Introdução: A esquistossomose (Sch) é uma das doenças infecciosas crônicas mais prevalentes do mundo. Entretanto, dados a respeito de uma de suas complicações, a hipertensão arterial pulmonar (HAP), são escassos. O objetivo deste estudo é avaliar a história natural de pacientes com HAP-Sch comparados a pacientes com HAP idiopática (HAPI). Métodos: Análise retrospectiva dos prontuários de todos os pacientes consecutivamente diagnosticados como HAP-Sch e HAPI no Instituto do Coração, São Paulo, Brasil, entre 2004 e 2008. Nenhum dos pacientes com Sch-PAH recebeu tratamento específico para HAP enquanto todos os pacientes com HAPI receberam. Resultados: Pacientes com HAP-Sch (n=54) apresentavam hipertensão pulmonar menos grave ao diagnóstico, com menores níveis de resistência vascular pulmonar (11.3 ± 11.3 vs 16.7 ± 10.6 UI; p=0.002) e pressão média de artéria pulmonar (56.7 ± 18.7 vs. 64.6 ± 17.4 mmHg; p=0.01) e ainda maior débito cardíaco (4.62 ± 1.5 vs. 3.87 ± 1.5 L/min; p=0.009) quando comparados com os pacientes com HAPI (n=95). Nenhum dos pacientes HAP-Sch apresentou resposta positiva ao teste agudo com vasodilatador enquanto 16.2% dos pacientes com HAPI apresentaram (p=0.015). As taxas de sobrevida em 1, 2 e 3 anos foram 95.1%, 95.1%, 85.9% e 95%, 86% e 82%, para HAP-Sch e HAPI, respectivamente (p=0.49). Ambos os grupos tinham uma maior taxa de sobrevida quando comparadas àquela estimada pela equação do NIH para os pacientes com HAPI sem tratamento específico para HAP (71%, 61% e 52%, respectivamente). Conclusão: HAP-Sch tem um curso clínico mais benigno do que HAPI apesar da falta de vasorreatividade aguda na avaliação hemodinâmica inicial / Background: Schistossomiasis (Sch) is one of the most prevalent chronic infectious diseases in the world. Nevertheless data regarding one of its most severe clinical complications, pulmonary arterial hypertension (PAH), is scarce. The objective of this study was to evaluate the natural history of Sch-PAH patients as compared to idiopathic PAH (IPAH). Methods: We retrospectively analyzed case notes of all consecutive patients diagnosed of Sch-PAH and IPAH referred to the Heart Institute in São Paulo, Brazil, between 2004 and 2008. None of the Sch-PAH received PAH specific treatment whereas all IPAH patients did. Findings: Sch-PH patients (n=54) had less severe pulmonary hypertension as evidenced by lower levels of pulmonary vascular resistance (11.3 ± 11.3 vs 16.7 ± 10.6 IU; p=0.002) and mean pulmonary artery pressure (56.7 ± 18.7 vs. 64.6 ± 17.4 mmHg; p=0.01) and higher cardiac output (4.62 ± 1.5 vs. 3.87 ± 1.5 L/min; p=0.009) at presentation than IPAH patients (n=95). None of the Sch- PAH patients demonstrated a positive response to acute vasodilator testing, whereas 16.2% of IPAH patients did (p=0.015). Survival rates at 1, 2 and 3 years were 95.1%, 95.1%, 85.9% and 95%, 86% and 82%, for Sch-PAH and IPAH, respectively (p=0.49). Both groups had a higher survival rate when compared to untreated IPAH survival as estimated by the NIH equation (71%, 61% and 52%, respectively). Conclusion: Sch-PAH has a more benign clinical course than IPAH despite a lack of demonstrable acute vasoreactivity at hemodynamic evaluation

Uma vez que a maioria das complicações relacionadas ao funcionamento das próteses de válvulas cárdicas é devida aos distúrbios de escoamento, a sua caracterização hidrodinâmica é um auxílio útil no projeto de novas válvulas. Simulações do escoamento pulsátil através de próteses de válvulas cardíacas começaram há cerca de 60 anos, por meio do desenvolvimento de diferentes simuladores cardíacos, melhorando a interpretação dos resultados clínicos. Para o presente estudo, um simulador cardíaco foi desenvolvido completamente na Escola Politécnica da Universidade de São Paulo, no Departamento de Engenharia Mecânica, para estudar o fluxo através de próteses mitrais e aórticas. A sua concepção é baseada na geometria e na fisiologia do lado esquerdo do coração humano, no estado da arte desses simuladores e na norma ISO 584:2010. Neste trabalho, o simulador cardíaco desenvolvido foi aplicado para estudar experimentalmente o fluxo pulsátil através de próteses cardíacas mitrais biológicas de pericárdio bovino. Para tanto, após a validação do simulador para algumas freqüências cardíacas, as biopróteses foram submetidas a ensaios de velocimetria não invasiva, por meio de um equipamento Particle Image Velocimetry (PIV). Os experimentos, que se concentraram principalmente logo após o começo da diástole, mostraram qualitativamente uma diferença significativa no escoamento intraventricular em função de dois posicionamentos das biopróteses, defasadas entre si de 180º no sentido do seu eixo longitudinal. Além disso, produziram significativas mudanças no escoamento próximo à prótese aórtica considerada. Com a continuidade deste estudo, os resultados poderão induzir a um dado procedimento clínico. / Since most complications related to the operation of prosthetic heart valves are due to disturbances of flow, their hydrodynamic characterization is a useful aid in the design of new prostheses. Simulations of pulsatile flow in cardiac prostheses began nearly 60 years ago, through the development of different mock human circulatory systems, improving the clinical results interpretation. A complete design of a cardiac simulator was developed at Polytechnic School of USP, Mechanical Engineering Department, to study mitral and aortic prosthetic heart valves. The simulator design is based on the both geometry and physiology of the left side of the human heart, on state-of-art studies and also considering the ISO 584:2010 standard. The cardiac simulator was applied to pulsatile flow testing of bovine pericardium mitral prosthetic valves. For this, after the cardiac simulator validation for some heart rates, the bioprostheses were assayed by noninvasive velocimetry technics, i.e., a Particle Image Velocimetry (PIV) system. The testing, which mainly were focused on just after the beginning of diastole, qualitatively have showed a significant difference in the intraventricular flow according two different positions for the bioprostheses, dephased of 180° in the direction of their longitudinal axis. Moreover, they produced significant changes in flow close to the aortic prosthesis considered. Future works may lead to a particular medical procedure.

O mecanismo hemodinâmico responsável pela hipotensão pós-exercício aeróbico varia entre os indivíduos, sendo interessante avaliar a possível influência da capacidade de vasodilatação periférica nesses mecanismos. Para tanto, 22 homens normotensos submeteram-se a 2 sessões experimentais: Controle (C - repouso) e Exercício (E- cicloergômetro, 45 min, 50% VO2pico). Antes e 60 min após as intervenções, a pressão arterial (PA) sistólica (PAS), diastólica (PAD) e média (PAM), o débito cardíaco (DC), a resistência vascular periférica (RVP), o volume sistólico (VS), a frequência cardíaca (FC), o fluxo sanguíneo muscular (FS) e a capacidade vasodilatadora periférica (avaliada pelo FS máximo póshiperemia - FSMax e pela área sob a curva pós-hiperemia - ASC) foram medidos. A ANOVA de 2 fatores para amostras repetidas foi empregada. A correlação de Pearson foi calculada entre os índices de capacidade vasodilatadora medidos préexercício e respostas ao exercício (pós-pré). O exercício diminuiu a PAS, PAM e impediu o aumento da PAD. Após o exercício, o DC diminuiu em alguns indivíduos e a RVP diminuiu em outros. O VS diminuiu pós-exercício, enquanto que a FC aumentou em alguns indivíduos e diminuiu em outros. O FS da região inativa e o FSMax da região ativa aumentaram após o exercício. Os índices de capacidade vasodilatadora (FSmax e ASC) não se correlacionaram com as respostas dos mecanismos hemodinâmicos avaliados pós-exercício, mas o FS pré-exercício da região inativa se correlacionou negativamente com a resposta da PA pós-exercício e o FS pré-exercício da região ativa se correlacionou negativamente com a resposta do FS dessa região, do VS e do DC, e positivamente com a resposta da RVP e da FC pós-exercício. Dessa forma, é possível concluir que a sessão de exercício físico proposta promove hipotensão pós-exercício cujos determinantes hemodinâmicos diferem entre os indivíduos. A xvii capacidade vasodilatadora avaliada pela resposta à hiperemia não se relaciona aos determinantes hemodinâmicos da hipotensão pós-exercício. Porém, o FS da região ativa se relaciona, de modo quanto maior for esse fluxo pré-exercício, menor é o aumento dele pós-exercício, menor a redução a RVP e maior a redução do DC e do VS / The hemodynamic mechanism responsible for post-aerobic exercise hypotension varies among individuals, which makes it interesting to evaluate the possible influence of peripheral vasodilatory capacity on them. For this purpose, 22 normotensive men underwent two experimental sessions: control (C rest) and Exercise (E cycle ergometer, 45 min, 50% VO2peak). Both prior to and 60 min after the interventions, systolic (SBP), diastolic (DBP) and mean (MBP) blood pressures (BP), cardiac output (CO), systemic vascular resistance (SVR), stroke volume (SV), heart rate (HR), muscle blood flow (BF) and peripheral vasodilatory capacity (assessed by the maximum BF after hyperemic maneuver BFMax, and the area under the curve after reactive hyperemia AUC) were measured. A two way ANOVA for repeated measures was employed. The Pearson correlation coefficient was calculated between the vasodilatory capacity measured pre exercise and the responses observed after exercise (post-pre). Exercise decreased both SBP and MBP, and prevented an increase in DBP. After exercise, CO decreased in some individuals, while SVR decreased in others. SV decreased after exercise, while HR increased in some subjects and decreased in others. BF of the inactive limb and BFMax of the active limb increased after exercise. The indices of vasodilatory capacity (BFMax and AUC) did not correlate with the hemodynamic mechanisms evaluated after exercise. However, pre-exercise BF measured on the inactive limb correlated negatively with the BP response after exercise, and pre-exercise BF of the active limb correlated negatively with SV, CO and BF of this limb after exercise, and positively with SVR and HR responses after exercise. Thus, we conclude that the exercise bout proposed in this study promotes post-exercise hypotension, but the hemodynamic determinants of this xix response differ between individuals. Vasodilatory capacity assessed by flow responses to hyperemia is not related to the hemodynamic determinants of postexercise hypotension, but the BF of the active limb is. Thus, the greater the preexercise BF of the active limb, the lower the increase in this flow and the reduction in SVR after exercise, and the greater the reduction in CO and SV

Justificativa e Objetivos - A indução anestésica em indivíduos em choque hipovolêmico pode agravar a instabilidade hemodinâmica. O anestésico inalatório xenônio (Xe) é gás inerte com propriedades que mantêm a estabilidade hemodinâmica, durante a anestesia, em individuos normais. O objetivo deste estudo foi avaliar os efeitos hemodinâmicos, metabólicos e sobre o transporte de oxigênio, durante anestesia com Xe, em cães submetidos a choque hipovolêmico. Método - Vinte e um cães sem raça definida foram submetidos a hipnose e relaxamento muscular por infusão venosa contínua de etomidato e vecurônio e ventilação controlada mecânica com FiO2 21% (oxigênio + ar comprimido). Sob anestesia local, inseriu-se cateter em artéria pulmonar para monitorização hemodinâmica e cateteres em artérias femorais direita e esquerda para medida da pressão arterial média e indução do choque hipovolêmico. Após indução do choque hemorrágico até a pressão arterial média atingir 40mmHg por 2 minutos, os animais foram randomizados em grupos controle e xenônio. O grupo xenônio recebeu ventilação controlada mecânica com O2 21% + Xe 79% durante 20 min. Realizou-se coleta de gasometria arterial e venosa mista e coleta de dados hemodinâmicos, com posterior cálculo hemodinâmico e do transporte de O2 antes da indução do choque, imediatamente após a sangria, após 5 min e 20 min, com administração de Xe, e 20 minutos após a suspensão do Xe. O grupo controle foi submetido ao mesmo procedimento, sem a administração de Xe. Os dois grupos foram comparados, utilizando análise de variância para medidas repetidas, considerando-se significativo p<0,05. Resultados: Os grupos foram comparáveis em relação aos valores médios de peso corpóreo e volume de sangramento. As variáveis hemodinâmicas, metabólicas e de transporte de oxigênio não apresentaram diferenças significativas entre os grupos controle e xenônio. Após a indução do choque, no grupo Xe a freqüência cardíaca variou de 130,22±20,57 para 131,89±24,34 em 5min e 138,44±33,66 após 20 minutos. No grupo controle esta variação foi de 144,33±21,03 para 143,75±22,58 após 5min (p=0,82) e para 149,50±23,52 após 20min(p=0,16). Conclusão: A administração de xenônio em cães, em estado de choque hipovolêmico, não altera a condição hemodinâmica, metabólica e de transporte de oxigênio, permitindo sugeri-lo como anestésico seguro em individuos nestas condições / Rationale and objectives - Anesthesia induction in subjects with hypovolemic shock may worsen a baseline hemodynamic instability. Xenon (Xe), an inhalation anesthetics, is an inactive gas with properties that, in normal subjects, maintain hemodynamic stability during anesthesia. The aim of this study was to assess Xe effects on hemodynamics, metabolism, and oxygen delivery during anesthesia in dogs with induced hypovolemic shock. Method - Twenty-one hybrid dogs were submitted to hypnosis and muscle relaxation by continuous venous infusion of etomidate and vecuronium and mechanichal controlled ventilation with a 21% FiO2 (oxigen + compressed air). Under local anesthesia, catheters were introduced into the pulmonary artery for hemodynamic monitoring, and in the left and right femoral arteries for mean arterial blood pressure measurements and hypovolemic shock induction. After induction of an hemorrhagic shock until a mean arterial blood pressure of 40mmHg for 2 minutes was reached, the animals were randomized into the Xenon or the control group. Dogs from the Xenon group received controlled mechanichal ventilation with a 21% FiO2 + 79% Xe for 20 minutes. Blood samples were collected for arterial e mixed venous gas analyses; hemodynamic data were also collected, with further hemodynamic calculation of O2 delivery before shock induction, immediately after the artificial bleeding, 5 min and 20 minutes after starting Xe administration, and 20 minutes after stopping Xe. The control group was submitted to the same procedures, without Xe administration. Both groups were compared using variance analysis for repeated measurements, considering statistical significance where a p<0,05 was reached. Results: Both groups were comparable in terms of mean body weight values and bleeding volume. Hemodynamic and metabolic variables and oxygen delviery had no significant differences between both groups, control and Xenon. In the Xenon group, after shock was induced, heart rate changed from 130.22 ± 20.57 to 131.89 ± 24.34 after 5 minutes, and to 138.44 ± 33.66 after 20 minutes. In the control group, heart rate varied from 144.33 ± 21.03 to 143.75 ± 22.58 after 5 minutes (p=0.82), and to 149.50 ± 23.52 after 20 minutes (p=0.16). Conclusion: Xenon administration does not cause changes in hemodynamics, metabolism, and oxygen delivery in dogs with induced hypovolemic shock, supporting its recommendation as a safe anesthetic in such conditions

Computer simulations have become a great tool to assist the medical field. The present work is a study of a non-invasive patient-specific methodology to evaluate the hemodynamic importance of coronary stenosis using computer simulations. The severity of the lesion is evaluated by the Fractional Flow Reserve, calculated by the pressure gradient before and after the lesion. The geometry models are obtained from medical images of Computed Tomography Angiography exams, and the simulations considers the pulsatile flow and the blood as a non-Newtonian fluid. The governing equations of the blood flow are solved by using Finite Element Method applied to the numerical method called Incremental Pressure Correction Scheme, and with the aid of the libraries from the open-source software FEniCS. Computer simulations of three different patients are performed and the results are compared with the invasive FFR measurements. The methodology proposed shows to be feasible in the study and analysis of stenosed coronaries. / Simulações computacionais tornaram-se uma excelente ferramenta para auxiliar a área médica. O presente trabalho é um estudo de uma metodologia não invasiva para avaliar a importância hemodinâmica de artérias coronárias com estenose através do uso de simulações computacionais. A severidade da lesão da artéria é avaliada através do Fractional Flow Reserve, calculado pelo gradiente de pressão antes e depois da lesão. Os modelos geométricos computacionais foram obtidos a partir de imagens médicas de exames de Angiografia por Tomografia Computadorizada e as simulações consideram o fluxo pulsátil e as propriedades não-Newtonianas do sangue. As equações governantes do fluxo de sangue são resolvidas utilizando o Método dos Elementos Finitos aplicado ao método numérico chamado Incremental Pressure Correction Scheme, e com o uso de bibliotecas do programa em código aberto FEniCS. Foram realizados simulações de três pacientes e os resultados foram confrontados com as medidas invasivas do FFR. A metodologia proposta mostrou-se viável para o estudo e análise de coronárias com estenose.

Introdução O papel das alterações hemodinâmicas sobre o remodelamento do ventrículo esquerdo tem sido pouco estudado, especialmente na hipertrofia cardíaca por sobrecarga de volume. A queda da pressão arterial sistêmica e o aumento da pressão de enchimento do ventrículo esquerdo afetam negativamente a pressão de perfusão miocárdica e podem, assim, prejudicar a perfusão subendocárdica, preferencialmente. As conseqüências para o remodelamento do ventrículo esquerdo ainda não foram determinadas. Objetivos Os objetivos do presente estudo foram investigar o papel da pressão de perfusão coronariana (PPC) no remodelamento subendocárdico e os possíveis efeitos sobre a função cardíaca em um modelo de fístula aorto-cava. Métodos Ratos machos Wistar, pesando 330-350 g, foram submetidos ao modelo de fístula aorto-cava (grupo FAC) ou à cirurgia fictícia - sham (grupo SH). Duas avaliações hemodinâmicas foram realizadas: hemodinâmica inicial, com uma semana de cirurgia e hemodinâmica final, com oito semanas de cirurgia. Duas regiões do ventrículo esquerdo foram examinadas: a região subendocárdica (SE) e a região não subendocárdica (não SE). O fluxo miocárdico foi determinado com microesferas coloridas na semana 1. A expressão e a atividade de metaloproteinase (MMP), o estresse oxidativo, os níveis de citocinas, a atividade de mieloperoxidase e a fração de volume do colágeno foram determinados na semana 8. A estrutura e a função cardíacas foram avaliadas com ecocardiografia realizada na semana 8. Resultados Comparado ao grupo SH, FAC apresentou PPC inicial (86+ - 3 mmHg vs. 52 + - 5 mmHg; P <0,0001) e PPC final (86+ - 2 mmHg vs. 54 + - 4 mmHg, P <0,0001) menores e +dP/dt (5917+ - 266 mmHg/s vs. 4511 + - 285 mmHg/s; P = 0,0021) e - dP/dt (5639 + - 396 mmHg/s vs. 4343 + - 274 mmHg/s; P = 0,0121) finais menores. Também, a fração de encurtamento (55,8 + - 1,2% vs. 45,1 + - 2,1%; P = 0,0014) e a espessura relativa de parede do ventrículo esquerdo (0,72 + - 0,02 vs. 0,58 + - 0,03; P = 0,0058) foram menores. Ainda em FAC, o fluxo miocárdico foi menor em SE (2,7 + - 0,5 mL/min/g) comparado a não SE (4,8 + - 0,8 mL/min/g) e também menor comparado a SE (6,7 + - 0,4 mL/min/g) e não SE (7,5 + - 0,5 mL/min/g) de SH. A expressão e a atividade da MMP-2 predominaram em SE de FAC, particularmente nos animais com PPC <60 mmHg. Aumento dos níveis de IL-1beta e IL-6 foram também predominantes em SE de FAC. Já a atividade da mieloperoxidase e os níveis de TNF-alfa e IL-10 foram comparáveis entre os grupos. Comparado a SH, FAC apresentou maior fração de volume do colágeno tanto em SE (1,1+ - 0,1% vs. 7,7 + - 0,4%; P <0,0001) quanto em não SE (1,0 + - 0,1% vs. 4,9 + - 0,3%, P <0,0001). Das variáveis hemodinâmicas, a análise multivariada demonstrou que a PPC inicial foi a única associada de forma independente com a fibrose SE (R2 = 0,76; P <0,0001), com a +dP/dt (R2= 0,55; P = 0,0004) e com a -dP/dt (R2= 0,91; P <0,0001). Houve correlação da PPC final com a expressão (R2 = 0,55; P <0,0001) e a atividade da MMP-2 (R2 = 0,88; P <0,0001) e da fibrose SE com a +dP/dt (R2 = 0,55; P = 0,0004) e com a -dP/dt (R2 = 0,85; P <0,0001). Conclusão Na fístula, a diminuição da PPC está associada a dano em SE, representado por isquemia, estresse oxidativo, aumento de citocinas e de MMP-2, com desenvolvimento de fibrose. O remodelamento de SE interfere negativamente na função do ventrículo esquerdo. / Introdution The role of hemodynamic changes in left ventricular remodeling has been poorly investigated, especially in the context of volume overload cardiac hypertrophy. Low diastolic blood pressure and high left ventricular filling pressure are expected to negatively affect coronary driving pressure and thereby put in jeopardy subendocardial perfusion, in particular. The consequences to global left ventricular remodeling remain undetermined. Objectives The aim of this study was to investigate the role of coronary driving pressure (CDP) in the development of subendocardial remodeling and the conceivable effects on cardiac function, using a rat model of aortocaval fistula. Methods Wistar rats weighting 330-350 g were submitted to aortocaval fistula (ACF group) or sham (SH group) operations. Two hemodynamic measurements were determined following surgery: initial, at week 1; and final, at week 8. Two distinct myocardial layers were examined: the subendocardium (SE) and the non-subendocardium (non SE). Myocardial blood flow was determined at week 1. Metalloproteinase expression and activity, oxidative stress, cytokine levels, myeloperoxidase activity, and fibrosis deposition were assessed at week 8. Cardiac structure and function were determined by means of echocardiography at week 8. Results Compared with SH, ACF showed lower initial (86 + - 3 mmHg vs. 52 + - 5 mmHg; P <0.0001) and final (86+ - 2 mmHg vs. 54 + - 4 mmHg, P <0.0001) CDP and lower final +dP/dt (5917 + - 266 mmHg/s vs. 4511+ - 285 mmHg/s; P = 0.0021) and -dP/dt (5639?396 mmHg/s vs. 4343 + - 274 mmHg/s; P = 0.0121). Left ventricular fractional shortening (55.8 + - 1.2% vs. 45.1+ - 2.1%; P = 0.0014) and relative wall thickness were also lower (0.72 + - 0.02 vs. 0.58 + - 0.03; P = 0.0058). ACF showed lower myocardial blood flow in SE (2.7 + - 0.5 mL/min/g) as compared with non SE (4.8 + - 0.8 mL/min/g) and as compared with both SE (6.7 + - 0.4 mL/min/g) and non SE (7.5 + - 0.5 mL/min/g) regions in SH. Metalloproteinase-2 expression and activity predominated in SE of ACF animals, particularly in those with CDP <60 mmHg. Increased levels of IL-6 and IL-1beta also predominated in SE of ACF. Otherwise, myeloperoxidase activity, and TNF-alfa and IL-10 levels were similar in both groups. Compared with SH, ACF showed higher collagen volume fraction in SE (1.1 + - 0.1% vs. 7.7 + - 0.4%; P <0.0001) and non SE (1.0 + - 0.1% vs. 4.9 + - 0.3%, P <0.0001) regions. Multivariate analyses disclosed initial CDP as the only hemodynamic parameter independently associated with SE fibrosis (R2 = 0.76; P <0.0001) and with +dP/dt (R2= 0.55; P = 0.0004) and -dP/dt (R2= 0.91; P <0.0001). Final CDP correlated with both the expression (R2 = 0.55; P <0.0001) and the activity of metalloproteinase-2 (R2 = 0.88; P <0.0001) and SE fibrosis correlated with both +dP/dt (R2 = 0.55; P = 0.0004) and -dP/dt (R2 = 0.85; P <0.0001). Conclusion Low coronary driving pressure early in the course of ACF is associated with SE damage characterized by ischemia, oxidative stress, increase in cytokines and MMP-2, the development of fibrosis and by this mechanism interferes negatively in left ventricular function.

Introdução: A fração de ejeção do ventrículo direito (FEVD) é um importante fator prognóstico em pacientes com hipertensão pulmonar (HP), porém a sua medida é complicada e demorada devido à complexidade anatômica do ventrículo direito (VD). O TAPSE (Tricuspid Annular Plane Systolic Excursion) é um bom índice da FEVD, mas ele avalia apenas o componente longitudinal da contração ventricular direita. A RVFAC (Right Ventricular Fractional Area Change) parece ser um melhor índice da FEVD por incluir os componentes longitudinal e transversal da contração ventricular direita. O objetivo deste estudo foi avaliar a performance da RVFAC de acordo com a gravidade do acometimento hemodinâmico em dois grupos distintos de pacientes portadores de HP pré-capilar: hipertensão arterial pulmonar (HAP) e tromboembolismo pulmonar crônico hipertensivo (TEPCH). Métodos: 62 pacientes realizaram cateterismo cardíaco direito e ressonância magnética cardíaca em ±72h. As áreas sistóica e diastólica finais do ventrículo direito (ASFVD, ADFVD), a área diastólica final do ventrículo esquerdo (ADFVE) e o TAPSE foram medidos nas imagens de quatro cavidades. A RVFAC (ADFVD-ASFVD/ADFVD) e a relação entre as áreas diastólica finais ventriculares (ADFVD/ADFVE) foram calculadas. Os diâmetros entre as paredes livre e septal (dL-S) e antero-posterior (dA-P) do ventículo esquerdo (VE) foram medidos nas imagens em eixo curto e o índice de excentricidade do VE (IE) foi calculado (=dA-P/dL-S). A FEVD foi calculada a partir de imagens consecutivas de 6mm no eixo curto. . Resultados: A população tinha 58 anos em média, a maioria era do sexo feminino e estava em classe funcional III, 23 tinham HAP e 39 TEPCH. A FEVD apresentou correlações fracas com as medidas hemodinâmicas de sobrecarga e de função do VD. A RVFAC apresentou melhor correlação (R2=0,65, p < 0,001) do que o TAPSE (R2=0,35, p<0,001) com a FEVD e melhor capacidade para estimar FEVD<35% do que o TAPSE (TAPSE: AUC 0,73 e RVFAC: AUC 0,93, p=0,0065). Dividimos a população pela mediana da resistência vascular pulmonar (RVP) e observamos que no grupo com maior gravidade hemodinâmica essa diferença se acentuou: no grupo com RVP<8,5UW (RVFAC: R2=0,66, p<0,001 e TAPSE: R2=0,30, e p=0,002) e no grupo com RVP>8,5UW (RVFAC: R2=0,51, p<0,001 e TAPSE: R2=0,14, e p=0,041). O grupo com RVP>8,5UW apresentou maior ADFVD/ADFVE e maior IE. As correlações da RVFAC e TAPSE com FEVD foram semelhantes entre os grupos HAP e TEPCH. Conclusão: A RVFAC se correlacionou melhor com a FEVD do que o TAPSE tanto no grupo com menor como no grupo com maior gravidade hemodinâmica. No grupo com maior gravidade as correlações da RVFAC com a FEVD foram ainda mais significativas, não havendo diferenças na performance da RVFAC entre os pacientes com HAP e TEPCH. A RVFAC foi um melhor índice da FEVD talvez por incluir o movimento transversal da contração ventricular / Introduction: The right ventricular ejection fraction (RVEF) is a surrogate marker in pulmonary hypertension (PH), but its measurement is complicated and time consuming. The TAPSE (Tricuspid Annular Plane Systolic Excursion) is a good index of RVEF, though it measures only the longitudinal component of right ventricular contraction. The RVFAC (Right Ventricular Fractional Area Change) seems to be a better index of RVEF because it takes into account the longitudinal and the transversal components of right ventricular contraction. The aim of our study was to evaluate the RVFAC performance according to hemodynamic severity in two groups of patients with PH: pulmonary arterial hypertension (PAH) and chronic thromboembolic pulmonary hypertension (CTEPH). Methos: Sixty-two patients with PAH and CTEPH underwent right heart catheterization and cardiac MR in a 72-hour delay. The right and left ventricle end diastolic areas (RVEDA, LVEDA), the right ventricle end systolic area (RVESA) and TAPSE were measured in the four chamber view. The RVFAC (=RVEDARVESA/RVEDA) and the RVEDA/LVEDA relationship were calculated. The diameter between the left ventricle (LV) free wall and the septum (dF-S) and the diameter between the LV anterior and posterior walls (dA-P) were measured and the LV eccentricity index (EI) was calculated (=dA-P/dF-S). The RVEF was calculated by using 6 mm RV short axis cines. Results: The population had mean age of 58 years with female majority, most of the patients were in functional class III, 23 had PAH and 39 CTEPH. The RVEF was weakly correlated to the hemodynamic variables of RV afterload and function. The RVFAC was more strongly correlated to RVEF (R2=0.65, p<0.001) than TAPSE (R2=0.35, p<0.001). RVEF<35% was better predicted by RVFAC than TAPSE (TAPSE: AUC 0.73 and RVFAC: AUC 0.93, p=0.0065). We divided the population by the median of the pulmonary vascular resistance (PVR) and we observed that in the group with worse hemodynamic severity this difference increased: in the group with PVR<8,5WU (RVFAC: R2=0.66, p<0.001 and TAPSE: R2=0.30, p=0.002) and in the group with PVR>8,5 WU (RVFAC: R2=0.51, p<0.001 and TAPSE: R2=0.14, p=0.041). The group with PVR>8,5WU had an increased RVEDA/LVEDA and an increased EI. There was no differences in the RVEF relationships between the groups of PAH and CETPH. Conclusion: The RVFAC was better correlated to RVEF than TAPSE in the groups with less severe and more severe hemodynamics. In patients with increased hemodynamic severity RVFAC perfomed even better, there was no difference in the performance of RVFAC in PAH or CTEPH. RVFAC was a better index of RVEF possibly because it takes into account the transversal component of right ventricular function

Os efeitos da hidratação sobre a pressão arterial (PA) e seus mecanismos hemodinâmicos e autonômicos pós-exercício foram pouco estudados e os resultados são controversos. Esse estudo avaliou esses efeitos, em normotensos jovens após uma sessão de exercício aeróbico. Assim, 16 rapazes submeteram-se a quatro sessões experimentais, realizadas em ordem aleatória: controle sem hidratação, exercício sem hidratação, controle com hidratação e exercício com hidratação. Nas sessões com hidratação, os sujeitos ingeriam 1l de água na noite anterior, 500ml 60min antes da intervenção (exercício ou repouso) e mais 1ml por 1g de massa corporal perdida logo após a intervenção. O exercício foi realizado por 45min em ciclo ergômetro em 50% do VO2pico. Em todas as sessões as PA sistólica (S), média (M) e diastólica (D), o débito cardíaco (DC), a frequência cardíaca (FC) e as variabilidades da FC e da PA foram medidos antes e após as intervenções. O exercício diminuiu a PAS e o volume sistólico (VS) e impediu os aumentos da FC, da PAD, da PAM e da sensibilidade baroreflexa, que ocorreram na sessão controle. A hidratação não modificou as respostas hemodinâmicas e autonômicas após o exercício. Em conclusão, em sujeitos jovens normotensos, a hidratação não modificou o efeito hipotensor promovido pelo exercício aeróbico no período de recuperação, não afetando seus mecanismos hemodinâmicos e autonômicos / The effects of hydration on post-exercise blood pressure (BP) and hemodynamic and autonomic mechanisms were poorly studied and results are controversial. This study evaluated these effects in young normotensives after an acute bout of aerobic exercise. Sixteen young men underwent four sessions in a random order: control without hydration, exercise without hydration, control with hydration and exercise with hydration. In the hydration sessions, subjects drank 1l of water in the night before, 500 ml 60 min before the intervention (rest or exercise) and 1ml for 1g of body mass lost immediately after the intervention. In exercise sessions, they exercised for 45 min on a cycle ergometer at 50% of VO2peak. Systolic (S), diastolic (D) and mean (M) BP, as well as cardiac output (CO), heart rate (HR), and HR and BP variabilities were measured before and after the interventions. Exercise produced a significant reduction in SBP and stroke volume (SV), and abolished the increase in HR, DBP, MBP and baroreflex sensitivity that occurred in the control sessions. Hydration did not change hemodynamic and autonomic responses after exercise. In conclusion, in healthy young subjects, hydration did not modify the hypotensive effect promoted by the aerobic exercise during the recovery period, not affecting its hemodynamic and autonomic mechanisms

臂叢阻滯麻醉可以阻斷同側正中神經，尺神經，橈神經和肌皮神經，故其經常被用於上肢手術中麻醉和/或鎮痛。臂叢阻滯麻醉也可以阻滯同側交感神經，導致同側上肢血管擴張（動脈和靜脈）和血流增加。脈沖多普勒超聲技術可以檢測到這些局部的血流動力學變化。文獻回顧表明迄今為止發表的大部分報道片面地評估了臂叢阻滯麻醉後上肢的局部血流動力學變化缺乏全面而系統的研究，並且報道中關於脈沖多普勒超聲技術用於上肢局部血流動力學測量的可靠性和可重復性的數據也很有限。此外，上肢的局部血流動力學變化是否與測量的位置或者使用的臂叢阻滯麻醉技術有關尚且未知。 / 我假設脈沖多普勒超聲是壹種可靠的測量上肢血流動力學變化的方法，它可以系統地定量測定臂叢阻滯麻醉後上肢的局部血流動力學變化，確定這些變化在上肢不同部位的差異，以及確定不同臂叢阻滯麻醉技術後局部血流動力學變化的差異。以下的部分列舉了本博士課題中開展的壹系列研究來證實我的假設。 / 第壹，我們在12個健康年輕誌願者中（年齡21-34歲）用脈沖多普勒超聲在上肢肱動脈和指掌側總動脈進行血流動力學測量，評估其在觀察者內和觀察者間的差異性。兩個觀察者獨立進行了測量。測量的指標包括收縮期峰值血流速度（厘米/秒），舒張末期血流速度（厘米/秒），收縮期峰值血流速度和舒張末期血流速度比值，平均速度（厘米/秒），時均速度（厘米/秒），阻力指數，搏動指數，動脈直徑（厘米），和血流量（毫升/分鐘）。結果顯示脈沖多普勒超聲是壹種可靠的方法，可用來重復測量上肢的局部血流動力學參數（組內相關系數>0.9）. / 第二，我們在8個病人中（年齡24-70歲）系統地評估了超聲波引導下的腋路臂叢神經阻滯後同側肱動脈的局部血流動力學變化。結果表明臂叢神經阻滯後最早的變化是脈沖多普勒頻譜波形的變化，其波形由三相變為單相，舒張期血流曲線擡升。隨著時間推移，收縮期峰值血流速度，舒張末期血流速度，平均速度，時均速度，動脈直徑，和血流量均顯著增加，收縮期峰值血流速度和舒張末期血流速度比值，阻力指數，搏動指數顯著降低。大部分變化發生在神經阻滯後5分鐘。在所有的局部血流動力學指標中，舒張末期血流速度表現出最顯著的變化（3.7倍），其增加超過收縮期峰值血流速度（1.5倍）和平均速度（2.8倍）。 / 第三，利用15個病人（年齡23-70歲），我們評估了超聲波引導下的鎖骨上臂叢神經阻滯後上肢近端動脈（肱動脈）和遠端動脈（指掌側總動脈）血流動力學變化的差異。臂叢神經阻滯之後，在能量多普勒圖像上，指掌側總動脈表現出更明顯的血管擴張。在脈沖多普勒頻譜波形中，兩個動脈均出現舒張早期的反流消失以及舒張期曲線擡升。另外，收縮期峰值血流速度，舒張末期血流速度，平均速度，時均速度，動脈直徑，和血流量增加，收縮期峰值血流速度和舒張末期血流速度比值，阻力指數，搏動指數顯著降低。這些指標的相對變化在指掌側總動脈比肱動脈更顯著。此研究中，4個病人出現對側手部溫度的增加，以此推測局部麻醉藥的雙側擴散。 / 第四，我們開展了壹項前瞻性隨機對照研究來比較腋路和鎖骨上臂叢神經阻滯引起的局部血流動力學變化的不同。兩組病人人口統計學資料類似。兩種臂叢神經阻滯技術均引起肱動脈和指掌側總動脈收縮期峰值血流速度，舒張末期血流速度，平均速度，時均速度，動脈直徑，和血流量的顯著增加，收縮期峰值血流速度和舒張末期血流速度比值，阻力指數，搏動指數顯著降低。跟腋窩方法相比，鎖骨上技術能夠引起肱動脈時均速度和血流量更顯著的增加。然而，在感覺神經阻滯起效方面，腋窩方法比鎖骨上方法更快。 / 總之，脈沖多普勒超聲可重復地測量肱動脈和指掌側總動脈的血流動力學參數及其變化。臂叢阻滯麻醉引起肱動脈和指掌側總動脈脈沖多普勒頻譜形態的變化，血流速度的增加和血流量的增加。這些局部血流動力學變化在指掌側總動脈中比肱動脈更顯著。鎖骨上臂叢神經阻滯比腋窩方法引起更顯著的局部血流動力學變化。臨床醫生可以利用上肢遠端動脈的局部血流動力學變化來評價臂叢阻滯麻醉的交感神經阻滯效應。麻醉醫師還可以根據這些發現為術後需要較好血流灌註的上肢血管手術選取臂叢神經阻滯方法。 / Brachial plexus block (BPB), which produces sensory and motor blockade of the ipsilateral median, ulnar, radial and musculocutaneous nerves, is frequently used for anesthesia and/or analgesia during surgical procedures of the upper extremity. BPB also produces ipsilateral sympathetic nerve blockade that is characterized by vasodilatation (venous and arterial), and an increase in blood flow to the ipsilateral upper extremity. Pulsed wave Doppler (PWD) ultrasound (US) has been used to evaluate these regional hemodynamic changes. A review of the literature shows that most published reports to date have only partially evaluated the regional hemodynamic changes in the upper extremity after a BPB. There are also limited data demonstrating that PWD US is a reliable or reproducible method of quantifying the regional hemodynamic changes in the upper extremity. Moreover, it is also not known whether the regional hemodynamic changes vary with the site of measurement or the technique of BPB used. / I hypothesized that PWD US is a reliable method for measuring regional hemodynamic parameters in the upper extremity. It can be used to comprehensively quantify the regional hemodynamic changes after a BPB and to determine the extent of these changes at different sites in the upper extremity and after different techniques for BPB. The following section outlines a series of studies that I undertook during this PhD project to corroborate my hypothesis. / Firstly, we sought to assess the intra-observer and inter-observer variability of measuring regional hemodynamic parameters, in the brachial and common palmar digital arteries of the upper extremity, using PWD US in 12 healthy young volunteers aged 21-34 yrs. The measurements were performed independently by two observers. Measured hemodynamic parameters included peak systolic velocity (PSV, cm/s), end diastolic velocity (EDV, cm/s), ratio of PSV and EDV (S/D), mean velocity (Vmean, cm/s), time-averaged mean velocity (TAVM, cm/s), resistance index (RI), pulsatility index (PI), the arterial diameter (d, cm), and blood flow (mL/min). The results showed that PWD US is a reliable and reproducible method of measuring regional hemodynamic parameters in the upper extremity (ICC>0.9). / Secondly, we comprehensively evaluated the regional hemodynamic changes in the ipsilateral brachial artery after an ultrasound guided (USG) axillary BPB in eight adult patients aged 24-70 yrs. Our results suggested that the earliest change after the BPB was a change in the morphology of the PWD spectral waveform from a triphasic to a monophasic waveform and an elevation in the diastolic blood flow velocity. Over time, there was also a significant increase in PSV, EDV, Vmean, TAVM, d, and blood flow, and a decrease in S/D ratio, RI, and PI. Most of these changes were seen as early as 5 minutes after the block. The increase in EDV (3.7-fold) was the most notable change, and it was significantly greater than the increase in PSV (1.5-fold) and Vmean (2.8-fold). / Thirdly, the regional hemodynamic changes in the proximal (brachial artery) and distal (common palmar digital artery) artery of the upper extremity after an USG supraclavicular BPB was investigated in 15 adult patients aged 23-70 yrs. After the block, the common palmar digital artery showed more obvious vasodilatation on the power Doppler US scan. In the PWD spectral waveform, and in both arteries studied, the protodiastolic blood flow disappeared and there was an elevation of the diastolic curve. Also there was a significant increase in PSV, EDV, Vmean, TAVM, d, and blood flow, and a significant reduction in S/D ratio, PI and RI in both arteries. Relative changes of these parameters were greater in the common palmar digital artery than in the brachial artery. In this study, bilateral spread of local anesthetic was observed in 4 patients, as evidenced by an increase of skin temperature on the contralateral hand. / Fourthly, a prospective and randomized study was conducted to compare the regional hemodynamic changes in the upper extremity after an axillary and supraclavicular BPB. The two study groups were similar with respect to demographic data. Both axillary and supraclavicular BPB caused a significant increase in PSV, EDV, Vmean, TAVM, d, and blood flow, and a significant reduction in S/D ratio, PI and RI in both the brachial and common palmar digital arteries. Compared with the axillary approach, the supraclavicular approach produced significantly greater increases in TAVM and blood flow in the brachial artery. However, the onset of sensory blockade was faster after the axillary BPB than with the supraclavicular BPB. / In conclusion, PWD US is a reliable and reproducible method for quantifying the regional hemodynamic parameters in both the brachial and common palmar digital arteries. BPB produces a change in the morphology of the PWD spectral waveform, arterial vasodilatation, an increase in blood flow velocity, and an increase in blood flow in both the ipsilateral brachial and common palmar digital arteries. These changes in regional hemodynamic parameters were more profound in the common palmar digital artery than in the brachial artery. Also these changes were more significant after a supraclavicular BPB than after an axillary BPB. These findings will allow clinicians to evaluate the sympathetic effect of a BPB using regional hemodynamic changes in the distal arteries of the upper extremity. These findings will also allow anesthesiologists to make an evidence-based choice on the techniques of BPB for vascular surgery of the upper extremity when good tissue perfusion is desirable postoperatively. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Detailed summary in vernacular field only. / Li, Jiawei. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2012. / Includes bibliographical references (leaves 182-192). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract also in Chinese. / TABLE OF CONTENTS / ABSTRACT / 中文摘要 / STATEMENT OF WORK / ACKNOWLEDGMENTS / PUBLICATIONS AND PRESENTATIONS / LIST OF ABBREVIATIONS / LIST OF TABLES / LIST OF FIGURES / Chapter CHAPTER 1 --- Introduction / Chapter 1.1 --- Introduction / Chapter 1.2 --- Aims of the project / Chapter 1.3 --- Outline of the thesis / Chapter CHAPTER 2 --- Literature Review / Chapter 2.1 --- Introduction / Chapter 2.2 --- Why regional hemodynamic changes occur after a BPB / Chapter 2.2.1 --- Anatomy of the sympathetic nervous system in the upper extremity / Chapter 2.2.2 --- The anatomic relationship between the sympathetic nerves and the brachial plexus / Chapter 2.2.3 --- Sympathetic efferents to blood vessels in the upper extremity / Chapter 2.3 --- Methods used to measure regional hemodynamic changes / Chapter 2.3.1 --- Skin and muscle blood flow / Chapter 2.3.2 --- Regional hemodynamic measurements using PWD US / Chapter 2.3.2.1 --- Basics of Doppler ultrasound / Chapter 2.3.2.2 --- Principles of blood flow / Chapter 2.3.2.3 --- Spectral analysis of blood flow using PWD US / Chapter 2.4 --- Published data on regional hemodynamic changes after BPB / Chapter 2.4.1 --- Skin temperature / Chapter 2.4.2 --- Cutaneous and muscular blood flow / Chapter 2.4.3 --- Regional hemodynamic measurements on major arterial branches of the upper extremity / Chapter 2.5 --- Introduction of BPB / Chapter 2.5.1 --- Anatomy of the brachial plexus / Chapter 2.5.2 --- Techniques for performing BPB / Chapter 2.5.3 --- USG BPB / Chapter 2.5.3.1 --- History / Chapter 2.5.3.2 --- Advantages of ultrasound guidance for peripheral nerve blockade / Chapter CHAPTER 3 --- Methodology / Chapter 3.1 --- Introduction / Chapter 3.2 --- Patient preparations / Chapter 3.3 --- Regional hemodynamic measurement / Chapter 3.3.1 --- Ultrasound equipment / Chapter 3.3.2 --- Patient position / Chapter 3.3.3 --- Regional hemodynamic measurements using PWD US / Chapter 3.3.3.1 --- Optimizing settings for B-Mode US / Chapter 3.3.3.2 --- Optimizing settings for PWD US / Chapter 3.3.3.3 --- Measurement of regional hemodynamic parameters / Chapter 3.3.4 --- Measurement of diameter (d) and blood flow (Q) / Chapter 3.4 --- USG BPB / Chapter 3.4.1 --- USG axillary BPB / Chapter 3.4.1.1 --- Scout scan / Chapter 3.4.1.2 --- Aseptic precautions / Chapter 3.4.1.3 --- USG axillary BPB / Chapter 3.4.2 --- USG supraclavicular BPB / Chapter 3.4.2.1 --- Scout scan / Chapter 3.4.2.2 --- Aseptic precautions / Chapter 3.4.2.3 --- USG supraclavicular BPB / Chapter 3.5 --- Outcome data after the BPB / Chapter CHAPTER 4 --- Measurement of Regional Hemodynamic Parameters in the Upper Extremity Using Pulsed Wave Doppler Ultrasound: A Reliability Study / Chapter 4.1 --- Introduction / Chapter 4.2 --- Methods / Chapter 4.2.1 --- Subjects / Chapter 4.2.2 --- Study design / Chapter 4.2.3 --- Data acquisition / Chapter 4.2.4 --- Statistical analysis / Chapter 4.3 --- Results / Chapter 4.4 --- Discussion / Chapter 4.4.1 --- Summary of main findings / Chapter 4.4.2 --- Compared with previous studies / Chapter 4.4.3 --- Sources of measurement variability / Chapter 4.4.4 --- Explanation for the variation in the changes in various regional hemodynamic parameters / Chapter 4.5 --- Conclusion / Chapter CHAPTER 5 --- Regional Hemodynamic Changes after an Axillary BPB: A Pulsed Wave Doppler Ultrasound Study / Chapter 5.1 --- Introduction / Chapter 5.2 --- Methods / Chapter 5.2.1 --- Patient enrollment / Chapter 5.2.2 --- Patient preparation / Chapter 5.2.3 --- Measurement of baseline regional hemodynamic parameters / Chapter 5.2.4 --- USG axillary BPB / Chapter 5.2.5 --- Outcome data after the BPB / Chapter 5.2.6 --- Sensory and motor assessments after the BPB / Chapter 5.2.7 --- Statistical Analysis / Chapter 5.3 --- Results / Chapter 5.4 --- Discussion / Chapter 5.4.1 --- Summary of main findings / Chapter 5.4.2 --- Limitations / Chapter 5.4.3 --- Changes in PWD spectral waveform / Chapter 5.4.4 --- Changes in regional hemodynamic parameters / Chapter 5.4.5 --- Increase in skin temperature / Chapter 5.4.6 --- Effects of local anesthetic / Chapter 5.5 --- Conclusion / Chapter CHAPTER 6 --- Does a Supraclavicular Brachial Plexus Block Induce Comparable Hemodynamic Changes in the Proximal and Distal Arteries of the Upper Extremity? / Chapter 6.1 --- Introduction / Chapter 6.2 --- Methods / Chapter 6.2.1 --- Patient recruitment / Chapter 6.2.2 --- Patient preparation / Chapter 6.2.3 --- Measurement of baseline regional hemodynamic parameters, arterial diameter and blood flow / Chapter 6.2.4 --- USG supraclavicular BPB / Chapter 6.2.5 --- Outcome measurements after the BPB / Chapter 6.2.6 --- Statistical analysis / Chapter 6.3 --- Results / Chapter 6.4 --- Discussion / Chapter 6.4.1 --- Summary of the main findings / Chapter 6.4.2 --- Limitations / Chapter 6.4.3 --- Changes in the PWD spectral waveform / Chapter 6.4.4 --- Explanation of the differences in regional hemodynamic changes in the distal and proximal arteries after BPB / Chapter 6.4.5 --- Increase in skin temperature and its relation to blood flow / Chapter 6.4.6 --- Bilateral sympathetic effect after supraclavicular BPB / Chapter 6.4.7 --- Other findings of this study / Chapter 6.5 --- Conclusion / Chapter CHAPTER 7 --- Does a Supraclavicular Brachial Plexus Block Induce Greater Changes in Regional Hemodynamics than an Axillary Brachial Plexus Block? / Chapter 7.1 --- Introduction / Chapter 7.2 --- Methods / Chapter 7.2.1 --- Sample size estimation / Chapter 7.2.2 --- Exclusion criteria / Chapter 7.2.3 --- Randomized allocation / Chapter 7.2.4 --- Preparations before the ultrasound scan / Chapter 7.2.5 --- Measurement of baseline regional hemodynamic parameters, diameter and blood / Chapter 7.2.6 --- USG axillary and supraclavicular BPB / Chapter 7.2.7 --- Outcome measurements after the BPB / Chapter 7.2.8 --- Statistical analysis / Chapter 7.3 --- Results / Chapter 7.4 --- Discussion / Chapter 7.4.1 --- Summary of the main findings / Chapter 7.4.2 --- Limitations / Chapter 7.4.3 --- Change in the PWD spectral waveform / Chapter 7.4.4 --- Differences in regional hemodynamic changes between the 2 study groups / Chapter 7.4.5 --- Differences in sensory and motor blockade between the 2 study groups / Chapter 7.4.6 --- Changes in skin temperature / Chapter 7.5 --- Conclusion / Chapter CHAPTER 8 --- Summary and Conclusions / APPENDIX / REFERENCES

Introdução: A esquistossomose (Sch) é uma das doenças infecciosas crônicas mais prevalentes do mundo. Entretanto, dados a respeito de uma de suas complicações, a hipertensão arterial pulmonar (HAP), são escassos. O objetivo deste estudo é avaliar a história natural de pacientes com HAP-Sch comparados a pacientes com HAP idiopática (HAPI). Métodos: Análise retrospectiva dos prontuários de todos os pacientes consecutivamente diagnosticados como HAP-Sch e HAPI no Instituto do Coração, São Paulo, Brasil, entre 2004 e 2008. Nenhum dos pacientes com Sch-PAH recebeu tratamento específico para HAP enquanto todos os pacientes com HAPI receberam. Resultados: Pacientes com HAP-Sch (n=54) apresentavam hipertensão pulmonar menos grave ao diagnóstico, com menores níveis de resistência vascular pulmonar (11.3 ± 11.3 vs 16.7 ± 10.6 UI; p=0.002) e pressão média de artéria pulmonar (56.7 ± 18.7 vs. 64.6 ± 17.4 mmHg; p=0.01) e ainda maior débito cardíaco (4.62 ± 1.5 vs. 3.87 ± 1.5 L/min; p=0.009) quando comparados com os pacientes com HAPI (n=95). Nenhum dos pacientes HAP-Sch apresentou resposta positiva ao teste agudo com vasodilatador enquanto 16.2% dos pacientes com HAPI apresentaram (p=0.015). As taxas de sobrevida em 1, 2 e 3 anos foram 95.1%, 95.1%, 85.9% e 95%, 86% e 82%, para HAP-Sch e HAPI, respectivamente (p=0.49). Ambos os grupos tinham uma maior taxa de sobrevida quando comparadas àquela estimada pela equação do NIH para os pacientes com HAPI sem tratamento específico para HAP (71%, 61% e 52%, respectivamente). Conclusão: HAP-Sch tem um curso clínico mais benigno do que HAPI apesar da falta de vasorreatividade aguda na avaliação hemodinâmica inicial / Background: Schistossomiasis (Sch) is one of the most prevalent chronic infectious diseases in the world. Nevertheless data regarding one of its most severe clinical complications, pulmonary arterial hypertension (PAH), is scarce. The objective of this study was to evaluate the natural history of Sch-PAH patients as compared to idiopathic PAH (IPAH). Methods: We retrospectively analyzed case notes of all consecutive patients diagnosed of Sch-PAH and IPAH referred to the Heart Institute in São Paulo, Brazil, between 2004 and 2008. None of the Sch-PAH received PAH specific treatment whereas all IPAH patients did. Findings: Sch-PH patients (n=54) had less severe pulmonary hypertension as evidenced by lower levels of pulmonary vascular resistance (11.3 ± 11.3 vs 16.7 ± 10.6 IU; p=0.002) and mean pulmonary artery pressure (56.7 ± 18.7 vs. 64.6 ± 17.4 mmHg; p=0.01) and higher cardiac output (4.62 ± 1.5 vs. 3.87 ± 1.5 L/min; p=0.009) at presentation than IPAH patients (n=95). None of the Sch- PAH patients demonstrated a positive response to acute vasodilator testing, whereas 16.2% of IPAH patients did (p=0.015). Survival rates at 1, 2 and 3 years were 95.1%, 95.1%, 85.9% and 95%, 86% and 82%, for Sch-PAH and IPAH, respectively (p=0.49). Both groups had a higher survival rate when compared to untreated IPAH survival as estimated by the NIH equation (71%, 61% and 52%, respectively). Conclusion: Sch-PAH has a more benign clinical course than IPAH despite a lack of demonstrable acute vasoreactivity at hemodynamic evaluation