<p>The burden of hypertension and subsequent in Tibet is quite profound and disproportionate when compared to other Chinese populations. Thus, there has a recent impetus to focus on low-cost sustainable health interventions to ameliorate this tremendous burden. Factors of compliance of first-line low dose hypertensive medications are not known in semi-nomadic Tibetan herdsmen at high altitude.</p><p>A retrospective analysis of a de-identified database for a single blinded equal allocation randomized control trial for a dietary reduced sodium salt substitute completed in 2009 using STATA 11.2 (STATA INC. College Station, TX) and logistic regression was performed. Patients were recruited from two townships at 4300 m altitude and northwest of Lhasa, the regional capital. Eligibility criteria included: age 40 years and older, with hypertension (&#8805; 140mmHg / &#8805; 90 mmHg) , enrollment in salt substitute trial, and prescription of hypertensive medication. Primary outcome was compliance to medication at three and six months of follow-up. Factor variables included and adjusted for included: sex, age, blood pressure, township, class of medication, and trial arm assignment.</p><p>The overall rate of non-compliance was 33.0% (38/115) after three months and 12.9% (28/217) after six months. After three months follow-up patients with Stage I and Stage II hypertension were at an adjusted odds ratio of 0.03(95%CI: 0.002-0.70) and 0.13(95%CI: 0.012-1.37) times lower odds of non-compliance when compared patients with only isolated systolic hypertension, (p=0.028 and 0.089, respectively). Furthermore, at six months of follow-up patients prescribed combination pharmacologic therapy had an adjusted odds ratios of 0.20 (95%CI: 0.05-0.81) times lower odds than those patients on diuretic only, p =0.023.</p> / Thesis

Research Objectives Heart failure (HF) is a common condition in persons older than 65 years. Existing literature indicated that hospital readmission rates after discharge for heart failure patients are immensely high. However, previous studies showed that almost half of the early hospital readmissions could be prevented. Moreover, Angiotensin-converting enzyme (ACE) inhibitor and Angiotensin receptor blocker (ARB) are the commonly used medications for heart failure patients to control blood pressure. Nevertheless, studies indicated that these two medications could also cause the risk of hospital readmission. Little studies examined the associations of medication use and hospital readmission of heart failure patients in Taiwan. This study aims to investigate the influence factors of hospital readmissions among heart failure patients in Taiwan. Study Design We collected the data from National Health Insurance (NHI) database during the period from year 2000 to 2006. Based on the rule of Bureau of National Health Insurance in Taiwan, the 14-day readmission is considered as a poor quality indicator. We categorized readmissions into 4 groups (14-day, 30-day, 180-day and over 180-day) and evaluated each group¡¦s demographic, hospital characteristics, medical resource utilization, Charlson Comorbidity Index and medication utilizations of ACE inhibitor and ARB. We conducted descriptive analyses by using chi-square and t tests and applied multivariate logistic regression analyses to estimate the probabilities of hospital readmissions of heart failure patients. Population Studied Patients aged 50 or older with heart failure were identified based on the International Classification of Diseases, Ninth Revision, Clinical Modification (ICD-9-CM). Principle Findings Among 1920 heart failure patients, 19.9% of them were readmitted within 14 days, 7.6% were readmitted within 30 days and 26% were readmitted within 180 days. The medical resource utilizations such as average inpatients cost per patient, average outpatients cost per patient, total medical cost, average of inpatients times per patient and average of outpatients times per patient were significantly higher in patients with readmissions than those without readmission. Age, Charlson Comorbidity Index, patients who had been treated with ACE inhibitors and patients who had been treated with ARB were significantly affected the probabilities of readmissions. Conclusion The heart failure patients with readmissions had significantly higher medical resource utilizations than those without readmission. The medication uses of ACE inhibitors or ARB were significantly affected the probabilities of hospital readmissions. By understanding more about the influence factors of readmissions among heart failure patients, we may provide continue improvements of quality of care and reduce unnecessary medical costs. This study results provide useful reference for policy-makers to establish effective disease management program and appropriate health care financing arrangement in the future.

Submitted by Jorge Silva (jorgelmsilva@ufrrj.br) on 2018-10-16T18:19:32Z No. of bitstreams: 1 2013 - Gabriela Ferreira de Oliveira.pdf: 1149006 bytes, checksum: e5df0fd5e246ea685fd7bb50c7ab42d5 (MD5) / Made available in DSpace on 2018-10-16T18:19:32Z (GMT). No. of bitstreams: 1 2013 - Gabriela Ferreira de Oliveira.pdf: 1149006 bytes, checksum: e5df0fd5e246ea685fd7bb50c7ab42d5 (MD5) Previous issue date: 2013-08-12 / Sodium is the major electrolyte of the extra cellular space, essential for the control of plasma osmolality and blood pressure. In addition, sodium is the only mineral for which there is a defined appetite. For sodium homeostasis and for the regulation of extra cellular fluid, the reported physiological systems include the renin angiotensin aldosterone system, atrial natriuretic peptide and oxytocin. In mice the feeding behavior of sodium is well established and the central inhibition of sodium appetite has been demonstrated. However, in some domestic species, especially in horses, subject of this study, this behavior has not yet been clarified. This study aimed to evaluate the clinical and hematological effects, beyond the assessment of fluid and electrolyte balance and feeding behavior of fluids after the central administration of enalaprilat in horses experimentally dehydrated. Six adult, gelding horses, were used. The animals were subjected to water and food restriction for 72 hours prior the study, associated with the administration of three doses of furosemide in the first 24 hours. After the 72 hours fasting, the animals were divided into two experimental groups. The first group was called Control Group (CG) and the second, Treaty Group (TG). The animals of TG received 2.75 mg/animal of enalaprilat by intracarotideal route. After administration of enalaprilat, the animals had free access to water and hypertonic saline solution (1.8% of NaCl), with ingested volumes monitored. All animals were submitted to a regular and periodical physical examination, measured blood pressure and collected blood samples every 12 hours until the administration of enalaprilat, to evaluate the effects of dehydration; and 30, 60, 120, 180 minutes and 24 hours after administration, to evaluate the drug effects. Weight loss was the parameter that best reflected dehydration, which was estimated at 10.5% at the end of 72 hours of food and water restriction. When the animals had free access to water and saline, we observed a higher total water consumption in TG (13.7 ? 12 L) than in the CG (9.1 ? 7.9 L), with no significant difference between groups (p = 0.3522). There was no significant difference between GC and GT in clinical and hematological parameters, in all moments evaluated. Evaluating the sodium appetite, as evidenced by the ratio between salt intake and the amount of fluid consumed, it was observed that the TG showed lower sodium appetite than the CG (p = 0 0396), observed 120 minutes after the central administration of enalaprilat, demonstrating the centrally action of ACE inhibitor (enalaprilat) in inhibition of sodium appetite in horses. / O s?dio ? o principal eletr?lito do espa?o extracelular, fundamental para o controle da osmolaridade plasm?tica e press?o arterial, al?m de ser o ?nico mineral para qual existe um apetite claramente definido. Para a homeostase do s?dio e do fluido extracelular, os sistemas fisiol?gicos relatados incluem o sistema renina angiotensina aldosterona (SRAA), pept?deo natriur?tico atrial (ANP) e ocitocina (OT). O comportamento ingestivo de s?dio em ratos j? est? bem estabelecido e a inibi??o central do apetite por s?dio j? foi demonstrada. Por?m, em algumas esp?cies dom?sticas, especialmente nos equinos, tema deste trabalho, este comportamento ainda n?o foi esclarecido. O objetivo deste trabalho foi avaliar os efeitos cl?nicos e hematol?gicos, al?m da avalia??o do equil?brio hidroeletrol?tico e do comportamento ingestivo de l?quidos ap?s a administra??o central de enalaprilato em equinos experimentalmente desidratados. Foram utilizados seis equinos adultos, machos, castrados, que permaneceram em jejum h?drico e alimentar por 72 horas, associado ? administra??o de furosemida. Ap?s 72 horas de jejum, os animais foram divididos em dois grupos experimentais, o Grupo Controle (GC) e o Grupo Tratado (GT), que recebeu 2,75 mg/animal de enalaprilato por via intracarot?dea. Ap?s, os animais tiveram livre acesso a ?gua e a solu??o salina hipert?nica (1,8% de NaCl). Os animais foram avaliados atrav?s de exame cl?nico, a cada 12 horas durante as 72 horas de jejum e 30, 60, 120, 180 minutos e 24 horas ap?s o Enalaprilato. Foram avaliados o peso corporal, a quantidade de l?quidos ingeridos, a press?o arterial m?dia, par?metros bioqu?micos e eletrol?ticos sangu?neos. A perda de peso corporal foi o par?metro que melhor refletiu a desidrata??o, estimada em 10,5% ao final de 72 horas de jejum. Com o restabelecimento do acesso ? ?gua e solu??o salina, observou-se maior consumo total de ?gua no GT (13,7 ? 12 L) que no GC (9,1 ? 7,9 L), sem diferen?a significativa entre os grupos (p = 0,3522). N?o houve diferen?a significativa nos par?metros cl?nicos e hematol?gicos avaliados entre o GC e o GT. O apetite por s?dio foi reduzido significativamente (p = 0, 0396) no GT comparado ao GC, evidenciado 120 minutos ap?s a administra??o do enalaprilato, demonstrando a a??o central do inibidor de ECA (Enalaprilato) na inibi??o do apetite por s?dio em equinos.

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Submitted by Diogo Misoguti (diogo.misoguti@gmail.com) on 2016-06-29T12:59:34Z No. of bitstreams: 1 cp118956.pdf: 11152798 bytes, checksum: 413c607598471e1abd0db7c49883c8ac (MD5) / Approved for entry into archive by Diogo Misoguti (diogo.misoguti@gmail.com) on 2016-06-29T13:00:23Z (GMT) No. of bitstreams: 1 cp118956.pdf: 11152798 bytes, checksum: 413c607598471e1abd0db7c49883c8ac (MD5) / Made available in DSpace on 2016-06-29T13:00:23Z (GMT). No. of bitstreams: 1 cp118956.pdf: 11152798 bytes, checksum: 413c607598471e1abd0db7c49883c8ac (MD5) Previous issue date: 2009 / Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) / Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) / Com o crescente aumento da prevalência mundial de diabetes mellitus, tem-se buscado modelos experimentais para melhor compreensão de sua fisiopatologia e tratamento que atendam de maneira mais adequada à preservação de células beta, proteção de órgãos-alvo e atenuação da aterosclerose. Objetivos: Desenvolver modelo experimental de diabetes mellitus tipo 2 induzido por meio de dieta, e utilizá-lo para examinar os efeitos de um inibidor da enzima conversora de angiotensina (IECA) e de um bloqueador do receptor de angiotensina (BRA) na proteção de órgãos-alvo. Métodos: Coelhos machos Nova Zelândia (n=49) receberam dieta acrescida de banha (10%), sacarose (40%) durante todo o protocolo do estudo além de colesterol (0,5% nos três primeiros meses e 0,1% nos meses subseqüentes). Os animais receberam aleatoriamente: apenas a dieta sem fármacos (G1), olmesartana 5 mg (G2), quinapril 30 mg (G3), ou a combinação de ambos (G4), acrescidos à mesma dieta por seis meses. Foram analisados lípides, frutosamina, glicose e insulina em jejum com cálculo dos índices para resistência à insulina e função de células beta pancreáticas. Foram ainda examinadas as áreas sob as curvas de insulina e glicose, após infusão de glicose intraperitoneal. Angiofluoresceinografias e análises histopatológicas avaliaram lesões em órgãos-alvo. Resultados: Os coelhos ganharam peso, e houve aumento dos níveis de glicose, colesterol total, LDL-C e triglicérides e redução do HDL-C (p <0,05 vs. basal). A frutosamina e o HOMA-IR se elevaram, enquanto houve redução do HOMA-β (p <0,05 vs. basal). Sinais precoces de retinopatia diabética foram observados a partir do terceiro mês, progredindo até o final do experimento (p<0,0005). Lesões ateroscleróticas em aorta, esteatofibrose hepática e infiltrado glomerular de macrófagos constituíram os principais achados histomorfológicos. O bloqueio do sistema renina-angiotensina modificou favoravelmente a glicemia e o HOMA-β (p<0,05) e houve atenuação do número e grau dos microaneurismas pelo tratamento com BRA isoladamente ou combinado com IECA (p<0,05 vs. G1). Conclusões: Nosso modelo reproduziu várias características glucometabólicas do diabetes mellitus tipo 2 humanóide, incluindo déficit de secreção e resistência à insulina. O bloqueio do sistema renina-angiotensina atenuou algumas alterações bioquímicas e as lesões microvasculares em retina. / With the increasing prevalence of diabetes mellitus worldwide, new experimental models are required to better understand the pathophysiology of this disease and to offer therapeutic options that can preserve pancreatic beta-cells, protect target organs and attenuate atherosclerosis. Objective: The aims of this study were to develop an experimental model of type 2 diabetes mellitus induced by diet and assess on this model the effects of an angiotensin-converting enzyme inhibitor (ACEI) and an antagonist of the angiotensin II type1 receptor (AT1R) on target organ protection. Methods: New Zealand male white rabbits (n=49) were fed high-fat/high-sucrose (10/40%) during the study protocol and cholesterol-enriched diet (0.5% in the first three months followed by 0.1% until the end of the study). These animals were randomized to receive: diet alone (G1), olmesartan 5 mg (G2), quinapril 30mg (G3), or combination of both drugs (G4), added to the same diet for six months. Fasting lipids, fructosamine, glucose and insulin, with calculation of insulin resistance and beta-cell function indexes were evaluated. The areas under the curves for glucose and insulin were obtained after intraperitoneal glucose bolus injection. Fluorescein angiography and histopathological analyses were performed to assess target-organs lesions. Results: The animals gained weight, and there were increases in blood glucose, total cholesterol, LDL-C and triglycerides, and decrease in HDL-C (p<0.05 vs. baseline). Fructosamine levels and the homeostasis model assessment of insulin resistance (HOMA-IR) were increased, while there was a reduction in the HOMA-β (p<0.05 vs. baseline). Early clinical features of diabetic retinopathy were seen since the third month, progressing up to the end of the experiment (p<0.0005). Aortic atherosclerosis, hepatic steatofibrosis and glomerular macrophage infiltration were the main histomorphologic findings of this study. The renin-angiotensin system (RAS) blockade favorably modified blood glucose and the HOMA- β (p<0.05) and promoted attenuation of the number and grade of microaneurysms in retina in the group of animals receiving AT1R antagonist or combined therapy with the ACEI (p<0.05 vs. G1). Conclusion: Our model reproduced several glucometabolic characteristics of humanoid type 2 diabetes, including decreased insulin secretion and insulin resistance. The RAS blockade attenuated some biochemical abnormalities and the diabetic retinopathy. / FAPESP: 07/51058-8

An Herzinsuffizienz sind in Deutschland weit mehr als 1 Mio. Menschen erkrankt. Ihre Häufigkeit steigt stetig an. Die Herzinsuffizienz wird als dominierende Herz-Kreislauf-Erkrankung des 21. Jahrhunderts angesehen. Die Hauptursache der Herzinsuffizienz ist die koronare Herzerkrankung besonderes nach stattgehabtem Myokardinfarkt. Sowohl für den akuten Myokardinfarkt als auch für die sich auf dieser Basis entwickelnde Herzinsuffizienz werden Veränderungen im Stoffwechsel der Sauerstoffradikale als pathophysiologisch bedeutsam angesehen. Es wird angenommen, dass als Folge der akuten Myokardischämie oxidativer Stress im Myokard hervorgerufen wird. Dieser kann über die akute Infarktphase hinaus prolongieren. Dadurch werden Mechanismen induziert (Hypertrophie und Apoptose, Störung myokardialer Signaltransduktion), die letztlich zur Herzinsuffizienz führen. Folgerichtig sollten therapeutische Maßnahmen, die zu einer Minimierung von oxidativem Stress führen, protektiv wirken. Im Rahmen dieser Arbeit wurde am Modell des Ligaturinfarktes der Ratte gezeigt, dass es in der Akutphase des Infarktes (30-36 h nach Ligatur) zu gesteigertem oxidativen Stress kommt. Dieser ließ sich anhand gesteigerter myokardialer Konzentration an Lipidperoxiden, die mit einer verminderten Konzentration antioxidativer Enzyme im Herz kombiniert war, dokumentieren. Werden solche Tiere 6 Wochen nach Ligatur untersucht, weisen sie im Herz im Vergleich zu scheinoperierten Tieren eine signifikant erhöhte Konzentration von Lipidperoxiden als Zeichen gesteigerten oxidativen Stresses auf. Parallel dazu werden typische Zeichen einer Herzinsuffizienz (Herzhypertrophie, erhöhter LVEDP, verminderte Kontraktilität) beobachtet. Wurden solche Tiere beginnend nach der akuten Myokardphase mit dem ACE-Hemmer Ramipril und dem Beta-Blocker Metoprolol behandelt - von beiden ist bekannt, dass sie protektiv in den Stoffwechsel der Sauerstoffradikale eingreifen können - wurde ein geringerer myokardialer oxidativer Stress beobachtet, der mit einer verminderten Ausprägung der morphologischen und funktionellen Herzinsuffizienzzeichen einherging. Die kombinierte Gabe von Beta-Blocker und ACE-Hemmer erwies sich dabei sowohl in der Reduktion von oxidativem Stress als auch in ihrem Einfluss auf Herzfunktion und Morphologie den Einzeltherapien überlegen. Als wesentlich für die Reduktion von oxidativem Stress durch Beta-Blockade und ACE-Hemmung wurde die kompensatorische Zunahme des enzymatischen antioxidativen Schutzes im Herz (GSH-Px, SOD) ausgewiesen. / In Germany, more than 1 million people suffer from heart failure and the incidence is continuously growing. Consequently, heart failure is accepted to be the dominant disease of the heart and circulatory system in the 21st century. The main reason for heart failure is coronary heart disease in general, and especially myocardial infarction (MI). Changes in the oxygen radical metabolism are thought to be essential in the pathogenesis of myocardial infarction and heart failure as its important consequence. It is supposed that, as a result of myocardial ischemia, oxidative stress arises in the heart, which can activate and prolong mechanisms (hypertrophy, apoptosis, disturbed signal transduction) well documented to result in heart failure. Consequently, treatment, which reduces the myocardial oxidative stress, should be beneficial. Using the model of ligature infarction in rats, our study shows increased myocardial oxidative stress in the acute phase of MI (30-36 h after ligature) documented by increased concentration of lipid peroxides (LPO) combined with reduced activity of the antioxidative enzymes. When the animals were analyzed 6 weeks after ligature in comparison to sham operated animals, increased oxidative stress and in parallel typical signs for heart failure (myocardial hypertrophy, increased LVEDP, reduced contractility) were observed. Treatment of the animals starting after acute myocardial infarction with the ACE-inhibitor Ramipril and the beta-blocker Metoprolol - both are known to interfere protectively with the oxygen radical metabolism - reduced the myocardial oxidative stress and the morphological and functional signs of failing heart. This effect was most impressive after combined treatment with Metoprolol and Ramipril. The elevated enzymatic antioxidative defense (GSH-Px, SOD) which we found in the heart after beta-blockade and ACE inhibition could be the reason.

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Part I. The aldosterone synthase gene (CYP11B2) polymorphism T-344C in blood pressure and left ventricular hypertrophy. BACKGROUND: Aldosterone is a key cardovascular hormone, it significantly influences volume, pressure and electrolyte balance. Aldosterone plays an important role in development of left ventricular (LV) hypertrophy and myocardial fibrosis. The aldosterone synthase gene (CYP11B2) is an important candidate gene region in essential hypertension. DESIGN AND METHODS: We assessed the influence of the T-344C polymorphism of aldosterone synthase - the rate-limiting enzyme in aldosterone biosynthesis - on the structure of the left ventricle in young normotensive men. The population included 113 normotensive mid-European Caucasian men aged 18-40 years (mean 27 +/- 5 years). We also studied the association of -344T/C polymorphism of the CYP11B2 gene with the presence and severity of hypertension in 369 individuals, of whom 213 were hypertensive patients (139 controlled hypertensive, 74 resistant hypertensive) and 156 were healthy normotensive subjects. The genotype was assessed using polymerase chain reaction with subsequent cleavage with restriction enzyme HAEIII (restriction fragment length polymorphism method) and visualization with ethidium bromide. Plasma renin activity (PRA) and plasma...