FABIANA GOULART MARCONDES BRAGA
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
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
5 resultados
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- Mode of Death on Chagas Heart Disease: Comparison with Other Etiologies. A Subanalysis of the REMADHE Prospective Trial(2013) AYUB-FERREIRA, Silvia M.; MANGINI, Sandrigo; ISSA, Victor S.; CRUZ, Fatima D.; BACAL, Fernando; GUIMARAES, Guilherme V.; CHIZZOLA, Paulo R.; CONCEICAO-SOUZA, Germano E.; MARCONDES-BRAGA, Fabiana G.; BOCCHI, Edimar A.Background: Sudden death has been considered the main cause of death in patients with Chagas heart disease. Nevertheless, this information comes from a period before the introduction of drugs that changed the natural history of heart failure. We sought to study the mode of death of patients with heart failure caused by Chagas heart disease, comparing with non-Chagas cardiomyopathy. Methods and results: We examined the REMADHE trial and grouped patients according to etiology (Chagas vs non-Chagas) and mode of death. The primary end-point was all-cause, heart failure and sudden death mortality; 342 patients were analyzed and 185 (54.1%) died. Death occurred in 56.4% Chagas patients and 53.7% non-Chagas patients. The cumulative incidence of all-cause mortality and heart failure mortality was significantly higher in Chagas patients compared to non-Chagas. There was no difference in the cumulative incidence of sudden death mortality between the two groups. In the Cox regression model, Chagas etiology (HR 2.76; CI 1.34-5.69; p = 0.006), LVEDD (left ventricular end diastolic diameter) (HR 1.07; CI 1.04-1.10; p<0.001), creatinine clearance (HR 0.98; CI 0.97-0.99; p = 0.006) and use of amiodarone (HR 3.05; CI 1.47-6.34; p = 0.003) were independently associated with heart failure mortality. LVEDD (HR 1.04; CI 1.01-1.07; p = 0.005) and use of beta-blocker (HR 0.52; CI 0.34-0.94; p = 0.014) were independently associated with sudden death mortality. Conclusions: In severe Chagas heart disease, progressive heart failure is the most important mode of death. These data challenge the current understanding of Chagas heart disease and may have implications in the selection of treatment choices, considering the mode of death.
- Hypertonic saline solution for prevention of renal dysfunction in patients with decompensated heart failure(2013) ISSA, Victor S.; ANDRADE, Lucia; AYUB-FERREIRA, Silvia M.; BACAL, Fernando; BRAGANCA, Ana C. de; GUIMARAES, Guilherme V.; MARCONDES-BRAGA, Fabiana G.; CRUZ, Fatima D.; CHIZZOLA, Paulo R.; CONCEICAO-SOUZA, Germano E.; VELASCO, Irineu T.; BOCCHI, Edimar A.Background: Renal dysfunction is associated with increased mortality in patients with decompensated heart failure. However, interventions targeted to prevention in this setting have been disappointing. We investigated the effects of hypertonic saline solution (HSS) for prevention of renal dysfunction in decompensated heart failure. Methods: In a double-blind randomized trial, patients with decompensated heart failure were assigned to receive three-day course of 100 mL HSS (NaCl 7.5%) twice daily or placebo. Primary end point was an increase in serumcreatinine of 0.3 mg/dL or more. Main secondary end point was change in biomarkers of renal function, including serum levels of creatinine, cystatin C, neutrophil gelatinase-associated lipocalin-NGAL and the urinary excretion of aquaporin 2 (AQP(2)), urea transporter (UT-A(1)), and sodium/hydrogen exchanger 3 (NHE3). Results: Twenty-two patients were assigned to HSS and 12 to placebo. Primary end point occurred in two (10%) patients in HSS group and six (50%) in placebo group (relative risk 0.3; 95% CI 0.09-0.98; P=0.01). Relative to baseline, serum creatinine and cystatin C levels were lower in HSS as compared to placebo (P=0.004 and 0.03, respectively). NGAL level was not statistically different between groups, however the urinary expression of AQP2, UT-A1 and NHE3 was significantly higher in HSS than in placebo. Conclusions: HSS administration attenuated heart failure-induced kidney dysfunction as indicated by improvement in both glomerular and tubular defects, a finding with important clinical implications. HSS modulated the expression of tubular proteins involved in regulation of water and electrolyte homeostasis.
conferenceObject Use of proliferation signal inhibitors in heart transplantation(2013) SAMUEL, M. Avila; BISELLI, B.; ULHOA JUNIOR, M. B.; NUSSBAUM, A. Santos; ESCALANTE, J. P.; MERCONDES-BRAGA, F. G.; AYUB-FERREIRA, S. M.; BRANDAO, S. M.; BACAL, F.; BOCCHI, E. A.- Insuficiência cardíaca descompensada(2013) MANGINI, Sandrigo; PIRES, Philippe Vieira; BRAGA, Fabiana Goulart Marcondes; BACAL, FernandoHeart failure is a disease with high incidence and prevalence in the population. The costs with hospitalization for decompensated heart failure reach approximately 60% of the total cost with heart failure treatment, and mortality during hospitalization varies according to the studied population, and could achieve values of 10%. In patients with decompensated heart failure, history and physical examination are of great value for the diagnosis of the syndrome, and also can help the physician to identify the beginning of symptoms, and give information about etiology, causes and prognosis of the disease. The initial objective of decompensated heart failure treatment is the hemodynamic and symptomatic improvement preservation and/or improvement of renal function, prevention of myocardial damage, modulation of the neurohormonal and/or inflammatory activation and control of comorbidities that can cause or contribute to progression of the syndrome. According to the clinical-hemodynamic profile, it is possible to establish a rational for the treatment of decompensated heart failure, individualizing the proceedings to be held, leading to reduction in the period of hospitalization and consequently reducing overall mortality.
- Myocarditis(2013) MONTERA, Marcelo Westerlund; MESQUITA, Evandro Tinoco; COLAFRANCESCHI, Alexandre Siciliano; OLIVEIRA JR., Amarino Carvalho de; RABISCHOFFSKY, Arnaldo; IANNI, Barbara Maria; ROCHITTE, Carlos Eduardo; MADY, Charles; MESQUITA, Claudio Tinoco; AZEVEDO, Clerio Francisco; BOCCHI, Edimar Alcides; SAAD, Eduardo Benchimol; BRAGA, Fabiana Goulart Marcondes; FERNANDES, Fabio; RAMIRES, Felix Jose Alvarez; BACAL, Fernando; FEITOSA, Gilson Soares; FIGUEIRA, Helio Roque; SOUZA NETO, Joao David de; MOURA, Lidia Ana Zytynski; CAMPOS, Luiz Antonio de Almeida; BITTENCOURT, Marcelo Imbroinise; BARBOSA, Marcia de Melo; MOREIRA, Maria da Consolacao Vieira; HIGUCHI, Maria de Lourdes; SCHWARTZMANN, Pedro; ROCHA, Ricardo Mourilhe; PEREIRA, Sabrina Bernardez; MANGINI, Sandrigo; MARTINS, Silvia Marinho; BORDIGNON, Solange; SALLES, Vitor Agueda