VIVIANE ZORZANELLI ROCHA GIRALDEZ
Projetos de Pesquisa
Unidades Organizacionais
Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico
62 resultados
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Agora exibindo 1 - 10 de 62
- I Brazilian Guidelines On Cardiovascular Prevention(2013) SIMAO, A. F.; PRECOMA, D. B.; ANDRADE, J. P.; CORREA FILHO, H.; SARAIVA, J. F. K.; OLIVEIRA, G. M. M.; MURRO, A. L. B.; CAMPOS, A.; ALESSI, A.; AVEZUM JUNIOR, A.; ACHUTTI, A. C.; MIGUEL, A. C. M. G.; SOUSA, A. C. S.; LOTEMBERG, A. M. P.; LINS, A. P.; FALUD, A. A.; BRANDAO, A. A.; SANJULIANI, A. F.; SBISSA, A. S.; ALENCAR FILHO, A. C.; HERDY, A. H.; POLANCZYK, C. A.; LANTIERI, C. J.; MACHADO, C. A.; SCHERR, C.; STOLL, C.; AMODEO, C.; ARAUJO, C. G. S.; SARAIVA, D.; MORIGUCHI, E. H.; MESQUITA, E. T.; CESENA, F. H. Y.; FONSECA, F. A. H.; CAMPOS, G. P.; SOARES, G. P.; FEITOSA, G. S.; XAVIER, H. T.; CASTRO, I; GIULIANO, I. C. B.; V, I. Rivera; GUIMARAES, I. C. B.; ISSA, J. S.; SOUZA, J. R. M.; FARIA NETO, J. R.; CUNHA, L. B. N.; PELLANDA, L. C.; BORTOLOTTO, L. A.; BERTOLAMI, M. C.; MINAME, M. H.; GOMES, M. A. M.; TAMBASCIA, M.; MALACHIAS, M. V. B.; SILVA, M. A. M.; IZA, M. C. O.; MAGALHAES, M. E. C.; BACELLAR, M. S. C.; MILANI, M.; WAJNGARTEN, M.; GHORAYEB, N.; COELHO, O. R.; VILLELA, P. B.; V, P. C. B. Jardim; SANTOS FILHO, R. D.; STEIN, R.; CASSANI, R. S. L.; D'AVILA, R. L.; FERREIRA, R. M.; BARBOSA, R. B.; POVOA, R. M. S.; KAISER, S. E.; ISMAEL, S. C.; CARVALHO, T.; GIRALDEZ, V. Z. R.; COUTINHO, W.; SOUZA, W. K. S. B.
- Activation of prostaglandin E-2-EP4 signaling reduces chemokine production in adipose tissue(2015) TANG, Eva H. C.; CAI, Yin; WONG, Chi Kin; ROCHA, Viviane Z.; SUKHOVA, Galina K.; SHIMIZU, Koichi; XUAN, Ge; VANHOUTTE, Paul M.; LIBBY, Peter; XU, AiminInflammation of adipose tissue induces metabolic derangements associated with obesity. Thus, determining ways to control or inhibit inflammation in adipose tissue is of clinical interest. The present study tested the hypothesis that in mouse adipose tissue, endogenous prostaglandin E-2 (PGE(2)) negatively regulates inflammation via activation of prostaglandin E receptor 4 (EP4). PGE(2) (5-500nM) attenuated lipopolysaccharide-induced mRNA and protein expression of chemokines, including interferon--inducible protein 10 and macrophage-inflammatory protein-1 in mouse adipose tissue. A selective EP4 antagonist (L161,982) reversed, and two structurally different selective EP4 agonists [CAY10580 and CAY10598] mimicked these actions of PGE(2). Adipose tissue derived from EP4-deficient mice did not display this response. These findings establish the involvement of EP4 receptors in this anti-inflammatory response. Experiments performed on adipose tissue from high-fat-fed mice demonstrated EP4-dependent attenuation of chemokine production during diet-induced obesity. The anti-inflammatory actions of EP4 became more important on a high-fat diet, in that EP4 activation suppressed a greater variety of chemokines. Furthermore, adipose tissue and systemic inflammation was enhanced in high-fat-fed EP4-deficient mice compared with wild-type littermates, and in high-fat-fed untreated C57BL/6 mice compared with mice treated with EP4 agonist. These findings provide in vivo evidence that PGE(2)-EP4 signaling limits inflammation. In conclusion, PGE(2), via activation of EP4 receptors, functions as an endogenous anti-inflammatory mediator in mouse adipose tissue, and targeting EP4 may mitigate adipose tissue inflammation.
conferenceObject PREDICTORS OF CORONARY ARTERY CALCIFICATION INCIDENCE IN SEVERE HYPERCHOLESTEROLEMIA(2023) MARTE, Ana; MINAME, Marcio Hiroshi; PARDI, Estevao Magalhaes; GANEM, Lucas; MIZUTA, Marjorie Hayashida; ROCHA, Viviane Zorzanelli; PEREIRA, Alexandre Costa; KRIEGER, Jose Eduardo; SANTOS, RaulconferenceObject HDL FUNCTIONALITY MODULATES CAROTID ARTERY INTIMA-MEDIA THICKNESS IN INDIVIDUALS WITH MARKED HYPERALPHALIPOPROTEINEMIA(2016) LAURINAVICIUS, Antonio; ROCHA, Viviane; BORTOLOTTO, Luiz; SANTOS, RaulconferenceObject ANALYSIS OF ELEVATED LIPOPROTEIN (A) LEVELS IN A REFERRAL CARDIOVASCULAR CENTER IN SAO PAULO, BRAZIL(2020) MIZUTA, Marjorie Hayashida; MINAME, Marcio Hiroshi; ROCHA, Viviane Z.; CHACRA, Ana Paula M.; SALGADO, Wilson; SANTOS, Raul D.- Subclinical carotid vascular disease and risk factors for atherosclerosis in type 1 and type 2 diabetes(2017) ROCHA, Viviane Z.; SANTOS, Raul D.
- Cholesterol lowering with inclisiran: a new chapter in the PCSK9 story book(2023) SANTOS, Raul D.; ROCHA, Viviane Z.This editorial refers to 'Inclisiran and cardiovascular events: a patient-level analysis of phase III trials, by K.K. Ray et al., https://doi.org/10. 1093/eurheartj/ehac594.
- Screening of ABCG5 and ABCG8 Genes for Sitosterolemia in a Familial Hypercholesterolemia Cascade Screening Program(2022) TADA, Mauricio Teruo; ROCHA, Viviane Zorzanelli; LIMA, Isabella Ramos; OLIVEIRA, Theo Gremen Mimary; CHACRA, Ana Paula; MINAME, Marcio Hiroshi; NUNES, Valeria Sutti; NAKANDAKARE, Edna Regina; CASTELO, Maria Helane Costa Gurgel; JANNES, Cinthia Elim; SANTOS, Raul D.; KRIEGER, Jose Eduardo; PEREIRA, Alexandre CostaBackground: Sitosterolemia is a rare autosomal recessive disorder caused by homozygous or compound heterozygous variants in ABCG5/ABCG8. The disease is characterized by increased plasma plant sterols. Small case series suggest that patients with sitosterolemia have wide phenotypic heterogeneity with great variability on either plasma cholesterol levels or development of atherosclerotic cardiovascular disease. The present study aims to characterize the prevalence and clinical features of sitosterolemia participating in a familial hypercholesterolemia genetic cascade screening program. Methods: From 443 familial hypercholesterolemia index cases, 260 were negative for familial hypercholesterolemia genes and were sequenced for the ABCG5/8 genes. Clinical and laboratory characteristics of affected individuals were determined. Results: Eight (3.1%) index cases were found to be homozygous or compound heterozygous variant for ABCG5/ABCG8 genes, confirming the genetic diagnosis of sitosterolemia. Screening their relatives led to the identification of 6 additional confirmed sitosterolemia cases (3 homozygous and 3 compound heterozygous variant) and 18 carriers (heterozygous). The mean age of identified sitosterolemia cases (n=14) was 37.2 +/- 19.8 years, 50% were females, and 78.6% (all adults) presented either clinical or subclinical atherosclerotic cardiovascular disease. As expected, affected individuals presented elevated plasma plant sterol levels (mean beta-Sitosterol and campesterol, respectively, 160.3 +/- 107.1 and 32.0 +/- 19.6 mu g/mL) and the highest plasma LDL (low-density lipoprotein)-cholesterol was 269.0 +/- 120.0 mg/dL (range: 122-521 mg/dL). LDL-cholesterol mean reduction with therapy among cases was 65%. Eighty-three percent (83%) of identified sitosterolemia patients presented hematologic abnormalities. Conclusions: Testing genes associated with sitosterolemia in the molecular routine workflow of a familial hypercholesterolemia cascade screening program allowed the precise diagnosis of sitosterolemia in a substantial number of patients with varying LDL-C levels and high incidence of early atherosclerotic cardiovascular disease and hematologic abnormalities.
- Use of statins and the incidence of type 2 diabetes mellitus(2015) BERNARDI, André; ROCHA, Viviane Zorzanelli; FARIA-NETO, José RochaIntroduction: the use of statins is associated with reduced cardiovascular risk in studies of primary and secondary prevention, and the reduction is directly proportional to the reduction of LDL-cholesterol. Recent evidence suggests that statins may be associated with a higher incidence of new cases of diabetes. The aim of this review is to explore this possibility, identifying factors associated with the increase in risk and the potential diabetogenic mechanisms of statins. In addition, we evaluated if the risk of diabetes interferes with the reduction in cardiovascular risk achieved with statins.Methods:we reviewed articles published in the Scielo and Pubmed databases, which assessed or described the association between use of statins and risk of diabetes up to June 2015.Results:use of statins is associated with a small increase in the incidence of new cases of diabetes. Age, potency of statin therapy, presence of metabolic syndrome, impaired fasting blood glucose, overweight and previously altered glycated hemoglobin levels are associated with increased risk of diabetes, but there is no consensus about the possible diabetogenic mechanisms of statins. In patients candidate to hypolipemiant drug therapy, the benefit of reducing cardiovascular risk outweighs any risk increase in the incidence of diabetes.Conclusion:statins are associated with a small increase in incidence of diabetes in patients predisposed to glycemic alteration. However, since the benefit of cardiovascular risk reduction prevails even in this group, there is no evidence to date that this finding should change the recommendation of starting statin therapy.
- CXCR3 Controls T-Cell Accumulation in Fat Inflammation(2014) ROCHA, Viviane Zorzanelli; FOLCO, Eduardo J.; OZDEMIR, Cafer; SHEIKINE, Yuri; CHRISTEN, Thomas; SUKHOVA, Galina K.; TANG, Eva H. C.; BITTENCOURT, Marcio Sommer; SANTOS, Raul D.; LUSTER, Andrew D.; COHEN, David E.; LIBBY, PeterObjective-Obesity associates with increased numbers of inflammatory cells in adipose tissue (AT), including T cells, but the mechanism of T-cell recruitment remains unknown. This study tested the hypothesis that the chemokine (C-X-C motif) receptor 3 (CXCR3) participates in T-cell accumulation in AT of obese mice and thus in the regulation of local inflammation and systemic metabolism. Approach and Results-Obese wild-type mice exhibited higher mRNA expression of CXCR3 in periepididymal AT-derived stromal vascular cells compared with lean mice. We evaluated the function of CXCR3 in AT inflammation in vivo using CXCR3-deficient and wild-type control mice that consumed a high-fat diet. Periepididymal AT from obese CXCR3-deficient mice contained fewer T cells than obese controls after 8 and 16 weeks on high-fat diet, as assessed by flow cytometry. Obese CXCR3-deficient mice had greater glucose tolerance than obese controls after 8 weeks, but not after 16 weeks. CXCR3-deficient mice fed high-fat diet had reduced mRNA expression of proinflammatory mediators, such as monocyte chemoattractant protein-1 and regulated on activation, normal T cell expressed and secreted, and anti-inflammatory genes, such as Foxp3, IL-10, and arginase-1 in periepididymal AT, compared with obese controls. Conclusions-These results demonstrate that CXCR3 contributes to T-cell accumulation in periepididymal AT of obese mice. Our results also suggest that CXCR3 regulates the accumulation of distinct subsets of T cells and that the ratio between these functional subsets across time likely modulates local inflammation and systemic metabolism.