VICTOR SARLI ISSA
Projetos de Pesquisa
Unidades Organizacionais
LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação, Hospital das Clínicas, Faculdade de Medicina
87 resultados
Resultados de Busca
Agora exibindo 1 - 10 de 87
bookPart Insuficiência cardíaca(2014) ISSA, Victor SarlibookPart Insuficiência cardíaca(2016) ISSA, Victor SarliconferenceObject Prevalence of Cognitive Impairment in Heart Transplant Waiting-List Patients in a Developing Country(2020) OLIVEIRA, F. M. de; IKEDA, E. T.; AVILA, M.; WOZNIAK, I.; SEGURO, L.; SANTOS, M.; FELTRIM, M.; BARONE, F.; ISSA, V.; LAGE, S.; BACAL, F.; BOCCHI, E.; GAIOTTO, F.; NOMURA, C.; MARCONDES-BRAGA, F.; MANGINI, S.conferenceObject The journey of patients with Chagas cardiomyopathy during episodes of descompensated heart failure(2018) ISSA, V. S.; GOMES, C.; TERHOCH, C. B.; MOREIRA, H. F.; PAES, T. M.; PADUA, V. P.; LAGE, S. G.; OLIVEIRA, M. T.; BOCCHI, E. A.- 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.
- Morphologic and immunohistochemical features of pulmonary vasculopathy in end-stage left ventricular systolic failure(2018) CAMPOS, Pompeu Tome Ribeiro de; LOPES, Antonio Augusto; ISSA, Victor Sali; AIELLO, Vera Demarchi
conferenceObject Type B natriuretic peptide as a rejection predictor in heart transplantation(2013) CRUZ, F. D. C.; ISSA, V. I.; FERREIRA, S. A.; CONCEICAO, G. E.; BACAL, F.; BOCCHI, E. A.- Impact of Exhaled Breath Acetone in the Prognosis of Patients with Heart Failure with Reduced Ejection Fraction (HFrEF). One Year of Clinical Follow-up(2016) MARCONDES-BRAGA, Fabiana G.; BATISTA, Guilherme L.; GUTZ, Ivano G. R.; SALDIVA, Paulo H. N.; MANGINI, Sandrigo; ISSA, Victor S.; AYUB-FERREIRA, Silvia M.; BOCCHI, Edimar A.; PEREIRA, Alexandre Costa; BACAL, FernandoBackground The identification of new biomarkers of heart failure (HF) could help in its treatment. Previously, our group studied 89 patients with HF and showed that exhaled breath acetone (EBA) is a new noninvasive biomarker of HF diagnosis. However, there is no data about the relevance of EBA as a biomarker of prognosis. Objectives To evaluate whether EBA could give prognostic information in patients with heart failure with reduced ejection fraction (HFrEF). Methods After breath collection and analysis by gas chromatography-mass spectrometry and by spectrophotometry, the 89 patients referred before were followed by one year. Study physicians, blind to the results of cardiac biomarker testing, ascertained vital status of each study participant at 12 months. Results The composite endpoint death and heart transplantation (HT) were observed in 35 patients (39.3%): 29 patients (32.6%) died and 6 (6.7%) were submitted to HT within 12 months after study enrollment. High levels of EBA (>= 3.7 mu g/L, 50th percentile) were associated with a progressively worse prognosis in 12-month follow-up (log-rank = 11.06, p = 0.001). Concentrations of EBA above 3.7 mu g/L increased the risk of death or HT in 3.26 times (HR = 3.26, 95% CI = 1.56-6.80, p = 0.002) within 12 months. In a multivariable cox regression model, the independent predictors of all-cause mortality were systolic blood pressure, respiratory rate and EBA levels. Conclusions High EBA levels could be associated to poor prognosis in HFrEF patients.
- Diagnostic discrepancies in clinical practice An autopsy study in patients with heart failure(2017) ISSA, Victor Sarli; DINARDI, Layara Fernanda Lipari; PEREIRA, Thiago Vicente; ALMEIDA, Lyna Kyria Rodrigues de; BARBOSA, Thaisa Silveira; BENVENUTTI, Luiz Alberto; AYUB-FERREIRA, Silvia Moreira; BOCCHI, Edimar AlcidesAutopsies are the gold standard for diagnostic accuracy; however, no recent study has analyzed autopsies in heart failure (HF). We reviewed 1241 autopsies (January 2000-May 2005) and selected 232 patients with HF. Clinical and autopsy diagnoses were analyzed and discrepancies categorized according to their importance regarding therapy and prognosis. Mean age was 63.3 +/- 15.9 years; 154 (66.4%) patients were male. The causes of death at autopsy were end-stage HF (40.9%), acute myocardial infarction (17.2%), infection (15.9), and pulmonary embolism 36 (15.5). Diagnostic discrepancies occurred in 191 (82.3%) cases; in 56 (24.1%), discrepancies were related to major diagnoses with potential influence on survival or treatment; pulmonary embolism was the cause of death for 24 (42.9%) of these patients. In 35 (15.1%), discrepancies were related to a major diagnosis with equivocal influence on survival or treatment; in 100 (43.1%), discrepancies did not influence survival or treatment. In multivariate analysis, age (OR: 1.03, 95% CI: 1.008-1.052, P=0.007) and presence of diabetes mellitus (OR: 0.359, 95% CI: 0.168-0.767, P=0.008) influenced the occurrence discrepancies. Diagnostic discrepancies with a potential impact on prognosis are frequent in HF. These findings warrant reconsideration in diagnostic and therapeutic practices with HF patients.
- 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.