CHARLES MADY
Projetos de Pesquisa
Unidades Organizacionais
Departamento de Cardio-Pneumologia, Faculdade de Medicina - Docente
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 - Líder
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 - Líder
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conferenceObject Impact of sympathectomy upon myocardium(2019) PESSOA, F. Fernanda; JORDAO, M. R.; FONSECA, K. C. B.; ZANONI, F.; SALEMI, V. M. C.; RIBEIRO, O. N.; SOUZA, L. E.; FERNANDES, F.; IRIGOYEN, M. C.; MOREIRA, L. F. P.; MADY, C.; RAMIRES, F. J. A.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 Effects of sympathectomy on myocardium(2014) JORDAO, M.; RAMIRES, F.; PESSOA, F.; FONSECA, K.; ZANONI, F.; SOUZA, L.; SALEMI, V.; MADY, C.conferenceObject Brain natriuretic peptide predicts mortality in patients undergoing pericardiectomy for constrictive pericarditis(2014) MELO, D. T. P.; FERNANDES, F.; GUALANDRO, D. M.; SALEMI, V. M. C.; OLIVETTI, N. Q. S.; BUCK, P. C.; DIAS, R. R.; RAMIRES, F. J. A.; CARAMELLI, B.; MADY, C.- Erythropoietin reduces collagen deposition after myocardial infarction but does not improve cardiac function(2018) PESSOA, Fernanda Gallinaro; MADY, Charles; FONSECA, Keila Cardoso Barbosa; OLIVEIRA-FONOFF, Adriana Morgan de; SALEMI, Vera Maria Cury; JORDAO, Mauricio Rodrigues; FERNANDES, Fabio; RAMIRES, Felix Jose AlvarezMyocardial remodeling includes inappropriate collagen deposition in the interstitium. Erythropoietin (EPO) may have cardioprotective effects. We aimed to assess the role of EPO on myocardial remodeling during the chronic phase. We studied 60 Wistar rats divided into the following groups: control (CT), control + EPO (CT + EPO), myocardial infarction + EPO (MI + EPO), and myocardial infarction (MI). The interstitial collagen volume fraction (ICVF) was quantified and echocardiography was performed. We quantified asymmetric dimethylarginine and glutathione by ELISA, and used real-time PCR to assess apoptosis and inflammation. Western blotting was used to evaluate inflammatory proteins and tissue inhibitors of metalloproteinases (TIMPs), and TUNEL staining was used to detect apoptosis. For matrix metalloproteinases (MMPs), we performed zymography. Parametric and nonparametric analyses were performed according to normality testing. ICVF was greater in MI groups (p < 0.001) and was attenuated by EPO (p = 0.05). The MMP-2 did not show any difference between groups. The TIMP-1 and TIMP-2 did not have difference between groups. The MI groups had worse fraction shortening (p < 0.001), without EPO protection (p = 0.666). The MI groups had increased left ventricle diastolic dimension (p < 0.001) without EPO attenuation (p = 0.79). EPO did not act on oxidative stress. Apoptosis and inflammation were not modulated by EPO. We concluded that EPO attenuated interstitial collagen accumulation, but did not protect from heart dilation or dysfunction.
conferenceObject Baroreflex and cardiac dysfunctions evaluated by transesophageal echocardiography, baroreflex sensitivity, autonomic control and invasive measurements in rats submitted to sinoaortic denervation(2012) SIRVENTE, R. A.; IRIGOYEN, M. C.; SOUZA, L.; MOSTARDA, C.; FUENTE, R. La; CANDIDO, G.; SOUZA, P.; MEDEIROS, A.; MADY, C.; SALEMI, V. M. C.Purpose: Sympathetic hyperactivity commonly seems to be related to cardiac dysfunction and baro and chemoreflexes impairment in hypertension. However, myocardial function has not been evaluated regarding the association of hypertension and baroreflex dysfunction using transesophageal echocardiography. Methods: Exercise test (ET), baroreflex sensitivity, cardiovascular autonomic control, transthoracic and transesophageal echocardiography using intracardiac echocardiographic catheter (AcuNav, Siemens, Mountain View, CA, USA), and invasively biventricular end-diastolic pressures (EDP) were evaluated in rats 10 weeks after sinoaortic denervation (SAD). The rats (n=32) were divided in 4 groups: 16 Wistar (W) with (n=8) or without SAD (n=8) and 16 spontaneously hypertensive rats (SHR) with (n=8) or without SAD (n=8). Results: Blood pressure (BP) and heart rate (HR) did not show any change between the groups SAD and without SAD, although, SHR showed higher BP levels in comparison to W. BP variability was increased in SHR groups compared to W. After SAD, BP variability increased in all groups compared to W (W: 15 mmHg2; *DSA: 49 mmHg2; *SHR: 60 mmHg2; *SHR-SAD:137 mmHg2, *p<0.05 vs. W). Exercise tests results showed that SHR had better functional capacity compared to SAD and SHRSAD (W: 1.16m/s; DSA: 0.9m/s; *SHR: 1.46; SHR-DSA: 1.02, *p<0.05 vs. SAD and SHRSAD). Left ventricular concentric hypertrophy, segmental systolic dysfunction and global diastolic LV dysfunction, segmental and global systolic dysfunction, and global diastolic RV dysfunction, indirect signals of pulmonary arterial hypertension were shown by echocardiography, mostly evident in SHRSAD. The RV-EDP increased in all groups compared to W(W:3±0.39mmHg, *SAD:4.7±0.52mmHg, *SHR: 6.6±1.1mmHg, *SHRSAD:7.8±0.87mmHg, *p<0.05 vs. W), and LV-EDP increased in SHR and SHRSAD groups compared to W, and in SHRSAD compared to SAD (W: 5,83±0,19 mmHg,SAD: 8.98±1.2 mmHg, *SHR: 12.51±4.73 mmHg, *#SHRSAD: 14.57±2.52mmHg, *p<0.05vs.W,#p<0.05 vs. DSA). There was a relation between invasive or noninvasive measurements of RV showing good accuracy of echocardiographic measurements. Conclusions: Our results suggest that baroreflex dysfunction impaired biventricular function. Moreover, the findings of RV dysfunction indicate that SAD may lead to increased pulmonary artery pressure, supporting a role for baroreflex dysfunction in the pathogenesis of the hypertensive cardiac disease.conferenceObject Lack of Effect of Simvastatin on Structural Remodeling in Animal Model of Chagas Cardiomyopathy(2012) IANNI, Barbara M.; RAMIRES, Felix J. A.; SALEMI, Vera M. C.; FERNANDES, Fabio; OLIVEIRA, Adriana M.; PESSOA, Fernanda G.; FONSECA, Keila C. B.; ARTEAGA, Edmundo; NASTARI, Luciano; MADY, CharlesPurpose: Chagas cardiomyopathy(CM) is characterized by a large amount of fibrosis and inflamation. As simvastatin (simva) has anti-inflamatory effects, we hypothetized that it could be an important drug in the treatment of patients with CM. The purpose was to evaluate simva in the myocardium remodeling and inflammation in na animal model of CM. Methods: 123 hamsters were divided: C-controls(25), CSimva-controls with simva 10mg/Kg/day(25), Simva1-infected treated from beginning with the same dose of simva(25), Simva2-infected treated after 4 months(24); Infect-untreated(24). Follow-up of 10 months. Interstitial collagen volume fraction (ICVF) RV and LV measured using videomorphometry and picrosirius red stained heart. Metalloproteinase9 (MMP9) was obtained by zymography. Gene expression of TNFalpha, IFNgamma, IL10 by real time PCR and ΔCt. Survival by Kaplan-Meier and log rank. Comparison between groups by Kruskal-Wallis; p≤0.05. Results: Infected animals Simva1=189±133 days Simva2=150±124; Infect=138±123) lived less than controls (C=257±80; CSimva=283±58)(p≤0.05) with no difference among infected. ICVF-RV(%) was greater in infected groups (Simva1=3.88±1.14, Simva2=2.22±0.64; Infect=4.38±0.83) than in controls C=1.12±0.31; CSimva=2.18±0.73)(p≤0.05)with no difference among infected groups. ICVF-LV(%) was greater in infected animals (Simva1=1.83±1.01, Simva2=1.52±0.93; Infect=3.01±0.66) than in controls (C=0.68±0.31; CSimva=0.81±0.28)(p≤0.05) with no difference among infected. MMP9 was higher in infected groups (Simva1=2394±2441, Simva2=5673±4091; Infect=2392±2042) compared to controls (C=954±2332; CSimva=454±1123)(p≤0.05) with no difference among infected. TNFalpha did not have difference among infected groups (Simva1=5.33±3.66, Simva2=4.44±2.17; Infect=6.13±3.24). IFNgamma in infected groups (Simva1=5.47±3.56, Simva2=4.46±2.08; Infect=4.21±2.09) was higher than in controls (C=8.50±2.59; CSimva=6.84±2.53)(p≤0.05) with no difference among infected. IL10 in infected animals (Simva1=9.07±4.62, Simva2=7.76±4.77; Infect=8.11±4.48) did not have difference and the values were greater than controls (C=14.11±4.40; CSimva=12.55±3.90)(p≤0.05). Conclusions: Simva did not attenuate deposition of interstitial collagen, did not change dynamics of collagen degradation, did not decrease inflammation, and did not reduce mortality.conferenceObject Neurovascular Control and Spontaneous Baroreflex Sensitivity in Heart Failure Patients with Preserved Ejection Fraction(2014) SAYEGH, Ana Luiza C.; SANTOS, Marcelo R. dos; SOUZA, Francis R. de; SALEMI, Vera Maria C.; OLIVEIRA, Carlos Augusto P.; FONSECA, Felipe X.; RODRIGUES, Sara; TROMBETTA, Ivani C.; TOSCHI-DIAS, Edgar; NEGRAO, Carlos Eduardo; ALVES, Maria-Janieire N.; MADY, CharlesconferenceObject Influence of air pollution upon myocardial remodeling(2013) OLIVEIRA, A. M.; RAMIRES, F.; FONSECA, K. C. B.; SALEMI, V. M.; PESSOA, F. G.; FERNANDES, F.; SALDIVA, P.; MADY, C.article 5 Citação(ões) na Scopus Tratamento de lesão de tronco da artéria coronária esquerda após radioterapia do tórax(2011) SALEMI, Vera Maria Cury; DABARIAN, Andre L.; NASTARI, Luciano; GAMA, Marcus; SOARES JUNIOR, Jose; MADY, CharlesPrevention of late cardiovascular complications after radiation therapy (RT) for treatment of a malignant tumor is challenging. We report the case of a young male patient with Hodgkin's lymphoma treated with RT, who developed ischemic heart disease during follow-up, although he had no cardiovascular risk factors. We conclude that patients undergoing RT who experience chest pain should be fully investigated for coronary artery disease.