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Made available in DSpace on 2013-09-27T14:54:31Z (GMT). No. of bitstreams: 1 WOS000312617200009.pdf: 741557 bytes, checksum: 1d8ed96b189668ac8d85325afa301b91 (MD5) Previous issue date: 2012-01-01 Made available in DSpace on 2013-09-30T18:38:41Z (GMT). No. of bitstreams: 1 WOS000312617200009.pdf: 741557 bytes, checksum: 1d8ed96b189668ac8d85325afa301b91 (MD5) Previous issue date: 2012-01-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:51:15Z No. of bitstreams: 1 WOS000312617200009.pdf: 741557 bytes, checksum: 1d8ed96b189668ac8d85325afa301b91 (MD5) Made available in DSpace on 2014-05-20T13:51:15Z (GMT). No. of bitstreams: 1 WOS000312617200009.pdf: 741557 bytes, checksum: 1d8ed96b189668ac8d85325afa301b91 (MD5) Previous issue date: 2012-01-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Background/Aims: Renin-angiotensin-aldosterone system blockade with a mineralocorticoid-receptor antagonist has not yet been studied in exposure to tobacco smoke (TS) models. Thus, this study investigated the role of spironolactone on cardiac remodeling induced by exposure to tobacco smoke. Methods: Male Wistar rats were divided into 4 groups: a control group (group C, n=11); a group with 2 months of cigarette smoke exposure (group TS-C, n=13); a group that received spironolactone 20 mg/kg of diet/day and no cigarette smoke exposure (group TS-S, n=13); and a group with 2 months of cigarette smoke exposure and spironolactone supplementation (group S, n=12). The rats were observed for a period of 60 days, during which morphological, biochemical and functional analyses were performed. Results: There was no difference in invasive mean arterial pressure among the groups. There were no interactions between tobacco smoke exposure and spironolactone in the morphological and functional analysis. However, in the echocardiographic analysis, the TS groups had left chamber enlargement, higher left ventricular mass index and higher isovolumetric relaxation time corrected by heart rate compared with the non-TS groups. In vitro left ventricular diastolic function also worsened in the IS groups and was not influenced by spironolactone. In addition, there were no differences in myocardial levels of IFN-gamma, TNF-alpha, IL-10, ICAM-1 and GLUT4 [TS: OR 0.52, 95%CI (-0.007; 0.11); Spironolactone: OR -0.01, 95%CI (-0.07;0.05)]. Conclusion: Our data do not support the participation of aldosterone in the ventricular remodeling process induced by exposed to cigarette smoke. Copyright (C) 2012 S. Karger AG, Basel Univ Estadual Paulista UNESP, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil São Paulo State Univ, Inst Biosci, Dept Microbiol & Immunol, Botucatu, SP, Brazil Univ Estadual Paulista UNESP, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil São Paulo State Univ, Inst Biosci, Dept Microbiol & Immunol, Botucatu, SP, Brazil FAPESP: 10/10187-2 CNPq: 473091/2010-0

Made available in DSpace on 2022-04-29T04:10:42Z (GMT). No. of bitstreams: 0 Previous issue date: 2012-01-01 Background: The objective of this study was to determine the early echocardiographic predictors of elevated left ventricular end-diastolic pressure (LVEDP) after a long follow-up period in the infarcted rat model. Material/Methods: Five days and three months after surgery, sham and infarcted animals were subjected to transthoracic echocardiography. Regression analysis and receiver-operating characteristic (ROC) curve were performed for predicting increased LVEDP 3 months after MI. Results: Among all of the variables, assessed 5 days after myocardial infarction, infarct size (OR: 0.760; CI 95% 0.563-0.900; p=0.005), end-systolic area (ESA) (OR: 0.761; CI 95% 0.564-0.900; p=0.008), fractional area change (FAC) (OR: 0.771; CI 95% 0.574-0.907; p=0.003), and posterior wall-shortening velocity (PWSV) (OR: 0.703; CI 95% 0.502-0.860; p=0.048) were predictors of increased LVEDP. The LVEDP was 3.6±1.8 mmHg in the control group and 9.4±7.8 mmHg among the infarcted animals (p=0.007). Considering the critical value of predictor variables in inducing cardiac dysfunction, the cut-off value was 35% for infarct size, 0.33 cm2 for ESA, 40% for FAC, and 26 mm/s for PWSV. Conclusions: Infarct size, FAC, ESA, and PWSV, assessed five days after myocardial infarction, can be used to estimate an increased LVEDP three months following the coronary occlusion. © Med Sci Monit. Department of Internal Medicine Botucatu Medical School UNESP, Botucatu Department of Internal Medicine Botucatu Medical School UNESP, Botucatu

FUNDAMENTO: A predição do processo de remodelação ventricular após o infarto agudo do miocárdio (IAM) pode ter importantes implicações clínicas. OBJETIVO: Analisar as variáveis ecocardiográficas preditoras da remodelação no modelo do infarto em ratos. MÉTODOS: Os animais foram submetidos ao ecocardiograma em dois momentos, cinco dias e três meses após o infarto (grupo IAM) ou a cirurgia simulada (grupo controle). A regressão linear foi utilizada para identificar as variáveis ecocardiográficas no quinto dia posteriormente ao infarto, as quais foram preditoras de remodelação depois de três meses da oclusão coronariana. Consideramos, como critério de remodelação, neste estudo, os valores do diâmetro diastólico do ventrículo esquerdo (DDVE) após três meses do infarto. RESULTADOS: O infarto induziu o aumento das câmaras esquerdas, associado com alterações das funções sistólica e diastólica. As variáveis peso corporal, índice do estresse parietal ventricular esquerdo (IEPVE), área sistólica (AS), área diastólica (AD), DDVE, diâmetro sistólico do ventrículo esquerdo (DSVE), fração de variação de área (FVA), fração de ejeção (FE), porcentagem de encurtamento endocárdico (% Enc), velocidade de encurtamento da parede posterior (VEPP) e tamanho do infarto, avaliadas cinco dias depois do infarto, foram preditoras do DDVE após três meses. Na análise de regressão multivariada, incluímos o tamanho do infarto, o IEPVE e a VEPP. O IEPVE (coeficiente: 4,402, erro padrão: 2,221, p = 0,05), mas não o tamanho do infarto e a VEPP, foi fator preditor de remodelação após três meses do infarto. CONCLUSÃO: O IEPVE foi preditor independente de remodelação após três meses do infarto e poderia ser incorporado na estratificação clínica depois da oclusão coronariana. BACKGROUND: The prediction of the ventricular remodeling process after acute myocardial infarction (AMI) may have important clinical implications. OBJECTIVE: To analyze echocardiographic variables predictors of remodeling in the infarction model in rats. MEHTODS: The animals underwent echocardiography in two moments, five days and three months after infarction (AMI group) or sham surgery (control group). Linear regression was used to identify the echocardiographic variables on the fifth day after the infarction, which were predictive of remodeling after three months of coronary occlusion. We considered as a criterion of remodeling in this study, the values of left ventricular diastolic diameter (LVDD) after three months of infarction. RESULTS: The infarction induced increase in the left chambers, associated with changes in systolic and diastolic functions. The variables body weight, left ventricular wall stress index (LVWSI), systolic area (SA), diastolic area (DA), LVDD, left ventricular systolic diameter (LVSD), area variation fraction (AVF), ejection fraction (EF), percent of endocardial shortening (%Short), posterior wall shortening velocity (PWSV) and infarct size assessed five days after infarction were predictors of LVDD after three months. At the multivariate regression analysis, we included the size of infarction, the LVWSI and PWSV. The LVWSI (coefficient: 4.402, standard error: 2.221, p = 0.05), but not the size of infarction and PWSV, was a predictor of remodeling after three months of infarction. CONCLUSION: LVPSI was an independent predictor of remodeling three months after the myocardial infarction and could be included in the clinical stratification after the coronary occlusion.

Made available in DSpace on 2013-08-12T18:57:41Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-01 Made available in DSpace on 2013-09-30T18:17:05Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:33:23Z No. of bitstreams: 0 Made available in DSpace on 2014-05-20T13:33:23Z (GMT). No. of bitstreams: 0 Previous issue date: 2011-07-01 Heart failure is a frequent complication of myocardial infarction. Several factors, such as recurrent myocardial ischemia, infarct size, ventricular remodeling, stunned myocardium, mechanical complications, and hibernating myocardium influence the appearance of left ventricular systolic dysfunction after myocardial infarction. Importantly, its presence increases the risk of death by at least 3- to 4-fold. The knowledge of the mechanisms and clinical features are essential for the diagnosis and treatment of left ventricular dysfunction and heart failure after myocardial infarction. Therefore, this review will focus on the clinical implications and treatment of heart failure after myocardial infarction. UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil UNESP Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil

Made available in DSpace on 2013-09-27T14:54:30Z (GMT). No. of bitstreams: 1 WOS000290594900015.pdf: 245307 bytes, checksum: b0a257abfedc947985c4d456f585bc8a (MD5) Previous issue date: 2011-01-01 Made available in DSpace on 2013-09-30T18:40:55Z (GMT). No. of bitstreams: 1 WOS000290594900015.pdf: 245307 bytes, checksum: b0a257abfedc947985c4d456f585bc8a (MD5) Previous issue date: 2011-01-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:50:52Z No. of bitstreams: 1 WOS000290594900015.pdf: 245307 bytes, checksum: b0a257abfedc947985c4d456f585bc8a (MD5) Made available in DSpace on 2014-05-20T13:50:52Z (GMT). No. of bitstreams: 1 WOS000290594900015.pdf: 245307 bytes, checksum: b0a257abfedc947985c4d456f585bc8a (MD5) Previous issue date: 2011-01-01 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Background: Recent studies have assessed the direct effects of smoking on cardiac remodeling and function. However, the mechanisms of these alterations remain unknown. The aim of this study was to investigate de role of cardiac NADPH oxidase and antioxidant enzyme system on ventricular remodeling induced by tobacco smoke. Methods: Male Wistar rats that weighed 200-230 g were divided into a control group (C) and an experimental group that was exposed to tobacco smoke for a period of two months (ETS). After the two-month exposure period, morphological, biochemical and functional analyses were performed. Results: The myocyte cross-sectional area and left ventricle end-diastolic dimension was increased 16.2% and 33.7%, respectively, in the ETS group. The interstitial collagen volume fraction was also higher in ETS group compared to the controls. In addition to these morphological changes, the ejection fraction and fractional shortening were decreased in the ETS group. Importantly, these alterations were related to augmented heart oxidative stress, which was characterized by an increase in NADPH oxidase activity, increased levels of lipid hydroperoxide and depletion of antioxidant enzymes (e.g., catalase, superoxide dismutase and glutathione peroxidase). In addition, cardiac levels of IFN-gamma, TNF-alpha and IL-10 were not different between the groups. Conclusion: Cardiac alterations that are induced by smoking are associated with increased NADPH oxidase activity, suggesting that this pathway plays a role in the ventricular remodeling induced by exposure to tobacco smoke. Copyright (C) 2011 S. Karger AG, Basel Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil Univ Estadual Paulista, Inst Biol Sci, Dept Chem & Biochem, Botucatu, SP, Brazil Univ São Paulo, Sch Med, Heart Inst InCor, Vasc Biol Lab, São Paulo, Brazil São Paulo State Univ, Inst Biosci, Dept Microbiol & Immunol, Botucatu, SP, Brazil Univ Estadual Paulista, Botucatu Med Sch, Dept Internal Med, Botucatu, SP, Brazil Univ Estadual Paulista, Inst Biol Sci, Dept Chem & Biochem, Botucatu, SP, Brazil São Paulo State Univ, Inst Biosci, Dept Microbiol & Immunol, Botucatu, SP, Brazil

Made available in DSpace on 2013-09-27T14:54:30Z (GMT). No. of bitstreams: 1 WOS000290594900013.pdf: 985087 bytes, checksum: e8d3ad68a7bd4c88c546df17eb21e0b5 (MD5) Previous issue date: 2011-01-01 Made available in DSpace on 2013-09-30T18:40:55Z (GMT). No. of bitstreams: 1 WOS000290594900013.pdf: 985087 bytes, checksum: e8d3ad68a7bd4c88c546df17eb21e0b5 (MD5) Previous issue date: 2011-01-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:50:53Z No. of bitstreams: 1 WOS000290594900013.pdf: 985087 bytes, checksum: e8d3ad68a7bd4c88c546df17eb21e0b5 (MD5) Made available in DSpace on 2014-05-20T13:50:53Z (GMT). No. of bitstreams: 1 WOS000290594900013.pdf: 985087 bytes, checksum: e8d3ad68a7bd4c88c546df17eb21e0b5 (MD5) Previous issue date: 2011-01-01 Background/Aims: To investigate the effect of taurine on cardiac remodeling induced by smoking. Methods: In the first step, rats were allocated into two groups: Group C (n=14): control; Group T (n=14): treated with taurine (3% in drinking water), for three months. In the second step, rats were allocated into two groups: Group ETS (n=9): rats exposed to tobacco smoke; Group ETS-T (n=9): rats exposed to tobacco smoke and treated with taurine for two months. Results: After three months, taurine presented no effects on morphological or functional variables of normal rats assessed by echocardiogram. on the other hand, after two months, ETS-T group presented higher LV wall thickness (ETS=1.30 (1.20-1.42); ETS-T=1.50 (1.40-1.50); p=0.029), E/A ratio (ETS=1.13 +/- 0.13; ETS-T=1.37 +/- 0.26; p=0.028), and isovolumetric relaxation time normalized for heart rate (ETS=53.9 +/- 4.33; ETS-T=72.5 +/- 12.0; p

Heart failure is characterized by a decreased exercise capacity due to the early appearance of symptoms like dyspnoea and muscle fatigability. Although these symptoms can be caused by reduced cardiac output, there is no clear association between exercise intolerance and hemodynamic parameters (Mancini et al. 1992; Harrington et al. 2001). It has been suggested that intrinsic skeletal muscle abnormalities play a role in decreased exercise capacity and heart failure symptoms (Vescovo et al. 1998). Muscle wasting is common in chronic illnesses such as those associated with HIV infection, some types of cancer, and heart failure (Mancini et al. 1992; Gonzalez-Cadavid et al. 1998; Bruera & Sweeney 2000). The mechanisms responsible for muscle atrophy in heart failure are not clear. Myostatin, a recently identified member of the transforming growth factor beta (TGF-β) superfamily of secreted growth and differentiation factors, regulates muscle growth, acting as a negative regulator of skeletal muscle mass (McPherron et al. 1997; Lee 2004). Several studies have shown a negative correlation between myostatin expression and muscle mass. Mutations of myostatin gene in cattle are associated with muscle hypertrophy (McPherron & Lee 1997). Similarly, myostatin-null mice present increased muscle mass, resulting from both muscle fibre hyperplasia and hyperthrophy (McPherron et al. 1997). Pharmacological treatment with a myostatin antibody increased skeletal muscle mass and grip strength (Whittemore et al. 2003). Furthermore, systemic overexpression of myostatin in adult mice was found to induce profound muscle and fat loss (Zimmers et al. 2002). In a clinical setting, recent investigations have suggested that myostatin may be involved in the muscle mass reduction observed in AIDS and cancer patients (Gonzalez-Cadavid et al. 1998; Acharyya & Gutttridge 2007). In HIV-infected men, increased levels of myostatin immunoreactive material in serum and skeletal muscle appear to correlate with the presence of cachexia (Gonzalez-Cadavid et al. 1998). In heart failure, the role of myostatin on skeletal muscle wasting remains unclear. Recently, Lenk et al. (2009) reported that myostatin was up-regulated in cardiac and skeletal muscle during experimental heart failure. The aim of this study was to evaluate myostatin mRNA and protein expression and skeletal muscle trophism in rats with myocardial infarction-induced heart failure. As myostatin expression can be modulated by follistatin, an antagonistic protein, we also evaluated follistatin expression.

Coronary heart disease (CHD) is the most common cause of death in many developed countries. The major risk factors for CHD are smoking, high blood pressure, diabetes, high cholesterol levels, and lack of physical activity. Importantly, passive smoke also increases the risk for CHD. The mechanisms involved in the effects of passive smoke in CHD are complex and include endothelial dysfunction, lipoprotein modification, increased inflammation and platelet activation. Recently, several studies have shown that exposure to tobacco smoke can result in cardiac remodeling and compromised cardiac function. Potential mechanisms for these alterations are neurohumoral activation, oxidative stress, and MAPK activation. Although the vascular effects of cigarette smoke exposure are well known, the effects of tobacco smoking on the heart have received less attention. Therefore, this review will focus on the recent findings as to the effects of passive smoking in acute and chronic phases of vascular and cardiac remodeling.

FUNDAMENTO: O papel do sistema adrenérgico na remodelação induzida pelo tabagismo é desconhecido. OBJETIVO: Investigar a influência do propranolol na remodelação induzida pela exposição à fumaça de cigarro. MÉTODOS: Ratos foram alocados em três grupos: 1) C, n=10 - animais controle; 2) F, n=10 - animais expostos à fumaça de cigarro; 3) BB, n=10 - animais expostos à fumaça de cigarro e que receberam propranolol (40 mg/kg/dia). Após dois meses, os animais foram submetidos a estudo ecocardiográfico e morfométrico. Utilizou-se análise de variância (ANOVA) de uma via (média ± desvio padrão) ou Kruskal-Wallis (mediana e intervalo interquartil). RESULTADOS: O Grupo BB apresentou menor frequência cardíaca que o Grupo F (C = 358 ± 74 btm, F = 374 ± 53 bpm, BB = 297 ± 30; P = 0,02). O Grupo F apresentou maiores diâmetros diastólicos (C = 18,6 ± 3,4 mm/kg, F = 22,8 ± 1,8 mm/kg, BB = 21,7 ± 1,8 mm/kg; P = 0,003) e sistólicos (C = 8,6 ± 2,1 mmkg, F = 11,3 ± 1,3 mm/kg, BB = 9,9 ± 1,2 mm/kg; P = 0,004) do ventrículo esquerdo (VE), ajustado ao peso corporal (PC) e tendência de menor fração de ejeção (C = 0,90 ± 0,03, F = 0,87 ± 0,03, BB =0,90 ± 0,02; P = 0,07) que o Grupo C. O Grupo BB apresentou tendência de menor relação VE/PC que o Grupo F (C = 1,94 (1,87 - 1,97), F = 2,03 (1,9-2,1) mg/g, BB = 1,89 (1,86-1,94); P = 0,09). CONCLUSÃO: A administração de propranolol atenuou algumas variáveis da remodelação ventricular induzida pela exposição à fumaça do cigarro em ratos. BACKGROUND: The role of the adrenergic system on ventricular remodeling induced by cigarette smoking is unknown. OBJECTIVES: To investigate the influence of propranolol on ventricular remodeling induced by exposure to tobacco smoke. METHODS: Rats were divided into three groups: 1) C, n=10 - control group; 2) F, n=10 - animals exposed to tobacco smoke; 3) BB, n=10 - animals receiving propranolol and exposed to tobacco smoke (40 mg/kg/day). After 2 months, the animals underwent echocardiographic and morphometric analyses. One-way ANOVA (mean ± standard deviation) or the Kruskal-Wallis test (median and interquartile interval) was used. RESULTS: Group BB showed a lower heart rate than group F (C = 358 ± 74 bpm, F = 374 ± 53 bpm, BB = 297 ± 30; P = 0.02). Group F showed greater end-diastolic diameters (C = 18.6 ± 3.4 mm/kg, F = 22.8 ± 1.8 mm/kg, BB = 21.7 ± 1.8 mm/kg; P = 0.003) and left ventricular (LV) end-systolic diameters (C = 8.6 ± 2.1 mm/kg, F = 11.3 ± 1.3 mm/kg, BB = 9.9 ± 1.2 mm/kg; P = 0.004), adjusted for body weight (BW) and a tendency towards a lower ejection fraction (C = 0.90 ± 0.03, F = 0.87 ± 0.03, BB =0.90 ± 0.02; P = 0.07) than group C. Group BB showed a tendency towards a lower LV/BW ratio than group F (C = 1.94 (1.87 - 1.97), F = 2.03 (1.9-2.1) mg/g, BB = 1.89 (1.86-1.94); P = 0.09). CONCLUSION: Administration of propranolol attenuated some of the variables of ventricular remodeling induced by the exposure to tobacco smoke in rats. FUNDAMENTO: Aún se desconoce el rol del sistema adrenérgico en la remodelación inducida por el tabaquismo. OBJETIVO: Investigar la influencia del propranolol en la remodelación inducida por la exposición al humo del cigarrillo. MÉTODOS: Se dividieron las ratas en tres grupos: 1) C, n=10 - animales control; 2) F, n=10 - animales expuestos al humo de cigarrillo; 3) BB, n=10 - animales expuestos al humo de cigarrillo y que recibieron propranolol (40 mg/kg/día). Tras dos meses, los animales fueron sometidos a estudio ecocardiográfico y morfométrico. Se empleó el análisis de varianza (ANOVA) de una vía (promedio ± desviación estándar) o Kruskal-Wallis (mediana e intervalo intercuartil). RESULTADOS: El Grupo BB presentó menor frecuencia cardiaca que el Grupo F (C = 358 ± 74 lpm, F = 374 ± 53 lpm, BB = 297 ± 30; P = 0,02). El Grupo F presentó mayores diámetros diastólicos (C = 18,6 ± 3,4 mm/kg, F = 22,8 ± 1,8 mm/kg, BB = 21,7 ± 1,8 mm/kg; P = 0,003) y sistólicos (C = 8,6 ± 2,1 mm/kg, F = 11,3 ± 1,3 mm/kg, BB = 9,9 ± 1,2 mm/kg; P = 0,004) del ventrículo izquierdo (VI), ajustado al peso corporal (PC) y tendencia de menor fracción de eyección (C = 0,90 ± 0,03, F = 0,87 ± 0,03, BB =0,90 ± 0,02; P = 0,07) que el Grupo C. El Grupo BB presentó tendencia de menor relación VI/PC que el Grupo F (C = 1,94 (1,87 - 1,97), F = 2,03 (1,9-2,1) mg/g, BB = 1,89 (1,86-1,94); P = 0,09). CONCLUSIÓN: La administración de propranolol atenuó algunas variables de la remodelación ventricular inducida por la exposición al humo del cigarrillo en ratas.

Made available in DSpace on 2018-12-11T17:29:34Z (GMT). No. of bitstreams: 0 Previous issue date: 2016-08-01. Added 1 bitstream(s) on 2019-10-09T18:32:39Z : No. of bitstreams: 1 S1807-59322016000800470.pdf: 341861 bytes, checksum: 531786629f0ab751fa3f3a1b78516fec (MD5) OBJECTIVE: The aim of this study was to evaluate the roles of the Taql and Bsml vitamin D receptor gene polymorphisms in hospital mortality of burn patients. METHODS: In total, 105 consecutive burn injury patients over 18 years in age who were admitted to the Burn Unit of Bauru State Hospital from January to December 2013 were prospectively evaluated. Upon admission, patient demographic information was recorded and a blood sample was taken for biochemical analysis to identify the presence of the Taql(rs731236) and Bsml(rs1544410) polymorphisms. All of the patients were followed over their hospital stay and mortality was recorded. RESULTS: Eighteen of the patients did not sign the informed consent form, and there were technical problems with genotype analysis for 7 of the patients. Thus, 80 patients (mean age, 42.5�16.1 years) were included in the final analysis. In total, 60% of the patients were male, and 16.3% died during the hospital stay. The genotype frequencies for the Taql polymorphism were 51.25% TT, 41.25% TC and 7.50% CC; for the Bsml polymorphism, they were 51.25% GG, 42.50% GA and 6.25% AA. In logistic regression analysis, after adjustments for age, gender and total body surface burn area, there were no associations between the Taql (OR: 1.575; CI95%: 0.148- 16.745; p=0.706) or Bsml (OR: 1.309; CI95%: 0.128-13.430; p=0.821) polymorphisms and mortality for the burn patients. CONCLUSIONS: Our results suggest that the Taql and Bsml vitamin D receptor gene polymorphisms are not associated with hospital mortality of burn patients. Universidade Estadual Paulista – UNESP Faculdade de Medicina de Botucatu Departamento de Medicina Interna Instituto Federal S�o Paulo – IFSP, Campus S�o Roque Universidade Estadual Paulista – UNESP Faculdade de Medicina de Botucatu Departamento de Medicina Interna

Background: Heart failure prediction after acute myocardial infarction may have important clinical implications. Objective: To analyze the functional echocardiographic variables associated with heart failure in an infarction model in rats. Methods: The animals were divided into two groups: control and infarction. Subsequently, the infarcted animals were divided into groups: with and without heart failure. The predictive values were assessed by logistic regression. The cutoff values predictive of heart failure were determined using ROC curves. Results: Six months after surgery, 88 infarcted animals and 43 control animals were included in the study. Myocardial infarction increased left cavity diameters and the mass and wall thickness of the left ventricle. Additionally, myocardial infarction resulted in systolic and diastolic dysfunction, characterized by lower area variation fraction values, posterior wall shortening velocity, E-wave deceleration time, associated with higher values of E / A ratio and isovolumic relaxation time adjusted by heart rate. Among the infarcted animals, 54 (61%) developed heart failure. Rats with heart failure have higher left cavity mass index and diameter, associated with worsening of functional variables. The area variation fraction, the E/A ratio, E-wave deceleration time and isovolumic relaxation time adjusted by heart rate were functional variables predictors of heart failure. The cutoff values of functional variables associated with heart failure were: area variation fraction < 31.18%; E / A > 3.077; E-wave deceleration time < 42.11 and isovolumic relaxation time adjusted by heart rate < 69.08. Conclusion: In rats followed for 6 months after myocardial infarction, the area variation fraction, E/A ratio, E-wave deceleration time and isovolumic relaxation time adjusted by heart rate are predictors of heart failure onset.

To investigate the role of MMP-2 and MMP-9 in cardiac remodelling induced by tobacco smoke exposure in rats.Rats were allocated into two groups: C (n=9): control animals; ETS (n=9): exposed to tobacco smoke. After 4months, the animals underwent echocardiography, morphometric study and determination of MMP-2 and MMP-9 activity.ETS rats had larger diastolic (C=15.6 +/-1.2 mm/kg, ETS=18.0+/-0.9 mm/kg; p0.001) and systolic (C=7.3+/-1.2 mm/kg, ETS=9.2+/-0.9 mm/kg; p=0.001) ventricular diameters adjusted for body weight. Fractional shortening (C=53+/-4.8%, ETS=48+/- 3.3%; p=0.031) and ejection fraction (C=0.89+/-0.03, ETS=0.86+/-0.02; p=0.030) were smaller in the ETS group. Myocyte cross-sectional area (C=245+/-8 microm2, ETS=253+/-8 microm2; p=0.028) was higher in ETS rats. There were no differences in MMP-2 (C=50+/-14%; ETS=43+/-11%, p=0.228) or MMP-9 (C=0.36+/-0.3%; ETS=0.62+/-0.3%, p=0.630) activity between the groups.MMP-2 and MMP-9 did not participate in the remodelling process induced by tobacco smoke exposure.

Made available in DSpace on 2021-07-14T10:37:25Z (GMT). No. of bitstreams: 0 Previous issue date: 2007-08. Added 1 bitstream(s) on 2021-07-14T11:34:31Z : No. of bitstreams: 1 S0100-55022007000200011.pdf: 218141 bytes, checksum: cba793d7bb59d9593956d016778f7c31 (MD5) Na Faculdade de Medicina de Botucatu (FMB), os cursos de clínica médica (CM) vêm sendo tradicionalmente ministrados nas enfermarias, ambulatórios, UTI e pronto-socorro do Hospital das Clínicas da FMB, sob a supervisão do Departamento de CM. Em outubro de 2002, a FMB passou a gerenciar o Hospital Estadual Bauru (HEB), tornando possível a transferência de parte do ensino de CM no internato para hospital secundário. Desde janeiro de 2004, grupos de internato, compostos por oito alunos, passaram a estagiar em enfermaria de clínica geral do HEB, sob a supervisão de preceptores da disciplina de CM geral. Entre as vantagens decorrentes dessa mudança, citamos a possibilidade de atender doentes com patologias mais simples, maior responsabilidade com o paciente, maior contato com o preceptor e o aprendizado sobre a necessidade de cumprir metas estabelecidas pelo hospital. A principal dificuldade na execução do estágio é a sobrecarga de trabalho para os preceptores, que é causada, em parte, pela ausência de residentes na enfermaria. Consideramos que a experiência em transferir parte do internato de CM para hospital secundário foi bem-sucedida e esta pode vir a estimular outras áreas da FMB para a busca de novos cenários de ensino. In the Botucatu School of Medicine (BSM), the internal medicine course has traditionally been run in the infirmaries, out-patient clinics, emergency unit, and intensive care unit of the BSM Hospital under the supervision of the Internal Medicine Department. In October 2002, BSM took over the management of the Bauru State Hospital (BSH) making possible to transfer part of the internal medicine training program to a secondary level hospital. Since January 2004, groups of eight students have stayed for a training program at the BSH Internal Medicine Infirmary under the supervision of internal medicine teaching doctors. Advantages of this scheme include exposing students to the simpler pathologies found in the general population, more responsibility with the patient, more contact between student and teacher, and learning about the need to reach the goals set by the hospital. The main functional difficulty of this training program is the heavy workload the teaching doctors have to face, in part due to the absence of residents in the infirmary. In conclusion, we consider the experience of transferring part of internal medicine training program to a secondary hospital has been a success and capable of stimulating other medical disciplines in the BSM to look for new settings for their training programs. Universidade Estadual Paulista Universidade Estadual Paulista, Hospital Estadual Bauru Universidade Estadual Paulista Universidade Estadual Paulista, Hospital Estadual Bauru

The aim of this study was to evaluate the effects of tomato supplementation on the normal rat heart and the role of oxidative stress in this scenario. Male Wistar rats were assigned to two groups: a control group (C, n = 16), in which animals received a control diet + 0.5 mL of corn oil/kg body weight/day, and a tomato group (T, n = 16), in which animals received a control diet supplemented with tomato +0.5 mL of corn oil/kg body weight/day. After three months, morphological, functional, and biochemical analyses were performed. Animals supplemented with tomato had a smaller left atrium diameter and myocyte cross-sectional area (CSA) compared to the control group (C group: 474 (415–539), T group: 273 (258–297) µm2, p = 0.004). Diastolic function was improved in rats supplemented with tomato. In addition, lipid hydroperoxide was lower (C group: 267 ± 46.7, T group: 219 ± 23.0 nmol/g, p = 0.039) in the myocardium of rats supplemented with tomato. Tomato intake was also associated with up-regulation of miR-107 and miR-486 and down-regulation of miR-350 and miR-872. In conclusion, tomato supplementation induces changes in miRNA expression and reduces oxidative stress. In addition, these alterations may be responsible for CSA reduction and diastolic function improvement.

Therefore The aim of this study is to investigate the cardiac glucose metabolism pathways in cardiac remodeling induced by TS . Methods 20 animals were allocated into 2 groups: group of animals exp...

Aim: To analyze the influence of rosemary (R) consumption on cardiac remodeling after myocardial infarction (MI). Material: Male Wistar rats were allocated into: 1) Sham group fed standard chow (SA...

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:34Z No. of bitstreams: 1 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:34Z No. of bitstreams: 1 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) Made available in DSpace on 2013-08-22T18:40:34Z (GMT). No. of bitstreams: 1 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) Previous issue date: 2006-02-01 Made available in DSpace on 2013-08-22T18:40:34Z (GMT). No. of bitstreams: 1 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) Previous issue date: 2006-02-01 Made available in DSpace on 2013-09-30T18:17:47Z (GMT). No. of bitstreams: 2 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) S0066-782X2006000200008.pdf.txt: 22760 bytes, checksum: cddd9a3fc8b9c96feca77f428933725a (MD5) Previous issue date: 2006-02-01 Made available in DSpace on 2013-09-30T18:17:47Z (GMT). No. of bitstreams: 2 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) S0066-782X2006000200008.pdf.txt: 22760 bytes, checksum: cddd9a3fc8b9c96feca77f428933725a (MD5) Previous issue date: 2006-02-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:33:41Z No. of bitstreams: 2 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) S0066-782X2006000200008.pdf.txt: 22760 bytes, checksum: cddd9a3fc8b9c96feca77f428933725a (MD5) Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:33:41Z No. of bitstreams: 2 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) S0066-782X2006000200008.pdf.txt: 22760 bytes, checksum: cddd9a3fc8b9c96feca77f428933725a (MD5) Made available in DSpace on 2014-05-20T13:33:41Z (GMT). No. of bitstreams: 2 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) S0066-782X2006000200008.pdf.txt: 22760 bytes, checksum: cddd9a3fc8b9c96feca77f428933725a (MD5) Previous issue date: 2006-02-01 Made available in DSpace on 2014-05-20T13:33:41Z (GMT). No. of bitstreams: 2 S0066-782X2006000200008.pdf: 175433 bytes, checksum: af4a40548486d7165ba55ee797af476b (MD5) S0066-782X2006000200008.pdf.txt: 22760 bytes, checksum: cddd9a3fc8b9c96feca77f428933725a (MD5) Previous issue date: 2006-02-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) OBJETIVO: Comparar as alterações estruturais cardíacas em modelos experimentais de sobrecarga de pressão e de volume. MÉTODOS: Foram analisados ratos com hipertensão renovascular (HRV, n = 8), normotensos com sobrecarga de volume por fístula aortocava (FAV, n = 10) e animais controles (CONT, n = 8). Após quatro semanas, registrou-se a pressão arterial caudal (PAS) e obtiveram-se os pesos dos ventrículos direito (PVD) e esquerdo (PVE). em cortes histológicos, foram medidas as áreas seccionais dos miócitos (AM), a espessura da parede do VE (E), o diâmetro da cavidade (DVE), a relação E/DVE, e a fração de colágeno (CVF). As comparações foram feitas pela ANOVA e teste de Tukey para nível de significância de 5%. RESULTADOS: A PAS (mmHg) foi maior no grupo HRV (HRV = 187 ± 22; CONT = 125 ± 10; FAV = 122 ± 6, p < 0,05). A hipertrofia do VE foi observada nos grupos HRV e FAV. O grupo FAV apresentou aumento significante do DVE, comparado ao CONT e HRV. As espessuras absoluta e normalizada da parede ventricular foram semelhantes entre os grupos. Houve aumento significante do CVF no grupo HRV em relação aos grupos CONT e FAV. CONCLUSÃO: A sobrecarga de volume causa padrão distinto de remodelação cardíaca, quando comparada com aquela decorrente da hipertensão arterial, sugerindo que as implicações funcionais de cada padrão não são intercambiáveis. OBJECTIVE: To compare cardiac structural changes in experimental pressure and volume overload models. METHODS: The study analysis included renovascular hypertensive rats (RVH, n=8), normotensive rats with volume overload caused by an aortocaval fistula (ACF, n=10) and control rats (CONT, n=8). After four weeks, tail cuff blood pressure (SBP) was recorded. Rats were killed, the hearts were excised and the right and left ventricles (RV&LV) were weighed (RVW&LVW). Using histological sections, myocyte cross sectional areas (MA). LV wall thickness (LVWT) LV cavity diameter (LVD), normalized LVWT (LVWT/LVD) and collagen volume fraction (CVF) were measured. The comparisons were made using the ANOVA and Tukey test for a significance level of 5%. RESULTS: Tail cuff blood pressure (mmHg) was higher in the RVH group (RVH = 187 ± 22; CONT = 125 ± 10; ACF = 122 ± 6, p

Objective We studied the effects of β-carotene (BC) on ventricular remodeling after myocardial infarction. Methods Myocardial infarction was induced in Wistar rats that were then treated with a BC diet (500 mg/kg of diet per day; MI-BC; n = 27) or a regular diet (MI; n = 27). Hearts were analyzed in vivo and in vitro after 6 mo. Results BC caused decreased left ventricular wall thickness (MI = 1.49 ± 0.3 mm, MI-BC = 1.23 ± 0.2 mm, P = 0.027) and increased diastolic (MI = 0.83 ± 0.15 cm 2 , MI-BC = 0.98 ± 0.14 cm 2 , P = 0.020) and systolic (MI = 0.56 ± 0.12 cm 2 , MI-BC = 0.75 ± 0.13 cm 2 , P = 0.002) left ventricular chamber areas. With respect to systolic function, the BC group presented less change in fractional area than did controls (MI = 32.35 ± 6.67, MI-BC = 23.77 ± 6.06, P = 0.004). There was no difference in transmitral diastolic flow velocities between groups. In vitro results showed decreased maximal isovolumetric systolic pressure (MI = 125.5 ± 24.1 mmHg, MI-BC = 95.2 ± 28.4 mmHg, P = 0.019) and increased interstitial myocardial collagen concentration (MI = 3.3 ± 1.2%, MI-BC = 5.8 ± 1.7%, P = 0.004) in BC-treated animals. Infarct sizes were similar between groups (MI = 45.0 ± 6.6%, MI-BC = 48.0 ± 5.8%, P = 0.246). Conclusion Taken together, these data suggest that BC has adverse effects on ventricular remodeling after myocardial infarction.

The objectives were to analyze the cardiac effects of exposure to tobacco smoke (ETS), for a period of 30 days, alone and in combination with beta-carotene supplementation (BC).Rats were allocated into: Air (control, n = 13); Air + BC (n = 11); ETS (n = 11); and BC + ETS (n = 9). In Air + BC and BC + ETS, 500 mg of BC were added to the diet. After three months of randomization, cardiac structure and function were assessed by echocardiogram. After that, animals were euthanized and morphological data were analyzed post-mortem. One-way and two-way ANOVA were used to assess the effects of ETS, BC and the interaction between ETS and BC on the variables.ETS presented smaller cardiac output (0.087 +/- 0.001 vs. 0.105 +/- 0.004 l/min; p = 0.007), higher left ventricular diastolic diameter (19.6 +/- 0.5 vs. 18.0 +/- 0.5 mm/kg; p = 0.024), higher left ventricular (2.02 +/- 0.05 vs. 1.70 +/- 0.03 g/kg; p0.001) and atrium (0.24 +/- 0.01 vs. 0.19 +/- 0.01 g/kg; p = 0.003) weight, adjusted to body weight of animals, and higher values of hepatic lipid hydroperoxide (5.32 +/- 0.1 vs. 4.84 +/- 0.1 nmol/g tissue; p = 0.031) than Air. However, considering those variables, there were no differences between Air and BC + ETS (0.099 +/- 0.004 l/min; 19.0 +/- 0.5 mm/kg; 1.83 +/- 0.04 g/kg; 0.19 +/- 0.01 g/kg; 4.88 +/- 0.1 nmol/g tissue, respectively; p0.05). Ultrastructural alterations were found in ETS: disorganization or loss of myofilaments, plasmatic membrane infolding, sarcoplasm reticulum dilatation, polymorphic mitochondria with swelling and decreased cristae. In BC + ETS, most fibers showed normal morphological aspects.One-month tobacco-smoke exposure induces functional and morphological cardiac alterations and BC supplementation attenuates this ventricular remodeling process.

Left ventricular (LV) and right ventricular (RV) function are known predictors of morbidity and mortality after an acute myocardial infarction (MI). However, the prognostic use of a late evaluation of cardiac function after an MI remains unclear.We analyzed echocardiograms obtained 1 year after MI in patients with LV dysfunction at baseline (ejection fraction [EF]or = 40%) from 291 patients enrolled in the SAVE echocardiographic substudy who did not develop heart failure (HF) or a recurrent MI during this first year. Left ventricular EF and RV fractional area change were assessed.After a median follow-up of 22 months after the 1-year echocardiogram, a low LVEF (30%) at 1 year was associated with an increased risk of death and/or HF (hazards ratio [HR] 2.7, 95% CI 1.3-5.3). Presence of RV dysfunction was also associated with an increased risk of death (HR 8.9, 95% CI 3.5-22.1), development of HF (HR 7.1, 95% CI 3.4-15.0), and the composite end point of death or HF (HR 7.6, 95% CI 4.1-14.2). In multivariate analyses, both low LVEF and RV dysfunction remained independently predictive of the composite end point of death or HF. Patients with biventricular dysfunction were at the greatest risk of death and/or HF (HR 19.4, 95% CI 8.2-46.0) in follow-up.In a stable population of survivors of MI, impaired LV and RV function at 1 year after MI are independently and additively predictive of increased risk of HF or death.

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:30Z No. of bitstreams: 1 S0066-782X2005000400006.pdf: 69487 bytes, checksum: be5f71973eb7529b54c000e994fcdacc (MD5) Made available in DSpace on 2013-08-22T18:40:31Z (GMT). No. of bitstreams: 1 S0066-782X2005000400006.pdf: 69487 bytes, checksum: be5f71973eb7529b54c000e994fcdacc (MD5) Previous issue date: 2005-04-01 Made available in DSpace on 2013-09-30T19:26:13Z (GMT). No. of bitstreams: 2 S0066-782X2005000400006.pdf: 69487 bytes, checksum: be5f71973eb7529b54c000e994fcdacc (MD5) S0066-782X2005000400006.pdf.txt: 28219 bytes, checksum: b02e9dbb6f941d9ba375f1092e7cd5b6 (MD5) Previous issue date: 2005-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:33:01Z No. of bitstreams: 2 S0066-782X2005000400006.pdf: 69487 bytes, checksum: be5f71973eb7529b54c000e994fcdacc (MD5) S0066-782X2005000400006.pdf.txt: 28219 bytes, checksum: b02e9dbb6f941d9ba375f1092e7cd5b6 (MD5) Made available in DSpace on 2014-05-20T13:33:02Z (GMT). No. of bitstreams: 2 S0066-782X2005000400006.pdf: 69487 bytes, checksum: be5f71973eb7529b54c000e994fcdacc (MD5) S0066-782X2005000400006.pdf.txt: 28219 bytes, checksum: b02e9dbb6f941d9ba375f1092e7cd5b6 (MD5) Previous issue date: 2005-04-01 OBJETIVO: Avaliar o papel do bloqueador dos receptores AT1 e do inibidor da enzima conversora da angiotensina na remodelação cardíaca induzida por estenose aórtica em ratos. MÉTODOS: Ratos Wistar foram divididos em 4 grupos: controle (C, n=13), estenose aórtica (EAo, n=11), EAo com lisinopril, 20 mg/kg/dia (LIS, n=11) e EAo com losartan, 40 mg/kg/dia (LOS, n=9). Os tratamentos foram iniciados 3 dias antes da cirurgia. Após 6 semanas, os animais foram submetidos ao estudo ecocardiográfico, quantificação da concentração de hidroxiprolina e da área seccional (CSA) miocitária do ventrículo esquerdo (VE). RESULTADOS: A EAo induziu aumento da espessura da parede do VE. Os animais LIS e LOS não apresentaram diferença em relação aos animais controles. Os ratos EAo e LIS apresentaram maiores diâmetros do átrio esquerdo que os ratos controles, enquanto nos animais LOS não houve diferença. Os animais com EAo apresentaram maiores valores da porcentagem de encurtamento que os controle. Esse fato não foi modificado com LIS ou LOS. A CSA dos animais do grupo EAo foi maior que a dos controle. Entretanto, o tratamento com LOS e com LIS atenuou o aumento da área induzida pela EAo. A EAo resultou em aumento na concentração de HOP, enquanto o grupo LOS não apresentou diferença em relação ao grupo controle. CONCLUSÃO: O bloqueio do sistema renina-angiotensina, com bloqueador AT1 e com IECA, pode atenuar o desenvolvimento de hipertrofia cardíaca, porém só o bloqueio dos receptores AT1 atenua a fibrose intersticial do VE. OBJECTIVE: To assess the role of the AT1 receptor blocker and the angiotensin-converting enzyme inhibitor in cardiac remodeling induced by aortic stenosis in rats. METHODS: Wistar rats were divided into the following 4 groups: 1) C - control (n=13); 2) AoS - aortic stenosis (n=11); 3) LIS - AoS treated with lisinopril, 20 mg/kg/day (n=11); and 4) LOS - AoS treated with losartan, 40 mg/kg/day (n=9). The treatments were initiated 3 days before surgery. After 6 weeks, the animals underwent echocardiographic study, and quantification of the hydroxyproline (HOP) concentration and the left ventricular (LV) myocyte cross-sectional area (CSA). RESULTS: Aortic stenosis induced an increase in left ventricular wall thickness. The LIS and LOS groups showed no difference as compared with the control group. The AoS and LIS rats had greater left atrial diameters than the control rats did, while no difference was observed in the LOS animals. The AoS animals had greater values of shortening percentage than control animals did. This fact was modified with neither LIS nor LOS. The cross-sectional area of the animals in the AoS group was greater than that in the control group. However, treatment with LOS and LIS attenuated the AoS-induced increase in area. Aortic stenosis caused an increase in HOP concentration, while the LOS group showed no difference as compared with the control group. CONCLUSION: Blockade of the renin-angiotensin system with AT1 blocker and ACEI may attenuate the development of heart hypertrophy, but only the blockade of AT1 receptors attenuates left ventricular interstitial fibrosis. Universidade Estadual Paulista Faculdade de Medicina de Botucatu Universidade Estadual Paulista Faculdade de Medicina de Botucatu

OBJETIVO: Verificar a ação do hormônio de crescimento (GH) sobre a remodelação miocárdica em ratos infartados. MÉTODOS: Ratos Wistar foram submetidos ao infarto e tratados com GH (IAM-GH; n=8), ou com o veículo (IAM; n=8). Ratos controles foram submetidos ao infarto simulado (C; n=8). Após 30 dias, os animais foram submetidos ao estudo funcional por meio de ecocardiograma e as alterações da contratilidade miocárdica estudadas no músculo papilar isolado do ventrículo esquerdo (VE). RESULTADOS: O ecocardiograma identificou aumento nos diâmetros (mm) diastólico (C=7,32±0,49; IAM=8,50±0,73; IAM-GH= 9,34± 0,73; P

Background— Patients with heart failure are at increased risk of sudden death and death attributed to progressive pump failure. We assessed the effect of candesartan on cause-specific mortality in patients enrolled in the Candesartan in Heart failure Assessment of Reduction in Mortality and morbidity (CHARM) program. Methods and Results— The CHARM program consisted of 3 component trials that enrolled patients with symptomatic heart failure: CHARM-Alternative (n=2028; LVEF⩽40% and ACE intolerant), CHARM-Added (n=2548; LVEF⩽40%, already on ACE inhibitors), and CHARM-Preserved (n=3023; LVEF >40%). Patients were randomized to candesartan, titrated to 32 mg QD, or placebo and were followed up for a median of 37.7 months. All deaths were reviewed by a blinded adjudication committee and categorized according to prespecified definitions on the basis of a narrative and source documentation. The number and rate of deaths by cause were calculated for each of the component trials and the overall program. Of all the patients, 8.5% died suddenly, and 6.2% died of progressive heart failure. Candesartan reduced both sudden death (HR 0.85 [0.73 to 0.99], P =0.036) and death from worsening heart failure (HR 0.78 [0.65 to 0.94], P =0.008). These reductions were most apparent in the patients with LVEF⩽40%. Conclusions— Candesartan reduced sudden death and death from worsening heart failure in patients with symptomatic heart failure, although this reduction was most apparent in patients with systolic dysfunction.

A piomiosite tropical é uma infecção primária dos músculos, que ocorre principalmente em países tropicais. Inicialmente, suas manifestações são leves e inespecíficas, o que dificulta o diagnóstico. A história natural dessa doença costuma ser benigna, com raras complicações. Essa apresentação descreve quatro casos de piomiosite, com manifestações e complicações peculiares.

Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:21Z No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:21Z No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:21Z No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Submitted by Guilherme Lemeszenski (guilherme@nead.unesp.br) on 2013-08-22T18:40:21Z No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-08-22T18:40:21Z (GMT). No. of bitstreams: 1 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2013-09-30T19:25:49Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:32:57Z No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 Made available in DSpace on 2014-05-20T13:32:57Z (GMT). No. of bitstreams: 2 S0066-782X2004000400008.pdf: 73437 bytes, checksum: dc571c9f8e360643ffaf5fd14f39ed7d (MD5) S0066-782X2004000400008.pdf.txt: 25059 bytes, checksum: 210081d944a2df910d26fe70b9388555 (MD5) Previous issue date: 2004-04-01 OBJETIVO: Comparar a mortalidade em 30 dias com a utilização de determinados grupos de medicamentos por pacientes, entre 1992-1997, quando não se dispunham de condutas consensuais para tratamento do infarto agudo do miocárdio, e de 2000-2002, após a padronização dessas condutas em nosso serviço. MÉTODOS: Avaliados, retrospectivamente, no 1º e 2º períodos, 172 e 143 pacientes respectivamente, admitidos com diagnóstico de infarto agudo do miocárdio: foram realizados os testes estatísticos: c² para comparar proporções, teste t de Student e o de Mann-Whitney para comparação de médias ou medianas. RESULTADOS: A análise não mostrou diferença em relação aos homens, brancos e a idade média de 61 anos, nos dois períodos. Com relação aos fatores de risco clássicos, foi observada diferença apenas na incidência de dislipidemia (17 e 29%) e, quanto à estratégia terapêutica, aumento significativo do uso de: trombolíticos (39 e 61,5%), ácido acetilsalicílico (70,9 e 96,5%), betabloqueadores (34,8 e 67,8%), inibidor da enzima conversora da angiotensina (45,9 e 74,8%), nitratos (61 e 85,3%) e a redução significativa de bloqueadores de cálcio (16,8 e 5,3%), antiarrítmicos (29,1 e 9,7%) e diuréticos (50,6 e 26,6%). O uso de inotrópicos não diferiu entre os períodos (29,6 e 32,1%). A mortalidade em 30 dias apresentou redução estatisticamente significante de 22,7 para 10,5%. CONCLUSÃO: A implementação das condutas consensuais para o tratamento do infarto agudo do miocárdio foi acompanhada por significante redução da taxa de mortalidade em 30 dias. OBJECTIVE: To compare 30-day mortality in patients receiving different types of medication from 1992 to 1997, when no consensual treatment for acute myocardial infarction was available, versus 30-day mortality in patients being treated between 2000 and 2002 after standardization of that treatment was obtained in our service. METHODS: In the first and second study periods, 172 and 143 patients, respectively, admitted with the diagnosis of acute myocardial infarction were retrospectively assessed. Their diagnoses were confirmed, and the following statistical tests were performed: the chi-square test for comparing proportions and the Student t test and the Mann-Whitney test for comparing the means or medians. RESULTS: The analysis showed no difference in regard to white men with a mean age of 61 years in the 2 study periods. In regard to the traditional risk factors, a difference was observed only in the incidence of dyslipidemia (17 and 29%). In regard to the therapeutic strategy adopted, the following was observed: 1) a significant increase in the use of thrombolytic agents (39 and 61.5%), acetylsalicylic acid (70.9 and 96.5%), beta-blockers (34.8 and 67.8%), angiotensin-converting enzyme inhibitors (45.9 and 74.8%), and nitrates (61 and 85.3%); and 2) a significant reduction in the use of calcium channel blockers (16.8 and 5.3%), antiarrhythmics (29.1 and 9.7%), and diuretics (50.6 and 26.6%). The use of inotropic agents did not differ between the study periods (29.6 and 32.1%). The 30-day mortality showed a statistically significant reduction from 22.7 to 10.5%. CONCLUSION: The implementation of standard protocols for the treatment of acute myocardial infarction was accompanied by a significant reduction in the 30-day mortality rate. UNESP Faculdade de Medicina de Botucatu UNESP Faculdade de Medicina de Botucatu

Thiamine is an essential component of cellular metabolism, and the lack of this vitamin can result in life-threatening biochemical damage (1). Specifically, thiamine is a cofactor in oxidative decarboxylation in three mitochondrial complexes (pyruvate, α-ketoglutarate and α-keto acids). In addition, this vitamin is also a cofactor of transketolase, an enzyme involved in the tricarboxylic acid cycle (2,3). Therefore, thiamine deficiency can lead to the onset of anaerobic metabolism, associated with severe lactic acidosis. The classical clinical presentations of thiamine deficiency are Wernicke-Korsakoff encephalopathy; peripheral neuropathy, muscle weakness and anorexia (dry beriberi), high-output heart failure (wet beriberi), and beriberi associated with shock (Shoshin beriberi) (4-6).

Retinoic acid (RA) plays a role in regulating cardiac geometry and function throughout life. The aim of this study was to analyze the cardiac effects of RA in adult rats. Wistar rats were randomly allocated to a control group ( n = 18) receiving standard rat chow and a group treated with RA ( n = 14) receiving standard rat chow supplemented with RA for 90 days. All animals were evaluated by echocardiography, isolated papillary muscle function, and morphological studies. Whereas the RA-treated group developed an increase in both left ventricular (LV) mass and LV end-diastolic diameter, the ratio of LV wall thickness to LV end-diastolic diameter remained unchanged when compared with the control group. In the isolated papillary muscle preparation, RA treatment decreased the time to peak developed tension and increased the maximum velocity of isometric relengthening, indicating that systolic and diastolic function was improved. Although RA treatment produced an increase in myocyte cross-sectional area, the myocardial collagen volume fraction was similar to controls. Thus our study demonstrates that small physiological doses of RA induce ventricular remodeling resembling compensated volume-overload hypertrophy in rats.

Made available in DSpace on 2015-10-21T13:08:47Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-01-01. Added 1 bitstream(s) on 2015-10-22T09:53:30Z : No. of bitstreams: 1 WOS000348048000014.pdf: 1507770 bytes, checksum: 6d4ada509f3ad39c009863c134ed89ce (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação para o Desenvolvimento da UNESP (FUNDUNESP) Background: Chronic heart failure is characterized by decreased exercise capacity with early exacerbation of fatigue and dyspnea. Intrinsic skeletal muscle abnormalities can play a role in exercise intolerance. Causal or contributing factors responsible for muscle alterations have not been completely defined. This study evaluated skeletal muscle oxidative stress and NADPH oxidase activity in rats with myocardial infarction (MI) induced heart failure. Methods and Results: Four months after MI, rats were assigned to Sham, MI-C (without treatment), and MI-NAC (treated with N-acetylcysteine) groups. Two months later, echocardiogram showed left ventricular dysfunction in MI-C; NAC attenuated diastolic dysfunction. In soleus muscle, glutathione peroxidase and superoxide dismutase activity was decreased in MI-C and unchanged by NAC. 3-nitrotyrosine was similar in MI-C and Sham, and lower in MI-NAC than MI-C. Total reactive oxygen species (ROS) production was assessed by HPLC analysis of dihydroethidium (DHE) oxidation fluorescent products. The 2-hydroxyethidium (EOH)/DHE ratio did not differ between Sham and MI-C and was higher in MI-NAC. The ethidium/DHE ratio was higher in MI-C than Sham and unchanged by NAC. NADPH oxidase activity was similar in Sham and MI-C and lower in MI-NAC. Gene expression of p47(phox) was lower in MI-C than Sham. NAC decreased NOX4 and p22(phox) expression. Conclusions: We corroborate the case that oxidative stress is increased in skeletal muscle of heart failure rats and show for the first time that oxidative stress is not related to increased NADPH oxidase activity. Universidade de São Paulo, Instituto do Coração do Hospital das Clínicas, Faculdade de Medicina Universidade Estadual Paulista, Departamento de Clínica Médica, Faculdade de Medicina de Botucatu FAPESP: 2010/50461-6 FAPESP: 2007/59500-1 CNPq: 306857/2012-0 CNPq: 306.845/2012-1

Made available in DSpace on 2015-10-21T13:08:55Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-01-01. Added 1 bitstream(s) on 2015-10-22T09:53:27Z : No. of bitstreams: 1 WOS000348048000024.pdf: 3141987 bytes, checksum: c7f7398f8ea48b5e5581e174fc423327 (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Background/Aims: The aim of this study was to evaluate the influence of pamidronate on ventricular remodeling after myocardial infarction. Methods: Male Wistar rats were assigned to four groups: a sham group, in which animals were submitted to simulated surgery and received weekly subcutaneous injection of saline (S group; n=14); a group in which animals received weekly subcutaneous injection of pamidronate (3 mg/kg of body weight) and were submitted to simulated surgery (SP group, n=14); a myocardial infarction group, in which animals were submitted to coronary artery ligation and received weekly subcutaneous injection of saline (MI group, n=13); and a myocardial infarction group with pamidronate treatment (MIP group, n=14). The rats were observed for three months. Results: Animals submitted to MI had left chamber enlargement and worse diastolic and systolic function compared with SHAM groups. E/A ratio, LV posterior and relative wall thickness were lower in the MIP compared with the MI group. There was no interaction between pamidronate administration and MI on systolic function, myocyte hypertrophy, collagen content, and calcium handling proteins. Conclusion: Pamidronate attenuates diastolic dysfunction following MI. Universidade Estadual Paulista, Departamento de Clínica Médica, Faculdade de Medicina de Botucatu Universidade Estadual Paulista, Departamento de Microbiologia e Imunologia, Instituto de Biociências de Botucatu FAPESP: 2011/10328-8

ObjectivesThe aim of this study was to determine the prognostic value of right ventricular (RV) function in patients after a myocardial infarction (MI).BackgroundRight ventricular function has been shown to predict exercise capacity, autonomic imbalance and survival in patients with advanced heart failure (HF).MethodsTwo-dimensional echocardiograms were obtained in 416 patients with left ventricular (LV) dysfunction (ejection fraction [LVEF] ≤40%) from the Survival And Ventricular Enlargement (SAVE) echocardiographic substudy (mean 11.1 ± 3.2 days post infarction). Right ventricular function from the apical four-chamber view, assessed as the percent change in the cavity area from end diastole to end systole (fractional area change [FAC]), was related to clinical outcome.ResultsRight ventricular function correlated only weakly with the LVEF (r = 0.12, p = 0.013). On univariate analyses, the RV FAC was a predictor of mortality, cardiovascular mortality and HF (p < 0.0001 for all) but not recurrent MI. After adjusting for age, gender, diabetes mellitus, hypertension, previous MI, LVEF, infarct size, cigarette smoking and treatment assignment, RV function remained an independent predictor of total mortality, cardiovascular mortality and HF. Each 5% decrease in the RV FAC was associated with a 16% increased odds of cardiovascular mortality (95% confidence interval 4.3% to 29.2%; p = 0.006).ConclusionsRight ventricular function is an independent predictor of death and the development of HF in patients with LV dysfunction after MI.

Made available in DSpace on 2018-12-11T17:11:36Z (GMT). No. of bitstreams: 0 Previous issue date: 2017-05-01 Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Background: Myocardial infarction (MI) is one of the leading causes of morbidity and mortality worldwide. Dietary intervention on adverse cardiac remodeling after MI has significant clinical relevance. Rosemary leaves are a natural product with antioxidant/anti-inflammatory properties, but its effect on morphology and ventricular function after MI is unknown. Methods and results: To determine the effect of the dietary supplementation of rosemary leaves on cardiac remodeling after MI, male Wistar rats were divided into 6 groups after sham procedure or experimental induced MI: 1) Sham group fed standard chow (SR0, n = 23); 2) Sham group fed standard chow supplemented with 0.02% rosemary (R002) (SR002, n = 23); 3) Sham group fed standard chow supplemented with 0.2% rosemary (R02) (SR02, n = 22); 4) group submitted to MI and fed standard chow (IR0, n = 13); 5) group submitted to MI and fed standard chow supplemented with R002 (IR002, n = 8); and 6) group submitted to MI and fed standard chow supplemented with R02 (IR02, n = 9). After 3 months of the treatment, systolic pressure evaluation, echocardiography and euthanasia were performed. Left ventricular samples were evaluated for: fibrosis, cytokine levels, apoptosis, energy metabolism enzymes, and oxidative stress. Rosemary dietary supplementation attenuated cardiac remodeling by improving energy metabolism and decreasing oxidative stress. Rosemary supplementation of 0.02% improved diastolic function and reduced hypertrophy after MI. Regarding rosemary dose, 0.02% and 0.2% for rats are equivalent to 11 mg and 110 mg for humans, respectively. Conclusion: Our findings support further investigations of the rosemary use as adjuvant therapy in adverse cardiac remodeling. Internal Medicine Department Botucatu Medical School UNESP Department of Biochemistry Botucatu Biosciences Institute UNESP Department of Microbiology and Immunology Botucatu Biosciences Institute UNESP Nutrition and Cancer Biology Laboratory Jean Mayer USDA Human Nutrition Research Center on Aging Tufts University Internal Medicine Department Botucatu Medical School UNESP Department of Biochemistry Botucatu Biosciences Institute UNESP Department of Microbiology and Immunology Botucatu Biosciences Institute UNESP FAPESP: 2011/08956-0 FAPESP: 2011/15059-5

Objectives The aim of this study was to evaluate the association between serum levels of 25(OH) vitamin D 3 with midupper arm muscle circumference (MUAMC), handgrip strength and length of hospital stay (LOS) after hip fracture. Methods In total, 102 consecutive patients with hip fracture over the age of 65 were admitted to the orthopedic unit and prospectively evaluated. All of the patients were treated according to specific protocols depending on the type of fracture. Anthropometric measurements and handgrip strength were performed, and blood samples were taken for serum biochemistry and 25(OH) vitamin D 3 analysis within the first 72 h of admission. All of the patients were followed during their hospital stay, and the length of stay was recorded. Results Of the patients, two were excluded because of pathologic fractures. In total, 100 patients with a mean age of 80 ± 7 y were included in the analysis. Among these patients, 73% were female, and 37% had vitamin D deficiency. The median LOS was 7 (5–11) d. Patients with vitamin D deficiency had lower handgrip strength in univariate analysis. In the multiple linear regression analysis with robust standard error, serum vitamin D levels adjusted by age and sex were associated with handgrip strength but not with MUAMC and LOS after hip fracture. Conclusions In conclusion, vitamin D serum levels were associated with handgrip strength but not with muscle mass or length of hospital stay after hip fracture.

Made available in DSpace on 2014-12-03T13:10:30Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-06-12Bitstream added on 2014-12-03T13:23:10Z : No. of bitstreams: 1 WOS000338701300020.pdf: 301785 bytes, checksum: 6b3c93312f42909464782db13e6fcef0 (MD5) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Background/Aims: The aim of this study was to evaluate whether supplementation of high doses of cholecalciferol for two months in normotensive rats results in increased systolic arterial pressure and which are the mechanisms involved. Specifically, this study assesses the potential effect on cardiac output as well as the changes in aortic structure and functional properties.Methods: Male Wistar rats were divided into three groups: 1) Control group (C, n = 20), with no supplementation of vitamin D, 2) VD3 (n = 19), supplemented with 3,000 IU vitamin D/kg of chow; 3) VD10 (n = 21), supplemented with 10,000 IU vitamin D/kg of chow. After two months, echocardiographic analyses, measurements of systolic arterial pressure (SAP), vascular reactivity, reactive oxygen species (ROS) generation, mechanical properties, histological analysis and metalloproteinase-2 and -9 activity were performed.Results: SAP was higher in VD3 and VD10 than in C rats (p = 0.001). Echocardiographic variables were not different among groups. Responses to phenylephrine in endothelium-denuded aortas was higher in VD3 compared to the C group (p = 0.041). Vascular relaxation induced by acetylcholine (p = 0.023) and sodium nitroprusside (p = 0.005) was impaired in both supplemented groups compared to the C group and apocynin treatment reversed impaired vasodilation. Collagen volume fraction (

Made available in DSpace on 2015-03-18T15:55:39Z (GMT). No. of bitstreams: 0 Previous issue date: 2014-01-01Bitstream added on 2015-03-18T16:28:35Z : No. of bitstreams: 1 WOS000343764600010.pdf: 1779097 bytes, checksum: 0e5005357de762c7419f95c003e1051d (MD5) Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq) Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Background: Intracellular signaling pathways involved in skeletal myosin heavy chain (MyHC) isofornn alterations during heart failure (HF) are not completely understood. We tested the hypothesis that diaphragm expression of mitogen-activated protein kinases (MAPK) and myogenic regulatory factors is changed in rats with myocardial infarction (MI) induced HF. Methods: Six months after MI rats were subjected to transthoracic echocardiography. After euthanasia, infarcted rats were subdivided in MI/HF- group (with no HF evidence; n=10), and MI/HF+ (with right ventricular hypertrophy and lung congestion; n=10). Sham operated rats were used as controls (n=10). MyHC isofornns were analyzed by electrophoresis. Statistical analysis: ANOVA and Pearson correlation. Results: MI/HF- had left cardiac chambers dilation with systolic and diastolic left ventricular dysfunction. Cardiac injury was more intense in MI/HF+ than MI/HF-. MyHC I isoform percentage was higher in MI/HF+ than MI/HF-, and IIb isoform lower in MI/HF+ than Sham. Left atrial diameter-to-body weight ratio positively correlated with MyHC I (p=0.005) and negatively correlated with MyHC IIb (p=0.02). TNF-alpha serum concentration positively correlated with MyHC I isoform. Total and phosphorylated ERK was lower in MI/HF- and MI/HF+ than Sham. Phosphorylated JNK was lower in MI/HF- than Sham. JNK and p38 did not differ between groups. Expression of NF-kappa B and the myogenic regulatory factors MyoD, myogenin, and MRF4 was similar between groups. Conclusion: Diaphragm MyHC fast-to-slow shift is related to cardiac dysfunction severity and TNF-alpha serum levels in infarcted rats. Reduced ERK expression seems to participate in MyHC isofornn changes. Myogenic regulatory factors and NF-kappa B do not modulate diaphragm MyHC distribution during chronic HF. Copyright (C) 2014 S. Karger AG, Basel UNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP, Brazil Fed Univ Mato Grosso Do Sul UFMS, Biol Sci & Hlth Ctr, Campo Grande, MS, Brazil UNESP, Biosci Inst, Dept Morphol, Botucatu, SP, Brazil UNESP, Botucatu Med Sch, Dept Internal Med, Botocutu, SP, Brazil UNESP, Biosci Inst, Dept Morphol, Botucatu, SP, Brazil CNPq: 306857/2012-0 CNPq: 306845/2012-1 FAPESP: 07/57499-6 FAPESP: 10/50084-8 FAPESP: 08/58655-4

Due to its antioxidant properties, tomato (Lycopersicon esculentum) and one of its primary constituents, lycopene have been evaluated in clinical and experimental studies. Our objective was to evaluate the influence of tomato and lycopene supplementation on the cardiac remodeling after acute myocardial infarction. Wistar rats were assigned to 6 groups: SHAM group, in which animals were submitted to simulated surgery (SHAM group; n=15); SHAM group that received lycopene 1mg/kg of body weight/day in the chow (SHAM-L group, n=9); SHAM group that received tomato in the chow (SHAM-T group, n=10); myocardial infarction (MI) group, in which animals were submitted to coronary artery ligation (MI group, n=16); MI group that received lycopene 1mg/kg of body weight/day in the chow (MI-L group, n=12); and MI group that received tomato in the chow (MI-T group, n=15). The amount of tomato supplemented had the same quantity of lycopene that was given for the groups supplemented only with this carotenoid. The rats were o...

Chronic inflammation presented in rheumatoid arthritis (RA) is associated with systemic manifestations, that include micronutrient deficiency, changes in body composition and cardiac morphofunctional alterations. The aim of this study is to evaluate the association of serum vitramin D and body composition with cardiac geometric pattern in patients with RA. Methods: 30 patients with RA were submitted to clinical, nutritional and biochemical evaluation. Bioimpedance analysis and dual-energy X-ray absorptiometry (DEXA) was performed to evaluate body composition. Transthoracic dopller- echocardiography was performed to evaluate left ventricle mass and relative wall thickness (RWT) in order to find cardiac geometry patterns. Patients were divided in Normal or abnormal pattern (concentric remodeling or concentric hypertrophy.) Results: The mean age was 53±9 years; 70% were woman, 43% presented with hypertension. All patients have been treated with methotrexate and a biological agent and presented with Disease a...

ACE inhibitors have shown beneficial results in several studies after myocardial infarction (MI). However, these studies have shown conflicting results about the ideal starting time of the ACE inhibitors administration after MI and the importance of infarct size.This study was designed to assess the long-term effects of lisinopril on mortality, cardiac function, and ventricular fibrosis after MI, in rats.Lisinopril (20 mg/kg/day) was given on day 1 or 21 days after coronary occlusion in small or large infarctions.The mortality rate was reduced by 39 % in early treatment and 30 % in delayed treatment in comparison to the untreated rats. Early treatment reduced cardiac dysfunction in small MIs; however, delayed treatment did not. No statistical difference was observed among the groups for large MIs. No statistical difference was observed among the groups with large or small MIs on myocardial hydroxyproline concentration.Both early and delayed treatments with lisinopril increased survival. Treatment exerts no marked effects on fibrosis; early treatment has exerted beneficial influences on cardiac function whereas delayed treatment had no consistent effects. The protective effect of lisinopril is detectable only in small (40 % of LV) MIs.

Endothelin levels are increased in rats with experimentally induced myocardial infarction. The purpose of this study was to determine whether endothelin-A (ETA) receptor antagonism alters ventricular remodeling and the development of heart failure after myocardial infarction (MI). We administered 10 mg/kg/day of A-127722 to rats post-MI for 6 weeks. A hemodynamic study was performed and passive pressure-volume curves obtained. In rats without infarcts, ETA receptor antagonist (n=8; vehicle, n = 5) had no effect. However, in rats with infarcts ETA antagonism (n = 14, MI = 35%; vehicle: n = 19, MI = 32%) reduced systemic arterial and LV systolic (but not end-diastolic) pressures and shifted the pressure-volume relationship to the right. Because LV mass was not changed, the volume-to-mass ratio was increased and was correlated inversely with the ability of the LV to maximally develop pressure. This increase in volume at low distending pressures was also coupled with a tendency (P < 0.06) for reduced scar thickness, suggesting that early initiation of an ETA receptor antagonism increased infarct expansion. The reduction in blood pressure offset the increase in volume such that wall stresses were unchanged, as was LV mass. The early use of ETA receptor antagonism in the rat model of myocardial infarction did not beneficially alter LV remodeling.

FUNDAMENTO: A relevância do padrão de geometria após o infarto do miocárdio não é conhecida. OBJETIVOS: Analisar a presença de diferentes padrões de geometria ventricular esquerda (VE) e seu impacto como preditor de remodelação em pacientes com infarto do miocárdio. MÉTODOS: Pacientes com infarto agudo anterior (n = 80) foram divididos de acordo com o padrão de geometria: normal (índice de massa [IMVE] normal e espessura relativa da parede [ERP] normal), remodelação concêntrica (IMVE normal e ERP aumentada), hipertrofia concêntrica (IMVE e ERP aumentadas) e hipertrofia excêntrica (IMVE aumentado e ERP normal). Após seis meses, foi repetido o ecocardiograma. RESULTADOS: Quatro pacientes foram a óbito. Dos sobreviventes, 41 apresentaram remodelação (R+), enquanto 39 não remodelaram (R-). Considerando-se o padrão geométrico, houve a seguinte distribuição: 24 pacientes com padrão normal, 13 com remodelação concêntrica, 29 com hipertrofia concêntrica e 14 com hipertrofia excêntrica. Os pacientes que remodelaram apresentaram maiores tamanhos de infarto analisados pelo pico da CPK (R+ = 4.610 (1.688 - 7.970), R- = 1.442 (775 - 4.247), p < 0,001) e da CK-MB (R+ = 441 (246 - 666), R- = 183 (101 - 465), p < 0,001), tendência a maior prevalência de remodelação concêntrica (R+ = 10, R- = 3, p = 0,08) e menor prevalência de hipertrofia excêntrica (R+ = 2, R- = 12, p = 0,006). Na análise de regressão multivariada, o tamanho do infarto foi preditor (OR = 1,01; p = 0,020) e a hipertrofia excêntrica foi fator protetor (OR = 0,189; p = 0,046) de remodelação ventricular após a oclusão coronariana. CONCLUSÃO: O padrão de geometria ventricular pode ter impacto no processo de remodelação em pacientes com infarto do miocárdio. BACKGROUND: The relevance of left ventricular (LV) geometric pattern after myocardial infarction is not known. OBJECTIVES: To analyze the presence of different LV geometric patterns and teir impact as a predictor of remodeling in patients with myocardial infarction. METHODS: Patients with anterior acute myocardial infarction (n = 80) were divided according to the geometric pattern: normal (normal left ventricular mass index [LVMI] and normal relative wall thickness [RWT]), concentric remodeling (normal LVMI and increased RWT), concentric hypertrophy (increased LVMI and RWT) and eccentric hypertrophy (increased LVMI and normal RWT). After six months, echocardiographic assessment was repeated. RESULTS: Four patients died. Of the survivors, 41 showed remodeling (R +), whereas 39 did not (R-). Considering the geometric pattern, the cases were distributed as follows: 24 patients with normal pattern, 13 with concentric remodeling, 29 with concentric hypertrophy and 14 with eccentric hypertrophy. Patients who showed remodeling had larger infarction sizes analyzed by peak CPK (R + = 4,610 (1,688-7,970), R- = 1,442 (775-4247), p

Purpose The purpose of the study is to determine the influence of serum thiamine, glutathione peroxidase (GPx) activity, and serum protein carbonyl concentrations in hospital mortality in patients with septic shock. Materials and Methods This prospective study included all patients with septic shock on admission or during intensive care unit (ICU) stay, older than 18 years, admitted to 1 of the 3 ICUs of the Botucatu Medical School, from January to August 2012. Demographic information, clinical evaluation, and blood sample were taken within the first 72 hours of the patient's admission or within 72 hours after septic shock diagnosis for serum thiamine, GPx activity, and protein carbonyl determination. Results One hundred eight consecutive patients were evaluated. The mean age was 57.5 ± 16.0 years, 63% were male, 54.6% died in the ICU, and 71.3% had thiamine deficiency. Thiamine was not associated with oxidative stress. Neither vitamin B1 levels nor the GPx activity was associated with outcomes in these patients. However, protein carbonyl concentration was associated with increased mortality. Conclusions In patients with septic shock, oxidative stress was associated with mortality. On the other hand, thiamine was not associated with oxidative stress or mortality in these patients.

FUNDAMENTO: Estudos de intervencao mostraram aumento da mortalidade em pacientes que receberam betacaroteno. Contudo, nao sao conhecidos os mecanismos envolvidos nesse fenomeno. OBJETIVO: Avaliar a influencia do betacaroteno sobre o estresse oxidativo e a expressao de conexina 43 em coracao de ratos. METODOS: Ratos Wistar, pesando aproximadamente 100 g, foram alocados em dois grupos: Grupo Controle (n = 30), que recebeu a dieta usada de rotina em nosso laboratorio, e Grupo Betacaroteno (n = 28), que recebeu betacaroteno (na forma de cristal, adicionado e misturado a dieta) na dose de 500 mg de betacaroteno/kg de dieta. Os animais receberam tratamento ate que atingissem entre 200 e 250 g, quando eram sacrificados. Foram coletados sangue, figado e coracao para realizacao de Western blotting e imunoistoquimica para conexina 43; foram realizados estudos morfometricos, dosagens de betacaroteno por cromatografia liquida de alta eficiencia bem como de glutationa reduzida, glutationa oxidada e hidroperoxidos de lipideos por analises bioquimicas. RESULTADOS: O betacaroteno foi detectado apenas no figado dos animais do Grupo Betacaroteno (288 ± 94,7 µg/kg). Os niveis de glutationa reduzida/glutationa oxidada foram maiores no figado e no coracao dos animais do Grupo Betacaroteno (figado - Grupo Controle: 42,60 ± 1,62; figado - Grupo Betacaroteno: 57,40 ± 5,90; p = 0,04; coracao: - Grupo Controle: 117,40 ± 1,01; coracao - Grupo Betacaroteno: 121,81 ± 1,32 nmol/mg proteina; p = 0,03). O conteudo de conexina 43 total foi maior no Grupo Betacaroteno. CONCLUSAO: O betacaroteno apresentou efeito benefico, caracterizado pelo aumento da comunicacao intercelular e melhora do sistema de defesa antioxidante. Nesse modelo, os mecanismos nao explicam a maior mortalidade observada com a suplementacao de betacaroteno em estudos clinicos. (Arq Bras Cardiol. 2013; [online].ahead print, PP.0-0)

Echocardiogram period Sh-Sed Sh-Ex MI-Sed MI-Ex Diastolic Area (cm2) 0.55 ± 0.07 0.55 ± 0.10 1.06 ± 0.16* 0.96 ± 0.23# Systolic Area (cm2) 0.16 ± 0.04 0.16 ± 0.03 0.82 ± 0.15* 0.68 ± 0.18#† Δ Area (%) 70.1 ± 6.35 70.0 ± 5.69 22.8 ± 7.86* 29.7 ± 5.51#† LVDD (mm) 8.73 ± 0.66 9,17 ± 0,34 11,79 ± 1,03* 11,26 ± 1,20# LVDD/BW (mm/Kg) 16.8 ± 1.24 18.3 ± 1.43 22.2 ± 2.35* 22.5 ± 2.29# LA (mm) 6.41 ± 0.55 6.13 ± 0.53 8.58 ± 1.41* 8.15 ± 1,09# LA/BW (mm/Kg) 12.4 ± 1.72 12.2 ± 0.94 16.2 ± 2.98* 16.2 ± 1.85# PWSV (mm/s) 38.3 ± 3.07 36.4 ± 3.16 20.1 ± 5.33* 21.6 ± 4.91#

FUNDAMENTO: A relevância do padrao de geometria apos o infarto do miocardio nao e conhecida. OBJETIVOS: Analisar a presenca de diferentes padroes de geometria ventricular esquerda (VE) e seu impacto como preditor de remodelacao em pacientes com infarto do miocardio. METODOS: Pacientes com infarto agudo anterior (n = 80) foram divididos de acordo com o padrao de geometria: normal (indice de massa [IMVE] normal e espessura relativa da parede [ERP] normal), remodelacao concentrica (IMVE normal e ERP aumentada), hipertrofia concentrica (IMVE e ERP aumentadas) e hipertrofia excentrica (IMVE aumentado e ERP normal). Apos seis meses, foi repetido o ecocardiograma. RESULTADOS: Quatro pacientes foram a obito. Dos sobreviventes, 41 apresentaram remodelacao (R+), enquanto 39 nao remodelaram (R-). Considerando-se o padrao geometrico, houve a seguinte distribuicao: 24 pacientes com padrao normal, 13 com remodelacao concentrica, 29 com hipertrofia concentrica e 14 com hipertrofia excentrica. Os pacientes que remodelaram apresentaram maiores tamanhos de infarto analisados pelo pico da CPK (R+ = 4.610 (1.688 - 7.970), R- = 1.442 (775 - 4.247), p < 0,001) e da CK-MB (R+ = 441 (246 - 666), R- = 183 (101 - 465), p < 0,001), tendencia a maior prevalencia de remodelacao concentrica (R+ = 10, R- = 3, p = 0,08) e menor prevalencia de hipertrofia excentrica (R+ = 2, R- = 12, p = 0,006). Na analise de regressao multivariada, o tamanho do infarto foi preditor (OR = 1,01; p = 0,020) e a hipertrofia excentrica foi fator protetor (OR = 0,189; p = 0,046) de remodelacao ventricular apos a oclusao coronariana. CONCLUSAO: O padrao de geometria ventricular pode ter impacto no processo de remodelacao em pacientes com infarto do miocardio.

Made available in DSpace on 2013-08-28T14:09:47Z (GMT). No. of bitstreams: 1 WOS000306687700090.pdf: 141400 bytes, checksum: 41b50410cc0558fe568f834ce2b9577a (MD5) Made available in DSpace on 2013-09-30T18:40:53Z (GMT). No. of bitstreams: 2 WOS000306687700090.pdf: 141400 bytes, checksum: 41b50410cc0558fe568f834ce2b9577a (MD5) WOS000306687700090.pdf.txt: 37081 bytes, checksum: bdfe065e7a523b5cf4259fe56d5437d8 (MD5) Previous issue date: 2012-07-23 Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-20T13:50:50Z No. of bitstreams: 2 WOS000306687700090.pdf: 141400 bytes, checksum: 41b50410cc0558fe568f834ce2b9577a (MD5) WOS000306687700090.pdf.txt: 37081 bytes, checksum: bdfe065e7a523b5cf4259fe56d5437d8 (MD5) Made available in DSpace on 2014-05-20T13:50:50Z (GMT). No. of bitstreams: 2 WOS000306687700090.pdf: 141400 bytes, checksum: 41b50410cc0558fe568f834ce2b9577a (MD5) WOS000306687700090.pdf.txt: 37081 bytes, checksum: bdfe065e7a523b5cf4259fe56d5437d8 (MD5) Previous issue date: 2012-07-23 Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES) Faculdade de Medicina de Botucatu - UNESP Introduction: Micronutrient deficiency is observed in heart failure patients. Taurine, for example, represents 50% of total free amino acids in the heart, and in vivo studies have linked taurine deficiency with cardiomyopathy.Methods: Thirty-four male Wistar rats (body weight = 100 g) were weighed and randomly assigned to one of two groups: Control (C) or taurine-deficient (T (-)). Beta-alanine at a concentration of 3% was added to the animals' water to induce taurine deficiency in the T (-) group. on day 30, the rats were individually submitted to echocardiography; morphometrical and histopathological evaluation and metalloproteinase activity, oxidative stress and inflammation evaluation were performed. Tissue samples were collected to determine the taurine concentration in the heart.Results: Taurine deficiency led to decreases in: ventricular wall thickness, left ventricle dry weight, myocyte sectional area, left ventricle posterior wall thickness and ventricular geometry. With regard to heart function, the velocity of the A wave, the ratio between the E and A wave, the ejection fraction, fractional shortening and cardiac output values were decreased in T () rats, suggesting abnormal diastolic and systolic function. Increased fibrosis, inflammation and increased activation of metalloproteinases were not observed. Oxidative stress was increased in deficient animals.Conclusions: These data suggest that taurine deficiency promotes structural and functional cardiac alterations with unique characteristics. Univ Estadual Paulista UNESP, Fac Med Botucatu, Dept Internal Med, Botucatu, SP, Brazil Univ Estadual Paulista UNESP, Inst Biociencias Botucatu, Dept Microbiol & Immunol, Botucatu, SP, Brazil Univ Estadual Paulista UNESP, Inst Biociencias Botucatu, Dept Chem & Biochem, Botucatu, SP, Brazil Univ São Paulo FMRP USP, Fac Med Ribeirao Preto, Dept Internal Med, Ribeirao Preto, SP, Brazil Univ Estadual Paulista UNESP, Fac Med Botucatu, Dept Internal Med, Botucatu, SP, Brazil Univ Estadual Paulista UNESP, Inst Biociencias Botucatu, Dept Microbiol & Immunol, Botucatu, SP, Brazil Univ Estadual Paulista UNESP, Inst Biociencias Botucatu, Dept Chem & Biochem, Botucatu, SP, Brazil

Submitted by Vitor Silverio Rodrigues (vitorsrodrigues@reitoria.unesp.br) on 2014-05-27T11:28:37Z No. of bitstreams: 0Bitstream added on 2014-05-27T14:48:14Z : No. of bitstreams: 1 2-s2.0-84876559654.pdf: 848952 bytes, checksum: d3fb094ff746b4c21fbb340cb75c967a (MD5) Made available in DSpace on 2014-05-27T11:28:37Z (GMT). No. of bitstreams: 0 Previous issue date: 2013-03-01 Background: In a previous study utilizing the rat model, exposure to tobacco smoke for 5 weeks increased survival after AMI, despite similar age and infarct size between the smokers and nonsmokers, and absence of reperfusion. Objective: Thus, this study aimed to analyze the effects of exposure to tobacco smoke on intensity, distribution or phosphorylation of connexin 43 in the rat heart. Methods: Wistar rats weighing 100 g were randomly allocated into 2 groups: 1) Control (n = 25); 2) Exposed to tobacco smoke (ETS), n = 23. After 5 weeks, left ventricular morphometric analysis, immunohisthochemistry and western blotting for connexin 43 (Cx43) were performed. Results: Collagen volume fraction, cross-sectional areas, and ventricular weight were not statistically different between control and ETS. ETS showed lower stain intensity of Cx43 at intercalated disks (Control: 2.32 ± 0.19; ETS: 1.73 ± 0.18; p = 0.04). The distribution of CX43 at intercalated disks did not differ between the groups (Control: 3.73 ± 0.12; ETS: 3.20 ± 0.17; p = 0.18). ETS rats showed higher levels of dephosphorylated form of Cx43 (Control: 0.45 ± 0.11; ETS: 0.90 ± 0.11; p = 0.03). On the other hand, total Cx43 did not differ between control and ETS groups (Control: 0.75 ± 0.19; ETS: 0.93 ± 0.27; p = 0.58). Conclusion: Exposure to tobacco smoke resulted in cardiac gap junction remodeling, characterized by alterations in the quantity and phosphorylation of the Cx43, in rats hearts. This finding could explain the smoker's paradox observed in some studies. Instituto de Biociências de Botucatu, Botucatu, SP