MAURO ROGERIO DE BARROS WANDERLEY JUNIOR

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LIM/11 - Laboratório de Cirurgia Cardiovascular e Fisiopatologia da Circulação, Hospital das Clínicas, Faculdade de Medicina

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  • conferenceObject
    Plasma Biomarkers Reflecting High Oxidative Stress Predicts Myocardial Injury Related to Anthracycline Chemotherapy in the CECCY Trial
    (2018) WANDERLEY JR., Mauro R.; AVILA, Monica S.; FERNANDES-SILVA, Miguel M.; CUNHA-NETO, Edecio; CRUZ, Fatima D.; BRANDAO, Goncalves Sara M.; RIGAUD, Vagner O.; HAJJAR, Ludhmila A.; KALIL FILHO, Roberto; BOCCHI, Edimar A.; AYUB-FERREIRA, Silvia M.
  • conferenceObject
    CARVEDILOL FOR PREVENTION OF CHEMOTHERAPY-INDUCED CARDIOTOXICITY: FINAL RESULTS OF THE PROSPECTIVE, RANDOMIZED, DOUBLE-BLIND, PLACEBO CONTROLLED CECCY TRIAL
    (2020) AYUB-FERREIRA, Silvia M.; AVILA, Monica; BRANDAO, Sara; CRUZ, Fatima D.; WANDERLEY JR., Mauro; RIGAUD, Vagner O. C.; HAJJAR, Ludhmila; KALIL-FILHO, Roberto; CRUZ, Cecilia B. V.; ALVES, Marco Stephan; GUIMARAES, Guilherme V.; ABDUCH, Maria; ISSA, Victor S.; SANTOS, Marilia; BITTENCOURT, Marcio; BOCCHI, Edimar Alcides
  • article 5 Citação(ões) na Scopus
    Plasma biomarkers reflecting high oxidative stress in the prediction of myocardial injury due to anthracycline chemotherapy and the effect of carvedilol: insights from the CECCY Trial
    (2022) WANDERLEY, M. R. de Barros; ÁVILA, M. S.; FERNANDES-SILVA, M. M.; CRUZ, F. das Dores; BRANDãO, S. M. G.; RIGAUD, V. O. C.; HAJJAR, L. A.; FILHO, R. K.; CUNHA-NETO, E.; BOCCHI, E. A.; AYUB-FERREIRA, S. M.
    Background: Anthracycline (ANT) is often used for breast cancer treatment but its clinical use is limited by cardiotoxicity (CTX). CECCY trial demonstrated that the β-blocker carvedilol (CVD) could attenuate myocardial injury secondary to ANT. Mieloperoxydase (MPO) is a biomarker of oxidative stress and galectin-3 (Gal-3) is a biomarker of fibrosis and cardiac remodeling. We evaluated the correlation between MPO and Gal-3 behavior with CTX. Materials and Methods: A post hoc analysis was performed in the patients who were included in the CECCY trial. A total of 192 women had her blood samples stored during the study at –80°C until the time of assay in a single batch. Stored blood samples were obtained at baseline, 3 and 6 months after randomization. We excluded samples from 18 patients because of hemolysis. MPO and Gal-3 were measured using Luminex xMAP technology through MILLIPLEX MAP KIT (Merck Laboratories). Results: 26 patients (14.9%) had a decrease of at least 10% in LVEF at 6 months after the initiation of chemotherapy. Among these, there was no significant difference in the MPO and Gal-3 when compared to the group without drop in LVEF (p = 0.85 for both MPO and Gal-3). Blood levels of MPO [baseline: 13.2 (7.9, 24.8), 3 months: 17.7 (11.1, 31.1), 6 months: 19.2 (11.1, 37.8) ng/mL] and Gal-3 [baseline: 6.3 (5.2, 9.6), 3 months: 12.3 (9.8, 16.0), 6 months: 10.3 (8.2, 13.1) ng/mL] increased after ANT chemotherapy, and the longitudinal changes were similar between the placebo and CVD groups (p for interaction: 0.28 and 0.32, respectively). In an exploratory analysis, as there is no normal cutoff value established for Gal-3 and MPO in the literature, the MPO and Gal-3 results were splited in two groups: above and below median. In the placebo group, women with high (above median) baseline MPO blood levels demonstrated a greater increase in TnI blood levels than those with low baseline MPO blood levels (p = 0.041). Compared with placebo, CVD significantly reduced TnI blood levels in women with high MPO blood levels (p < 0.001), but did not reduce the TnI levels in women with low baseline MPO blood levels (p = 0.97; p for interaction = 0.009). There was no significant interaction between CVD treatment and baseline Gal-3 blood levels (p for interaction = 0.99). Conclusions: In this subanalysis of the CECCY trial, MPO and Gal-3 biomarkers did not predict the development of CTX. However, MPO blood levels above median was associated with more severe myocardial injury and identified women who were most likely to benefit from carvedilol for primary prevention (NCT01724450). © 2022 Wanderley Jr. et al.
  • article 343 Citação(ões) na Scopus
    Carvedilol for Prevention of Chemotherapy-Related Cardiotoxicity
    (2018) AVILA, Monica Samuel; AYUB-FERREIRA, Silvia Moreira; WANDERLEY JR., Mauro Rogerio de Barros; CRUZ, Fatima das Dores; BRANDAO, Sara Michelly Goncalves; RIGAUD, Vagner Oliveira Carvalho; HIGUCHI-DOS-SANTOS, Marilia Harumi; HAJJAR, Ludhmila Abrahao; KALIL FILHO, Roberto; HOFF, Paulo Marcelo; SAHADE, Marina; FERRARI, Marcela S. M.; COSTA, Romulo Leopoldo de Paula; MANO, Max Senna; CRUZ, Cecilia Beatriz Bittencourt Viana; ABDUCH, Maria Cristina; ALVES, Marco Stephan Lofrano; GUIMARAES, Guilherme Veiga; ISSA, Victor Sarli; BITTENCOURT, Marcio Sommer; BOCCHI, Edimar Alcides
    BACKGROUND Anthracycline (ANT) chemotherapy is associated with cardiotoxicity. Prevention with beta-blockers remains controversial. OBJECTIVES This prospective, randomized, double-blind, placebo-controlled study sought to evaluate the role of carvedilol in preventing ANT cardiotoxicity. METHODS The authors randomized 200 patients with HER2-negative breast cancer tumor status and normal left ventricular ejection fraction (LVEF) referred for ANT (240 mg/m(2)) to receive carvedilol or placebo until chemotherapy completion. The primary endpoint was prevention of a >= 10% reduction in LVEF at 6 months. Secondary outcomes were effects of carvedilol on troponin I, B-type natriuretic peptide, and diastolic dysfunction. RESULTS Primary endpoint occurred in 14 patients (14.5%) in the carvedilol group and 13 patients (13.5%) in the placebo group (p = 1.0). No differences in changes of LVEF or B-type natriuretic peptide were noted between groups. A significant difference existed between groups in troponin I levels over time, with lower levels in the carvedilol group (p = 0.003). Additionally, a lower incidence of diastolic dysfunction was noted in the carvedilol group (p = 0.039). A nonsignificant trend toward a less-pronounced increase in LV end-diastolic diameter during the follow-up was noted in the carvedilol group (44.1 +/- 3.64 mm to 45.2 +/- 3.2 mm vs. 44.9 +/- 3.6 mm to 46.4 +/- 4.0 mm; p = 0.057). CONCLUSIONS In this largest clinical trial of beta-blockers for prevention of cardiotoxicity under contemporary ANT dosage, the authors noted a 13.5% to 14.5% incidence of cardiotoxicity. In this scenario, carvedilol had no impact on the incidence of early onset of LVEF reduction. However, the use of carvedilol resulted in a significant reduction in troponin levels and diastolic dysfunction.(Carvedilol Effect in Preventing Chemotherap-Induced Cardiotoxicity [CECCy] NCTO1724450)(C) 2018 by the American College of Cardiology Foundation.