MARCELO DANTAS TAVARES DE MELO

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  • article 5 Citação(ões) na Scopus
    Exercise training in heart failure with reduced ejection fraction and permanent atrial fibrillation: A randomized clinical trial
    (2022) ALVES, Leandro S.; BOCCHI, Edimar Alcides; CHIZZOLA, Paulo Roberto; CASTRO, Rafael Ertner; SALEMI, Vera Maria Cury; MELO, Marcelo Dantas Tavares de; ANDRETA, Camila Rocon de Lima; GUIMARAES, Guilherme Veiga
    BACKGROUND Heart failure (HF) associated with atrial fibrillation increases patients' physical inactivity, worsening their clinical condition and mortality. Exercise training is safe and has clear benefits in HF. However, little is known about the effects of exercise training on patients with HF with reduced ejection fraction and permanent atrial fibrillation (HFAF). OBJECTIVE The purpose of this study was to test the hypothesis that exercise training improves functional capacity, cardiac function, and quality of life in patients with HFAF. METHODS This randomized clinical trial was conducted at the Heart Institute. Patients with HFAF, left ventricular ejection fraction <= 40%, and resting heart rate (HR) <= 80 beats/min were included in the study. Cardiopulmonary testing, echocardiography, nervous system, and quality of life assessment were performed before and after the 12-week protocol period. RESULTS Twenty-six patients (mean age 58 +/- 1 years) were randomized to exercise training (HFAF-trained group; n = 13) or no training (HFAF-untrained group; n = 13). At baseline, no differences between the groups were found. Exercise improved peak oxygen consumption, slope of ventilation per minute/carbon dioxide production, and quality of life. The HFAF-trained group had significantly decreased resting HR (from 73 +/- 2 to 69 +/- 2 beats/ min; P = .02) and recovery HR (from 148 +/- 11 to 128 +/- 9 beats/min; P = .001). Concomitantly, left ventricular ejection fraction increased (from 31% 61% to 36% +/- 0.9%; P=.01), left atrial dimension decreased (from 52 +/- 1.2 to 47 +/- 1 mm; P = .03), and left ventricular end-systolic volume and left ventricular enddiastolic volume deceased (from 69 +/- 2 to 64 +/- 1.8 mL/m(2) and from 9962.1 to 9162 mL/m(2), respectively; P<.05). No changes were observed in the HFAF-untrained group. CONCLUSION Exercise training can improve exercise capacity, quality of life, and cardiac function in patients with HF with reduced ejection fraction and permanent atrial fibrillation.
  • article 0 Citação(ões) na Scopus
    Usefulness of Myocardial Deformation Indices in Preventing Cardiotoxicity in Breast Cancer Patients
    (2019) MELO, Marcelo Dantas Tavares de; SALEMI, Vera Maria Cury
  • article 36 Citação(ões) na Scopus
    Myocardial T1 mapping and extracellular volume quantification in patients with left ventricular non-compaction cardiomyopathy
    (2018) ARAUJO-FILHO, Jose A. B.; ASSUNCAO JR., Antonildes N.; MELO, Marcelo D. Tavares de; BIERE, Loic; LIMA, Camila R.; DANTAS JR., Roberto N.; NOMURA, Cesar H.; SALEMI, Vera M. C.; JEROSCH-HEROLD, Michael; PARGA, Jose R.
    Aims From pathophysiological mechanisms to risk stratification and management, much debate and discussion persist regarding left ventricular non-compaction cardiomyopathy (LVNC). This study aimed to characterize myocardial T1 mapping and extracellular volume (ECV) fraction by cardiovascular magnetic resonance (CMR), and investigate how these biomarkers relate to left ventricular ejection fraction (LVEF) and ventricular arrhythmias (VA) in LVNC. Methods and results Patients with LVNC (n = 36) and healthy controls (n = 18) were enrolled to perform a CMR with T1 mapping. ECV was quantified in LV segments without late gadolinium enhancement (LGE) areas to investigate diffuse myocardial fibrosis. Patients with LVNC had slightly higher native T1 (1024 +/- 43ms vs. 995 +/- 22 ms, P = 0.01) and substantially expanded ECV (28.0 +/- 4.5% vs. 23.5 +/- 2.2%, P < 0.001) compared to controls. The ECV was independently associated with LVEF (beta = -1.3, P = 0.001). Among patients without LGE, VAs were associated with higher ECV (27.7% with VA vs. 25.8% without VA, P = 0.002). Conclusion In LVNC, tissue characterization by T1 mapping suggests an extracellular expansion by diffuse fibrosis in myocardium without LGE, which was associated with myocardial dysfunction and VA, but not with the amount of noncompacted myocardium.
  • article 7 Citação(ões) na Scopus
    Smoking accelerates renal cystic disease and worsens cardiac phenotype in Pkd1-deficient mice
    (2021) SOUSA, Marciana V.; AMARAL, Andressa G.; FREITAS, Jessica A.; MURATA, Gilson M.; WATANABE, Elieser H.; BALBO, Bruno E.; TAVARES, Marcelo D.; HORTEGAL, Renato A.; ROCON, Camila; SOUZA, Leandro E.; IRIGOYEN, Maria C.; SALEMI, Vera M.; ONUCHIC, Luiz F.
    Smoking has been associated with renal disease progression in ADPKD but the underlying deleterious mechanisms and whether it specifically worsens the cardiac phenotype remain unknown. To investigate these matters, Pkd1-deficient cystic mice and noncystic littermates were exposed to smoking from conception to 18 weeks of age and, along with nonexposed controls, were analyzed at 13-18 weeks. Renal cystic index and cyst-lining cell proliferation were higher in cystic mice exposed to smoking than nonexposed cystic animals. Smoking increased serum urea nitrogen in cystic and noncystic mice and independently enhanced tubular cell proliferation and apoptosis. Smoking also increased renal fibrosis, however this effect was much higher in cystic than in noncystic animals. Pkd1 deficiency and smoking showed independent and additive effects on reducing renal levels of glutathione. Systolic function and several cardiac structural parameters were also negatively affected by smoking and the Pkd1-deficient status, following independent and additive patterns. Smoking did not increase, however, cardiac apoptosis or fibrosis in cystic and noncystic mice. Notably, smoking promoted a much higher reduction in body weight in Pkd1-deficient than in noncystic animals. Our findings show that smoking aggravated the renal and cardiac phenotypes of Pkd1-deficient cystic mice, suggesting that similar effects may occur in human ADPKD.
  • article 5 Citação(ões) na Scopus
    The Expression of Lipoprotein Receptors Is Increased in the Infarcted Area After Myocardial Infarction Induced in Rats With Cardiac Dysfunction
    (2018) LIMA, Aline D. de; GUIDO, Maria C.; TAVARES, Elaine R.; CARVALHO, Priscila O.; MARQUES, Alyne F.; MELO, Marcelo D. T. de; SALEMI, Vera M. C.; KALIL-FILHO, Roberto; MARANHAO, Raul C.
    Left ventricular (LV) remodeling after myocardial infarction constitutes the structural basis for ventricular dysfunction and heart failure. The characterization underlying the expression of lipoprotein receptors in cardiac dysfunction is scarcely explored. The aim of this study was to analyze the status of lipoprotein receptors on the infarcted and noninfarcted areas of LV and to verify whether nano particles that mimic the lipid structure of low-density lipoprotein (LDL) and have the ability to bind to LDL receptors (LDE) are taken up more avidly by the noninfarcted LV. 13 male Wistar rats with left coronary artery ligation (myocardial infarction [MI]) and 12 animals with SHAM operation (SHAM) were used in this study. 6 weeks after the procedure, the quantification of low-density lipoprotein receptor (LDLR), LDL receptor-related protein 1 (LRP1), scavenger receptor-class B type I (SR-BI) lipoprotein receptors, and PCNA proliferation marker, and tissue uptake of radioactively labeled LDE were performed. Immunohistochemistry and Western blot analysis showed that LDLR, LRP1, SR-BI, and PCNA, expression in infarcted area of MI was remarkably higher than SHAM and noninfarcted subendocardial (SEN) and interstitial (INT) areas. In addition, in SEN noninfarcted area of MI, the presence of LDLR was about threefold higher than in SHAM SEN and INT noninfarcted areas. The LDE uptake of noninfarcted LV of MI group was about 30% greater than that of SHAM group. In conclusion, these findings regarding the status of lipoprotein receptors after MI induction could help to establish mechanisms on myocardial repairing. In conclusion, infarcted rats with LV dysfunction showed increased expression of lipoprotein receptors mainly in the infarcted area.
  • article 1 Citação(ões) na Scopus
    Position Statement on the Use of Myocardial Strain in Cardiology Routines by the Brazilian Society of Cardiology's Department Of Cardiovascular Imaging-2023
    (2023) ALMEIDA, Andre Luiz Cerqueira; MELO, Marcelo Dantas Tavares de; BIHAN, David Costa de Souza Le; VIEIRA, Marcelo Luiz Campos; PENA, Jose Luiz Barros; CASTILLO, Jose Maria Del; ABENSUR, Henry; HORTEGAL, Renato de Aguiar; OTTO, Maria Estefania Bosco; PIVETA, Rafael Bonafim; DANTAS, Maria Rosa; ASSEF, Jorge Eduardo; BECK, Adenalva Lima de Souza; SANTO, Thais Harada Campos Espirito; SILVA, Tonnison de Oliveira; SALEMI, Vera Maria Cury; ROCON, Camila; LIMA, Marcio Silva Miguel; BARBERATO, Silvio Henrique; RODRIGUES, Ana Clara; RABSCHKOWISKY, Arnaldo; FROTA, Daniela do Carmo Rassi; GRIPP, Eliza de Almeida; BARRETTO, Rodrigo Bellio de Mattos; SILVA, Sandra Marques e; CAUDURO, Sanderson Antonio; PINHEIRO, Aurelio Carvalho; ARAUJO, Salustiano Pereira de; TRESSINO, Cintia Galhardo; SILVA, Carlos Eduardo Suaide; MONACO, Claudia Gianini; PAIVA, Marcelo Goulart; FISHER, Claudio Henrique; ALVES, Marco Stephan Lofrano; GRAU, Claudia R. Pinheiro de Castro; SANTOS, Maria Veronica Camara dos; GUIMARAES, Isabel Cristina Britto; MORHY, Samira Saady; LEAL, Gabriela Nunes; SOARES, Andressa Mussi; CRUZ, Cecilia Beatriz Bittencourt Viana; GUIMARAES FILHO, Fabio Villaca; ASSUNCAO, Bruna Morhy Borges Leal; FERNANDES, Rafael Modesto; SARAIVA, Roberto Magalhaes; TSUTSUI, Jeane Mike; SOARES, Fabio Luis de Jesus; FALCAO, Sandra Nivea dos Reis Saraiva; HOTTA, Viviane Tiemi; ARMSTRONG, Anderson da Costa; HYGIDIO, Daniel de Andrade; MIGLIORANZA, Marcelo Haertel; CAMAROZANO, Ana Cristina; LOPES, Marly Maria Uellendahl; CERCI, Rodrigo Julio; SIQUEIRA, Maria Eduarda Menezes de; TORREAO, Jorge Andion; ROCHITTE, Carlos Eduardo; FELIX, Alex
  • article 0 Citação(ões) na Scopus
    New Paradigms in the Evaluation of Diastolic Function by Cardiac Magnetic Resonance Imaging in Aortic Valvopathy
    (2020) SALEMI, Vera Maria Cury; MELO, Marcelo Dantas Tavares de; ARAUJO FILHO, Jose De Arimateia Batista
  • article 29 Citação(ões) na Scopus
    Nicotinamide attenuates streptozotocin-induced diabetes complications and increases survival rate in rats: role of autonomic nervous system
    (2021) CRUZ, Paula L.; MORAES-SILVA, Ivana C.; RIBEIRO, Amanda A.; MACHI, Jacqueline F.; MELO, Marcelo Dantas Tavares de; SANTOS, Fernando dos; SILVA, Maikon Barbosa da; STRUNZ, Celia Maria Cassaro; CALDINI, Elia Garcia; IRIGOYEN, Maria-Claudia
    Background To evaluate the effect of nicotinamide prior to streptozotocin-induced (STZ) diabetes in baroreflex sensitivity and cardiovascular autonomic modulation, and its association with hemodynamics and metabolic parameters. Methods Methods: Male Wistar rats were divided into control (Cont) and STZ-induced diabetes (Diab). Half of the rats from each group received a single dose of nicotinamide (100 mg/Kg) before STZ injection (Cont+NicA and Diab+NicA). All groups were followed-up for 5 weeks. Results Body weight loss of more than 40% was observed in Diab throughout the period (Diab: 271.00 +/- 12.74 g; Diab+NicA: 344.62 +/- 17.82). Increased glycemia was seen in Diab rats (541.28 +/- 18.68 mg/dl) while Diab+NicA group had a slight decrease (440.87 +/- 20.96 mg/dl). However, insulin resistance was observed only in Diab. In relation to Cont, heart rate, mean blood pressure and diastolic function were reduced when compared to Diab, together with parasympathetic modulation and baroreflex sensitivity. All of these parameters were improved in Diab+NicA when compared to Diab. Improved baroreflex sensitivity and parasympathetic modulation were correlated with glycemia, insulin resistance, and body weight mass. Additionally, Diab+NicA group increased survival rate. Conclusions Results suggest that the association of nicotinamide in STZ-induced diabetic rats prevents most of the expected derangements mainly by preserving parasympathetic and baroreflex parameters.
  • article 5 Citação(ões) na Scopus
    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 Cury
    Aims 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.
  • article 4 Citação(ões) na Scopus
    Left ventricular basal region involvement in noncompaction cardiomyopathy
    (2013) MELO, Marcelo Dantas Tavares de; BENVENUTI, Luiz A.; MADY, Charles; KALIL-FILHO, Roberto; SALEMI, Vera M. C.
    A previously healthy 16-year-old woman experienced progressive dyspnea on exertion. The echocardiogram and cardiac magnetic resonance imaging showed a significant increase in cardiac chambers, severe biventricular systolic dysfunction, and prominent ventricular trabeculations suggesting noncompaction cardiomyopathy (NCC). The patient underwent heart transplantation 5 years after the NCC diagnosis, and the anatomopathological examination evidenced diffuse biventricular hypertrabeculation compromise, including the basal region of the biventricular wall. There is no consensus about the gold-standard diagnostic criteria, which demands a conceptual review and attention to another point: the relation of trabeculation volume and prognosis.