BARBARA MARIA IANNI
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
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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.- The effect of beta-blockade on myocardial remodelling in Chagas' cardiomyopathy(2012) PIMENTEL, Walace de Souza; RAMIRES, Felix Jose Alvarez; IANNI, Barbara Maria; SALEMI, Vera Maria Cury; BILATE, Angelina Morand Bianchi; CUNHA-NETO, Edecio; OLIVEIRA, Adriana Morgan de; FERNANDES, Fabio; MADY, CharlesOBJECTIVE: Chagas' disease has spread throughout Latin America because of the high rate of migration among these countries. Approximately 30% of Chagas' patients will develop cardiomyopathy, and 10% of these will develop severe cardiac damage leading to heart failure. Beta-blockade improves symptoms and survival in heart failure patients; however, its efficacy has not been well established in Chagas' disease. We evaluated the role of carvedilol in cardiac remodeling and mortality in a Chagas' cardiomyopathy animal model. METHODS: We studied Trypanosoma cruzi infection in 55 Syrian hamsters that were divided into three groups: control (15), infected (20), and infected + carvedilol (20). Animals underwent echocardiography, electrocardiography, and morphometry for collagen evaluation in ventricles stained with picrosirius red. RESULTS: The left ventricular diastolic diameter did not change between groups, although it was slightly larger in infected groups, as was left ventricular systolic diameter. Fractional shortening also did not change between groups, although it was slightly lower in infected groups. Collagen accumulation in the interstitial myocardial space was significantly higher in infected groups and was not attenuated by carvedilol. The same response was observed in the perivascular space. The survival curve showed significantly better survival in the control group compared with the infected groups; but no benefit of carvedilol was observed during the study. However, in the acute phase (up to 100 days of infection), carvedilol did reduce mortality. CONCLUSION: Carvedilol did not attenuate cardiac remodeling or mortality in this model of Chagas' cardiomyopathy. The treatment did improve survival in the acute phase of the disease.
- Myocardial Chemokine Expression and Intensity of Myocarditis in Chagas Cardiomyopathy Are Controlled by Polymorphisms in CXCL9 and CXCL10(2012) NOGUEIRA, Luciana Gabriel; SANTOS, Ronaldo Honorato Barros; IANNI, Barbara Maria; FIORELLI, Alfredo Inacio; MAIRENA, Eliane Conti; BENVENUTI, Luiz Alberto; FRADE, Amanda; DONADI, Eduardo; DIAS, Fabricio; SABA, Bruno; WANG, Hui-Tzu Lin; FRAGATA, Abilio; SAMPAIO, Marcelo; HIRATA, Mario Hiroyuki; BUCK, Paula; MADY, Charles; BOCCHI, Edimar Alcides; STOLF, Noedir Antonio; KALIL, Jorge; CUNHA-NETO, EdecioBackground: Chronic Chagas cardiomyopathy (CCC), a life-threatening inflammatory dilated cardiomyopathy, affects 30% of the approximately 8 million patients infected by Trypanosoma cruzi. Even though the Th1 T cell-rich myocarditis plays a pivotal role in CCC pathogenesis, little is known about the factors controlling inflammatory cell migration to CCC myocardium. Methods and Results: Using confocal immunofluorescence and quantitative PCR, we studied cell surface staining and gene expression of the CXCR3, CCR4, CCR5, CCR7, CCR8 receptors and their chemokine ligands in myocardial samples from end-stage CCC patients. CCR5+, CXCR3+, CCR4+, CCL5+ and CXCL9+ mononuclear cells were observed in CCC myocardium. mRNA expression of the chemokines CCL5, CXCL9, CXCL10, CCL17, CCL19 and their receptors was upregulated in CCC myocardium. CXCL9 mRNA expression directly correlated with the intensity of myocarditis, as well as with mRNA expression of CXCR3, CCR4, CCR5, CCR7, CCR8 and their ligands. We also analyzed single-nucleotide polymorphisms for genes encoding the most highly expressed chemokines and receptors in a cohort of Chagas disease patients. CCC patients with ventricular dysfunction displayed reduced genotypic frequencies of CXCL9 rs10336 CC, CXCL10 rs3921 GG, and increased CCR5 rs1799988CC as compared to those without dysfunction. Significantly, myocardial samples from CCC patients carrying the CXCL9/CXCL10 genotypes associated to a lower risk displayed a 2-6 fold reduction in mRNA expression of CXCL9, CXCL10, and other chemokines and receptors, along with reduced intensity of myocarditis, as compared to those with other CXCL9/CXCL10 genotypes. Conclusions: Results may indicate that genotypes associated to reduced risk in closely linked CXCL9 and CXCL10 genes may modulate local expression of the chemokines themselves, and simultaneously affect myocardial expression of other key chemokines as well as intensity of myocarditis. Taken together our results may suggest that CXCL9 and CXCL10 are master regulators of myocardial inflammatory cell migration, perhaps affecting clinical progression to the life-threatening form of CCC.
conferenceObject TEN-YEAR INCIDENCE OF CHAGAS CARDIOMYOPATHY AMONG ASYMPTOMATIC T. CRUZI SEROPOSITIVE, FORMER BLOOD DONORS(2012) MURPHY, E. L.; SABINO, E.; RIBEIRO, A.; SALEMI, V; ANTUNES, A.; MENEZES, M.; IANNI, B.; NASTARI, L.; FERNANDEZ, F.; PATAVINO, G.; SACHDEV, V; CAPUANI, L.; ALMEIDA NETO, C. De; OLIVEIRA, C. Di Lorenzo; CARRICK, D.; WRIGHT, D.; CUSTER, B.; BUSCH, M. P.; MURPHY, E. L.- Effect of Colchicine on Myocardial Injury Induced by Trypanosoma cruzi in Experimental Chagas Disease(2012) FERNANDES, Fabio; RAMIRES, Felix Jose Alvarez; IANNI, Barbara Maria; SALEMI, Vera Maria Cury; OLIVEIRA, Adriana Morgan; PESSOA, Fernanda Gallinaro; CANZIAN, Mauro; MADY, CharlesBackground: The hallmark of Chagas disease (CD) is multifocal myocarditis and extensive fibrosis. We investigated the potential effect of colchicine on myocardial remodeling in experimental CD. Methods and Results: One hundred Syrian hamsters were randomly divided into noninfected untreated control (CG), noninfected control treated with colchicine (COLG 0.4 mg kg(-1) d(-1) by gavage), infected (IG), and infected treated with colchicine (ICOLG, 0.4 mg kg(-1) d(-1)) groups. The interstitial collagen volume fraction (ICVF) was evaluated by videomorphometry with picrosirius red staining. The gelatinolytic activities of matrix metalloproteinase (MMP) 2 were examined with the use of zymography. Myocarditis was described according to the Dallas criteria. Statistical comparisons were performed with parametric analysis of variance and Tukey test. ICVF (%) accumulation was attenuated in infected colchicine-treated animals in the left (CG 0.81 +/- 0.13, COLG 0.85 +/- 0.13, IG: 1.35 +/- 0.31,* ICOLG 1.06 +/- 0.19; *P < .05 compared with ICOLG) and right ventricles (CG 1.4 +/- 0.36, COLG 1.26 +/- 0.14, IG 1.97 +/- 0.058,* ICOLG: 1.52 +/- 0.23; *P < .05 compared with ICOLG). A significant increase in MMP-2 enzymatic activity (UA) was observed in ICOLG (17,432.8*) compared with GC (3731.6), COLG (2,792.6), and IG (4,286.3; *P < .001). In IG, 66% of animals had myocarditis compared with only 49% in ICOLG. Conclusions: Colchicine had a protective effect on myocardium, indicated by decreased interstitial myocardial fibrosis, increased intensity of MMP-2, and attenuated myocardial inflammation. (J Cardiac Fail 2012;18:654-659)
conferenceObject Lack of effect of simvastatin on structural remodeling in animal model of chagas cardiomyopathy(2012) IANNI, B. M.; RAMIRES, F. J. A.; SALEMI, V. M. C.; FERNANDES, F.; OLIVEIRA, A. M.; PESSOA, F. G.; FONSECA, K. C. B.; CUNHA NETO, E.; MADY, C.Purpose: 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 an animal model of CM. Methods: 123 hamsters were divided:C-controls (25), CSimva-controls with simva 10mg/kg/day (25), Simva1-infected treated from the beginning with the same dose of simva (25), Simva2-infected treated after 4 months (24); Infectuntreated(24). Follow-up of 10 months. Interstitial collagen volume fraction (ICVF) RV and LV measured using videomorphometry and picrosirius red stained heart. Metalloproteinase 9 (MMP9) was obtained by zymography. Gene expression of TNFalpha, IFNgamma, IL10 by real time PCR and Ct. Survival by Kaplan-Meierand log rank. Comparison between groups by Kruskal-Wallis; p≤0.05. Results: Infected animals (Simva1=189±133days; 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. TNFal-pha 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.