VERA MARIA CURY SALEMI
Projetos de Pesquisa
Unidades Organizacionais
LIM/65, Hospital das Clínicas, Faculdade de Medicina
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação, Hospital das Clínicas, Faculdade de Medicina
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação, Hospital das Clínicas, Faculdade de Medicina
15 resultados
Resultados de Busca
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conferenceObject Echocardiographic findings of Trypanosoma cruzi seropositive blood donors(2017) SALEMI, V. M. C.; OLIVEIRA, C. D. L.; RIBEIRO, A. L.; MENEZES, M. M.; ANTUNES, A. P.; FERREIRA-FILHO, J. C.; SACHDEV, V.; FERNANDES, F.; NASTARI, L.; IANNI, B. M.; MADY, C.; CARNEIRO-PROIETTI, A. B.; KEATING, S. M.; BUSCH, M. P.; SABINO, E. G.conferenceObject METHOTREXATE CARRIED IN LIPID CORE NANOPARTICLES REDUCED THE INFARCTION SIZE AND IMPROVED LEFT VENTRICLE FUNCTION FOLLOWING ACUTE MYOCARDIUM INFARCTION INDUCED IN RATS(2017) MARANHAO, Raul Cavalcante; GUIDO, Maria Carolina; MARQUES, Alyne Franca; TAVARES, Elaine Rufo; BISPO, Deborah Lima; MELO, Marcelo Dantas Tavares De; LIMA, Aline Derisio; NICOLAU, Jose Carlos; SALEMI, Vera Maria; KALIL-FILHO, Roberto- Caracterização das Variáveis do Teste de Esforço Cardiopulmonar em Pacientes com Endomiocardiofibrose após Cirurgia de Ressecção Endocárdica(2017) SAYEGH, Ana Luiza C.; SANTOS, Marcelo R. dos; OLIVEIRA, Patricia de; FERNANDES, Fabio; RONDON, Eduardo; SOUZA, Francis R. de; SALEMI, Vera M. C.; ALVES, Maria Janieire de N. N.; MADY, CharlesBackground: Endomyocardial fibrosis (EMF) is a rare disease, characterized by diastolic dysfunction which leads to reduced peak oxygen consumption (VO2). Cardiopulmonary exercise testing (CPET) has been proved to be a fundamental tool to identify central and peripheral alterations. However, most studies prioritize peak VO2 as the main variable, leaving aside other important CPET variables that can specify the severity of the disease and guide the clinical treatment. Objective: The aim of this study was to evaluate central and peripheral limitations in symptomatic patients with EMF by different CPET variables. Methods: Twenty-six EMF patients (functional class III, NYHA) were compared with 15 healthy subjects (HS). Functional capacity was evaluated using CPET and diastolic and systolic functions were evaluated by echocardiography. Results: Age and gender were similar between EMF patients and HS. Left ventricular ejection fraction was normal in EMF patients, but decreased compared to HS. Peak heart rate, peak workload, peak VO2, peak oxygen (O-2) pulse and peak pulmonary ventilation (V-E) were decreased in EMF compared to HS. Also, EMF patients showed increased Delta heart rate /Delta oxygen uptake and Delta oxygen uptake /Delta work rate compared to HS. Conclusion: Determination of the aerobic capacity by noninvasive respiratory gas exchange during incremental exercise provides additional information about the exercise tolerance in patients with EMF. The analysis of different CPET variables is necessary to help us understand more about the central and peripheral alterations cause by both diastolic dysfunction and restrictive pattern.
- Vitamin C mitigates oxidative/nitrosative stress and inflammation in doxorubicin-induced cardiomyopathy(2017) AKOLKAR, Gauri; DIAS, Danielle da Silva; AYYAPPAN, Prathapan; BAGCHI, Ashim K.; JASSAL, Davinder S.; SALEMI, Vera Maria Cury; IRIGOYEN, Maria Claudia; ANGELIS, Katia De; SINGAL, Pawan K.Increase in oxidative/nitrosative stress is one of the mechanisms associated with the development of cardiotoxicity due to doxorubicin (Dox), a potent chemotherapy drug. Previously, we reported mitigation of Dox-induced oxidative/nitrosative stress and apoptosis by vitamin C (Vit C) in isolated cardiomyocytes. In the present in vivo study in rats, we investigated the effect of prophylactic treatment with Vit C on Dox-induced apoptosis, inflammation, oxidative/nitrosative stress, cardiac dysfunction, and Vit C transporter proteins. Dox (cumulative dose: 15 mg/kg) in rats reduced systolic and diastolic cardiac function and caused structural damage. These changes were associated with a myocardial increase in reactive oxygen species, reduction in antioxidant enzyme activities, increased expression of apoptotic proteins, and inflammation. Dox also caused an increase in the expression of proapoptotic proteins Bax, Bnip-3, Bak, and caspase-3. An increase in oxidative/nitrosative stress attributable to Dox was indicated by an increase in superoxide, protein carbonyl formation, lipid peroxidation, nitric oxide (NO), NO synthase (NOS) activity, protein nitrosylation, and inducible NOS protein expression. Dox increased the levels of cardiac proinflammatory cytokines TNF-alpha, IL-1 beta, and IL-6, whereas the expression of Vit C transporter proteins (sodium-ascorbate cotransporter 2 and glucose transporter 4) was reduced. Prophylactic and concurrent treatment with Vit C prevented all these changes and improved survival in the Vit C + Dox group. Vit C also improved Dox-mediated systolic and diastolic dysfunctions and structural damage. These results suggest a cardioprotective role of Vit C in Dox-induced cardiomyopathy by reducing oxidative/nitrosative stress, inflammation, and apoptosis, as well as improving Vit C transporter proteins. NEW & NOTEWORTHY This in vivo study provides novel data that vitamin C improves cardiac structure and function in doxorubicin-induced cardiomyopathy by reducing oxidative/nitrosative stress, apoptosis, and inflammation along with upregulation of cardiac vitamin C transporter proteins. The latter may have a crucial role in improving antioxidant status in this cardiomyopathy.
- Decreased glycolytic metabolism in non-compaction cardiomyopathy by F-18-fluoro-2-deoxyglucose positron emission tomography: new insights into pathophysiological mechanisms and clinical implications(2017) MELO, Marcelo Dantas Tavares de; GIORGI, Maria Clementina Pinto; ASSUNCAO JR., Antonildes Nascimento; DANTAS JR., Roberto Nery; ARAUJO FILHO, Jose de Arimateia; PARGA FILHO, Jose Rodrigues; BIERRENBACH, Ana Luiza de Souza; LIMA, Camila Rocon de; SOARES JR., Jose; MENEGUETTI, Jose Claudio; MADY, Charles; HAJJAR, Ludhmila Abrahao; KALIL FILHO, Roberto; BOCCHI, Edimar Alcides; SALEMI, Vera Maria CuryAims The pathophysiological mechanisms of left ventricular non-compaction cardiomyopathy (LVNC) remain controversial. This study performed combined F-18-fluoro-2-deoxyglucose dynamic positron emission tomography (FDG-PET) and 99mTc-sestamibi single-photon emission computed tomography (SPECT) studies to evaluate myocardial glucose metabolism and perfusion in patients with LVNC and their clinical implications. Methods and results Thirty patients (41 +/- 12 years, 53% male) with LVNC, diagnosed by cardiovascular magnetic resonance (CMR) criteria, and eight age-matched healthy controls (42 +/- 12 years, 50% male) were prospectively recruited to undergo FDG-PET with measurement of the myocardial glucose uptake rate (MGU) and SPECT to investigate perfusion-metabolism patterns. Patients with LVNC had lower global MGU compared with that in controls (36.9 +/- 8.8 vs. 44.6 +/- 5.4 mu mol/min/100 g, respectively, P = 0.02). Of 17 LV segments, MGU levels were significantly reduced in 8, and also a reduction was observed when compacted segments from LVNC were compared with the segments from control subjects (P < 0.001). Perfusion defects were also found in 15 (50%) patients (45 LV segments: 64.4% match, and 35.6% mismatch perfusion-metabolism pattern). Univariate and multivariate analyses showed that beta-blocker therapy was associated with increased MGU (beta coefficient = 10.1, P = 0.008). Moreover, a gradual increase occurred in MGU across the beta-blocker dose groups (P for trend = 0.01). Conclusion The reduction of MGU documented by FDG-PET in LVNC supports the hypothesis that a cellular metabolic pathway may play a role in the pathophysiology of LVNC. The beneficial effect of beta-blocker mediating myocardial.
- The role of air pollution in myocardial remodeling(2017) OLIVEIRA-FONOFF, A. M. de; MADY, C.; PESSOA, F. G.; FONSECA, K. C. B.; SALEMI, V. M. C.; FERNANDES, F.; SALDIVA, P. H. N.; RAMIRES, F. J. A.Background Excessive air pollution in urban environments can impact morbidity and mortality. The authors evaluated the role of particulate matter(2.5) (PM2.5) in structural, geometric, and functional remodeling in hearts, using an experimental model of myocardial infarction. Methods and findings Seventy-five rats were divided into 5 groups: control (CG), CG exposed to PM2.5 pollution (CGP), myocardial infarcted group (MI), infarcted group immediately exposed to pollution (IGP-I), and infarcted group previously exposed to pollution and kept exposed after infarction (IGP-II). Greater deposition of interstitial collagen occurred in the left ventricle in CGP, MI, IGP-I, and IGP-II groups compared with that in controls (p = 0.002 CG vs CGP and p<0.0001 CG vs MI, IGP-I, and IGP-II). In the right ventricle, greater collagen deposition existed in CGP, MI, IGP-I, and IGP-II compared with that in CG (p<0.021 CG vs CGP and p<0.0001 CG vs MI, IGP-I, and IGP-II). At the end of the study, CG had a higher mean shortening fraction than the other groups had (p <= 0.03). Left ventricular systolic diameter was lower in CG than in infarcted groups (p <= 0.003). The infarcted groups had greater expression of TGF-beta (p <= 0.04). PM2.5 increased the expression of TGF-beta in the IGP-II compared with the MI group (p = 0.004). The TNF-alpha gene was overexpressed in the IGP-II compared with the CGP group (p = 0.012). INF-gamma gene expression was greater in IGP-II (p <= 0.01). Oxidative stress analysis showed a higher glutathione concentration in CGP (p = 0.03), MI (p = 0.014), and IGP-I (p = 0.008) compared with that in CG. Conclusions PM2.5 stimulates the deposition of fibrosis in the myocardium of healthy hearts, but not in infarcted hearts. PM2.5 modulates the inflammatory response, which was greater in the IGP-II group. It also modulates oxidative stress in healthy hearts but not in infarcted hearts.
- Methotrexate carried in lipid core nanoparticles reduces myocardial infarction size and improves cardiac function in rats(2017) MARANHAO, Raul C.; GUIDO, Maria C.; LIMA, Aline D. de; TAVARES, Elaine R.; MARQUES, Alyne F.; MELO, Marcelo D. Tavares de; NICOLAU, Jose C.; SALEMI, Vera Mc; KALIL-FILHO, RobertoPurpose: Acute myocardial infarction (MI) is accompanied by myocardial inflammation, fibrosis, and ventricular remodeling that, when excessive or not properly regulated, may lead to heart failure. Previously, lipid core nanoparticles (LDE) used as carriers of the anti-inflammatory drug methotrexate (MTX) produced an 80-fold increase in the cell uptake of MTX. LDE-MTX treatment reduced vessel inflammation and atheromatous lesions induced in rabbits by cholesterol feeding. The aim of the study was to investigate the effects of LDE-MTX on rats with MI, compared with commercial MTX treatment. Materials and methods: Thirty-eight Wistar rats underwent left coronary artery ligation and were treated with LDE-MTX, or with MTX (1 mg/kg intraperitoneally, once/week, starting 24 hours after surgery) or with LDE without drug (MI-controls). A sham-surgery group (n=12) was also included. Echocardiography was performed 24 hours and 6 weeks after surgery. The animals were euthanized and their hearts were analyzed for morphometry, protein expression, and confocal microscopy. Results: LDE-MTX treatment achieved a 40% improvement in left ventricular (LV) systolic function and reduced cardiac dilation and LV mass, as shown by echocardiography. LDE-MTX reduced the infarction size, myocyte hypertrophy and necrosis, number of inflammatory cells, and myocardial fibrosis, as shown by morphometric analysis. LDE-MTX increased antioxidant enzymes; decreased apoptosis, macrophages, reactive oxygen species production; and tissue hypoxia in non-infarcted myocardium. LDE-MTX increased adenosine bioavailability in the LV by increasing adenosine receptors and modulating adenosine catabolic enzymes. LDE-MTX increased the expression of myocardial vascular endothelium growth factor (VEGF) associated with adenosine release; this correlated not only with an increase in angiogenesis, but also with other parameters improved by LDE-MTX, suggesting that VEGF increase played an important role in the beneficial effects of LDE-MTX. Overall effects of commercial MTX were minor, and did not improve LV function or infarction size. Both treatments did not induce any toxicity. Conclusion: The remarkable improvement in heart function and reduction in infarction size achieved by LDE-MTX supports future clinical trials.
conferenceObject EFFECTS OF TREATMENT WITH METHOTREXATE ASSOCIATED TO LIPID NANOPARTICLES ON DIABETIC CARDIOMYOPATHY IN RATS(2017) MARANHAO, Raul Cavalcante; MARQUES, Alyne Franca; GUIDO, Maria Carolina; TAVARES, Elaine Rufo; BISPO, Deborah Lima; MELO, Marcelo Dantas Tavares de; SALEMI, Vera MariaconferenceObject Relationship between autonomic activity, beta receptors and catecholamines after sympathectomy(2017) JORDAO, M. R.; ZANONI, F.; PESSOA, F. G.; FONSECA, K. C. B.; SALEMI, V. M. C.; SOUZA, L. E.; RIBEIRO, O. N.; FERNANDEZ, F.; MADY, C.; RAMIRES, F. J. A.conferenceObject Effect of exercise training on functional capacity and left atrium volume in patients with restrictive cardiomyopathy(2017) SAYEGH, A. L.; SANTOS, M. Dos; OLIVEIRA, P.; RONDON, E.; SOUZA, F. R. De; SALEMI, V. M. C.; ALVES, M. J. N. N.; MADY, C.