-millimeter 32-detector CT angiography (32x0.5-MDCTA) in patients with advanced CAD and a high likelihood of having elevated coronary calcium scores. ECG-gated coronary 32x0.5-MDCTA (32x0.5 mm cross-sections, 0.35x0.35x0.35 mm³ isotropic voxels, 400 ms gantry rotation) was performed in 30 consecutive patients (25 male, 59±13 years-old, 26.2±4.9 Kg/m²) with advanced CAD. Major coronary arteries, including >=1.5-mm first order branches, and bypass grafts were independently evaluated for >= 50% stenoses. Stents were excluded. Conventional coronary angiography (performed on average 18±12 days before their corresponding 32x0.5-MDCTAs) was analyzed by quantitative coronary angiography. Median Agatston calcium score was 510 (3-5066 range). Sensitivity, specificity, positive and negative predictive values for detection of >= 50% stenoses in the native coronary arteries were: 76% (29/38), 94% (190/202), 71% (29/41), and 96% (190/199), respectively. Overall diagnostic accuracy was 91% (219/240). Twenty percent (69/352) of the vessels were excluded from the analysis due to one of the following artifacts: motion, noise, and low contrast enhancement isolated or in combination (45/69 or 65%), image distortion secondary to an ICD or pacemaker lead (18/69 or 26%), and severe arterial calcification (6/69 or 9%). We concluded that 32x0.5-MDCTA accurately excludes >= 50% coronary stenoses in patients with advanced CAD and high calcium scores, showing an overall diagnostic accuracy of 91%

Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 5 uppsatser.

A doença arterial coronária (DAC) avançada caracteriza-se pela presença de vasos calcificados e difusamente estenosados, o que reduz a acurácia da angiografia coronária não-invasiva por meio dos atuais aparelhos de tomografia computadorizada (CT) com 16 colunas de detectores (16-MDCTA). O principal objetivo deste estudo foi tentar demonstrar uma acurácia diagnóstica global de pelo menos 90% para a detecção de estenoses coronárias >= 50% em pacientes com DAC avançada e alta probabilidade de possuírem escores de cálcio coronário elevados, mediante a utilização de um sistema de CT com 32 colunas de detectores, todas capazes de adquirir simultaneamente cortes com 0,5 mm de espessura (32x0,5-MDCTA). Angiografias coronárias sincronizadas ao traçado de ECG foram obtidas por meio da 32x0,5-MDCTA (32 cortes de 0,5 mm, voxels isotrópicos de 0,35x0,35x0,35 mm³, rotação do gantry a 400 ms) em 30 pacientes consecutivos (25 do sexo masculino, com idade média igual a 59±13 anos e índice de massa corpórea médio de 26,2±4,9 Kg/m²) e portadores de DAC avançada. As principais artérias nativas, incluindo seus ramos de primeira ordem com diâmetro >= 1,5 mm bem como os enxertos coronários existentes, foram avaliados de forma independente quanto à presença de estenoses >= 50%. Os stents foram excluídos. As angiografias coronarianas convencionais (realizadas em média 18±12 dias antes das respectivas 32x0,5-MDCTAs) foram analisadas de maneira quantitativa (angiografia coronária quantitativa). A mediana do escore de cálcio de Agatston foi igual a 510 (variação entre 3 e 5066). A sensibilidade, a especificidade e os valores preditivos positivo e negativo para a detecção de estenoses >= 50% nas artérias coronárias nativas foram seguintes: 76% (29/38), 94% (190/202), 71% (29/41), e 96% (190/199), respectivamente. A acurácia diagnóstica global foi de 91% (219/240). Do total de vasos analisados, 20% (69/352) foram excluídos devido à existência de um dos seguintes artefatos: movimento, ruído e baixo realce do contraste radiológico isoladamente ou em conjunto (45/69 ou 65%), distorção da imagem secundária à presença de eletrodo de desfibrilador ou marcapasso (18/69 ou26%), e calcificação arterial excessiva (6/69 ou 9%). Conclui-se que a 32x0,5-MDCTA exclui com precisão as estenoses coronarianas >= 50% em pacientes com DAC avançada e escore de cálcio coronário elevado, com acurácia diagnóstica global de 91% / Advanced coronary artery disease (CAD) is characterized by calcified and diffusely stenotic vessels, hampering accuracy of noninvasive coronary angiography with current 16-detector computed tomography (CT) scanners. The main purpose of this study was to try to demonstrate an overall diagnostic accuracy of at least 90% for detection of coronary stenoses >= 50% by half-millimeter 32-detector CT angiography (32x0.5-MDCTA) in patients with advanced CAD and a high likelihood of having elevated coronary calcium scores. ECG-gated coronary 32x0.5-MDCTA (32x0.5 mm cross-sections, 0.35x0.35x0.35 mm³ isotropic voxels, 400 ms gantry rotation) was performed in 30 consecutive patients (25 male, 59±13 years-old, 26.2±4.9 Kg/m²) with advanced CAD. Major coronary arteries, including >=1.5-mm first order branches, and bypass grafts were independently evaluated for >= 50% stenoses. Stents were excluded. Conventional coronary angiography (performed on average 18±12 days before their corresponding 32x0.5-MDCTAs) was analyzed by quantitative coronary angiography. Median Agatston calcium score was 510 (3-5066 range). Sensitivity, specificity, positive and negative predictive values for detection of >= 50% stenoses in the native coronary arteries were: 76% (29/38), 94% (190/202), 71% (29/41), and 96% (190/199), respectively. Overall diagnostic accuracy was 91% (219/240). Twenty percent (69/352) of the vessels were excluded from the analysis due to one of the following artifacts: motion, noise, and low contrast enhancement isolated or in combination (45/69 or 65%), image distortion secondary to an ICD or pacemaker lead (18/69 or 26%), and severe arterial calcification (6/69 or 9%). We concluded that 32x0.5-MDCTA accurately excludes >= 50% coronary stenoses in patients with advanced CAD and high calcium scores, showing an overall diagnostic accuracy of 91%

A perda da permeabilidade seletiva de membrana celular causada pela isquemia leva ao acúmulo de sódio e edema miocárdico. Este fenômeno tem implicações importantes na estrutura e função do ventrículo esquerdo, nas primeiras horas após infarto do miocárdio. Objetivou-se investigar a hipótese de que, durante as primeiras horas após oclusão coronária prolongada e restabelecimento de fluxo completo, a taxa de acúmulo de sódio miocárdico é determinado pela integridade da microvasculatura. Utilizou-se imagem de ressonância magnética do sódio-23 em 3 dimensões, para monitorizar as alterações do conteúdo de sódio miocárdico no tempo, em um modelo canino in vivo e com tórax fechado (n = 19) de infarto do miocárdio e reperfusão. Seis animais apresentaram fibrilação ventricular durante a oclusão ou imediatamente após reperfusão coronária, não completando o protocolo. Em quatro experimentos não se detectou nenhuma área de infarto, por nenhum dos métodos utilizados. Um animal foi submetido a oclusão coronária permanente. Os oito animais restantes constituíram o grupo de infartos reperfundidos. Destes, infartos com obstrução microvascular (n = 4), detectados por microesfera radioativa e por imagem por ressonância magnética do hidrogênio realçada com contraste, mostraram uma taxa menor de acúmulo de sódio, assim como um menor fluxo sangüíneo 20 minutos e 6 horas após reperfusão. A ausência de obstrução microvascular nos infartos (n = 4) esteve associada a taxas maiores de acúmulo do sódio e maior restabelecimento do fluxo sangüíneo miocárdico. Além disso, o tamanho do infarto por imagem por ressonância magnética do sódio-23 apresentou boa correlação com o tamanho do infarto pela anatomopatologia (cloreto de trifeniltetrazólio ou TTC) e pela imagem de ressonância do hidrogênio realçada por contraste (hiperintensificação ou realce tardio) 9 horas após reperfusão. Conclui-se que, em infartos do miocárdio reperfundidos, o acúmulo de sódio é dependente da integridade microvascular e está diminuído em regiões de obstrução microvascular, comparado com regiões miocárdicas com microvasculatura patente. A imagem por ressonância do sódio-23 pode ser um instrumento útil para a monitorização in vivo do conteúdo do sódio no infarto agudo do miocárdio. / Loss of membrane permeability caused by ischemia leads to cellular sodium accumulation and myocardial edema. This phenomenon has important implications to left ventricular structure and function in the first hours after myocardial infarction. We hypothesized that during this period of time, after prolonged coronary occlusion and complete reflow, the rate of myocardial sodium accumulation is governed by microvascular integrity. We used 3-dimensional 23 Na magnetic resonance imaging to monitor myocardial sodium content changes over time in an in vivo closed-chest canine model (n = 19) of myocardial infarction and reperfusion. Six animals had ventricular fibrillation during occlusion or immediately after coronary reperfusion, and did not finish the protocol. Myocardial infarction was not detected in four experiments, by any of utilized methods. In one experiment, we produced permanent coronary occlusion. The remaining eight animals constituted the reperfused myocardial infarction group. From those, infarcts with microvascular obstruction n = 4) defined by both radioactive microsphere and contrast-enhanced 1 H magnetic resonance imaging showed a slower rate of sodium accumulation as well as lower blood flow at 20 minutes and 6 hours after reperfusion. Conversely, the absence of microvascular obstruction (n = 4) was associated with faster rates of sodium accumulation and greater blood flow restoration. In addition, infarct size by 23 Na magnetic resonance imaging correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced 1 H magnetic resonance imaging at 9 hours after reperfusion. We conclude that in reperfused myocardial infarction, sodium accumulation is dependent on microvascular integrity and is slower in regions of microvascular obstruction compared with those with patent microvasculature. Finally, 23 Na magnetic resonance imaging can be a useful tool for monitoring in vivo myocardial sodium content in acute myocardial infarction.

A perda da permeabilidade seletiva de membrana celular causada pela isquemia leva ao acúmulo de sódio e edema miocárdico. Este fenômeno tem implicações importantes na estrutura e função do ventrículo esquerdo, nas primeiras horas após infarto do miocárdio. Objetivou-se investigar a hipótese de que, durante as primeiras horas após oclusão coronária prolongada e restabelecimento de fluxo completo, a taxa de acúmulo de sódio miocárdico é determinado pela integridade da microvasculatura. Utilizou-se imagem de ressonância magnética do sódio-23 em 3 dimensões, para monitorizar as alterações do conteúdo de sódio miocárdico no tempo, em um modelo canino in vivo e com tórax fechado (n = 19) de infarto do miocárdio e reperfusão. Seis animais apresentaram fibrilação ventricular durante a oclusão ou imediatamente após reperfusão coronária, não completando o protocolo. Em quatro experimentos não se detectou nenhuma área de infarto, por nenhum dos métodos utilizados. Um animal foi submetido a oclusão coronária permanente. Os oito animais restantes constituíram o grupo de infartos reperfundidos. Destes, infartos com obstrução microvascular (n = 4), detectados por microesfera radioativa e por imagem por ressonância magnética do hidrogênio realçada com contraste, mostraram uma taxa menor de acúmulo de sódio, assim como um menor fluxo sangüíneo 20 minutos e 6 horas após reperfusão. A ausência de obstrução microvascular nos infartos (n = 4) esteve associada a taxas maiores de acúmulo do sódio e maior restabelecimento do fluxo sangüíneo miocárdico. Além disso, o tamanho do infarto por imagem por ressonância magnética do sódio-23 apresentou boa correlação com o tamanho do infarto pela anatomopatologia (cloreto de trifeniltetrazólio ou TTC) e pela imagem de ressonância do hidrogênio realçada por contraste (hiperintensificação ou realce tardio) 9 horas após reperfusão. Conclui-se que, em infartos do miocárdio reperfundidos, o acúmulo de sódio é dependente da integridade microvascular e está diminuído em regiões de obstrução microvascular, comparado com regiões miocárdicas com microvasculatura patente. A imagem por ressonância do sódio-23 pode ser um instrumento útil para a monitorização in vivo do conteúdo do sódio no infarto agudo do miocárdio. / Loss of membrane permeability caused by ischemia leads to cellular sodium accumulation and myocardial edema. This phenomenon has important implications to left ventricular structure and function in the first hours after myocardial infarction. We hypothesized that during this period of time, after prolonged coronary occlusion and complete reflow, the rate of myocardial sodium accumulation is governed by microvascular integrity. We used 3-dimensional 23 Na magnetic resonance imaging to monitor myocardial sodium content changes over time in an in vivo closed-chest canine model (n = 19) of myocardial infarction and reperfusion. Six animals had ventricular fibrillation during occlusion or immediately after coronary reperfusion, and did not finish the protocol. Myocardial infarction was not detected in four experiments, by any of utilized methods. In one experiment, we produced permanent coronary occlusion. The remaining eight animals constituted the reperfused myocardial infarction group. From those, infarcts with microvascular obstruction n = 4) defined by both radioactive microsphere and contrast-enhanced 1 H magnetic resonance imaging showed a slower rate of sodium accumulation as well as lower blood flow at 20 minutes and 6 hours after reperfusion. Conversely, the absence of microvascular obstruction (n = 4) was associated with faster rates of sodium accumulation and greater blood flow restoration. In addition, infarct size by 23 Na magnetic resonance imaging correlated best with infarct size by triphenyltetrazolium chloride and contrast-enhanced 1 H magnetic resonance imaging at 9 hours after reperfusion. We conclude that in reperfused myocardial infarction, sodium accumulation is dependent on microvascular integrity and is slower in regions of microvascular obstruction compared with those with patent microvasculature. Finally, 23 Na magnetic resonance imaging can be a useful tool for monitoring in vivo myocardial sodium content in acute myocardial infarction.