VIVIANE ZORZANELLI ROCHA GIRALDEZ

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Instituto do Coração, Hospital das Clínicas, Faculdade de Medicina - Médico

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Autor: ROCHA, Viviane Z. ×

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Agora exibindo 1 - 10 de 29
  • article 3 Citação(ões) na Scopus
  • article 5 Citação(ões) na Scopus
    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.
  • article 10 Citação(ões) na Scopus
    Cholesterol and inflammation: The lesser the better in atherothrombosis
    (2018) ROCHA, Viviane Z.; SANTOS, Raul D.
  • article 26 Citação(ões) na Scopus
    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, Aimin
    Inflammation 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.
  • article 5 Citação(ões) na Scopus
    Cardiovascular disease onset in old people with severe hypercholesterolemia
    (2023) COUTINHO, Elaine R.; MINAME, Marcio H.; ROCHA, Viviane Z.; BITTENCOURT, Marcio S.; JANNES, Cinthia E.; KRIEGER, Jose E.; PEREIRA, Alexandre C.; SANTOS, Raul D.
    Background and aims: Familial hypercholesterolemia (FH) variants are associated with higher atherosclerotic cardiovascular disease risk (ASCVD) even when compared with other forms of severe hypercholesterolemia, especially in young people. Lipid lowering therapies (LLT) may change hypercholesterolemia natural history. This study aimed at evaluating factors associated with occurrence of ASCVD in old severe hypercholesterolemics diagnosed or not with FH and undergoing LLT.Methods: Hypercholesterolemic individuals >= 60 years participating on a genetic cascade screening for FH were divided in 4 groups (2 x 2) according to the presence (variant+) or not (variant-) of FH genetic variants and previous ASCVD (ASCVD+ and ASCVD-). Biomarkers associated with new incident ASCVD events were tested using Cox models. Continuous data shown as medians (%25; %75).Results: From 4,111 genotyped individuals, 377 (9.1%) were elderly [age 66 (63; 71) years], 28.9% males, 42.7% variant+, 32.1% with previous ASCVD, LLT duration 9 (5; 16) years, and on treatment LDL-cholesterol 144 (109; 200) mg/dL. After 4.8 (7; 3) years of follow up there were 47 incident events (12.4%, 2.7% patient/year). The annualized event rates were 0.8% (95% CI 0.36%; 1.70%), 2.3% (95% CI 1.3%; 4.1%), 5.2% (95% CI 2.8%; 9.7%) and 6.3% (95% CI 4.0%; 10.0%) respectively for groups variant-/ASCVD-, variant+/ASCVD-, variant-/ ASCVD+ and, variant+/ASCVD+ (p log rank p < 0.001). Only presence of previous ASCVD was independently associated with incident ASCVD [hazard ratio 3.236 (95%CI 1.497-6.993, p = 0.003)]. No interaction was found for previous ASCVD and variants.Conclusions: In old severe hypercholesterolemic individuals undergoing long-term LLT previous ASCVD was associated with incident events while FH causing variants were not.
  • article 0 Citação(ões) na Scopus
  • article 17 Citação(ões) na Scopus
    Familial hypercholesterolemia and cardiovascular disease in older individuals
    (2021) COUTINHO, Elaine R.; MINAME, Marcio H.; ROCHA, Viviane Z.; BITTENCOURT, Marcio S.; JANNES, Cinthia E.; TADA, Mauricio T.; LIMA, Isabella R.; SALGADO FILHO, Wilson; CHACRA, Ana P.; PEREIRA, Alexandre C.; KRIEGER, Jose E.; SANTOS, Raul D.
    Background and aims: Familial hypercholestemlemia (FH) is characterized by high LDL-cholesterol (LDL-C) and early atherosclerotic cardiovascular disease (ASCVD). With a lipid lowering therapy (LLT), most individuals with FH may have a longer ASCVD-free survival. However, there is scant data about older individuals with FH. Methods: We compared characteristics of genetically defined FH older individuals with age-matched non-FH counterparts. Results: From 4111 genotyped individuals, 462 older than 60 years were included (198 positive and 264 negative for FH variants). There were no differences regarding median age [%25; 75%] 66.0 (62.0; 71.0) and 66.0 (62.2; 71.0) years, p = 0.68 for FH and non-FH, respectively. In both groups, there was a higher frequency of females, however, there were more males in the FH group 37.4% vs. 24.2%, p = 0.002. No differences were seen between FH and non-FH in LLT use: 88.5% vs. 91.5%, p = 0.29. Despite a longer LLT duration in FH patients (with 11.0 (7.0; 20.0) vs. 7.0 (3.0; 13.0) years, p < 0.001), treatment was started late in both groups: at 54.0 (47.0; 61.0) and 59.0 (52.0; 64.0) years, p < 0.001, in FH and non-FH, respectively. FH had greater frequencies of previous and early ASCVD (40.9% vs. 27.3%, p = 0.002, and 22.2% vs. 9.0%, p < 0.001). In FH, male sex [HR (95%C01 2.67 (1.50-4.73), p = 0.001, and LLT onset age 0.96 (0.93-0.99), p = 0.009, were independently associated with ASCVD. Conclusions: Among hypercholesterolemic older individuals participating in a cascade screening program, the genetic diagnosis of FH was associated with higher ASCVD rates, emphasizing the relevance of a monogenic defect as the cause of long-lasting hypercholesterolemia and ASCVD risk, particularly in men.
  • conferenceObject
    STATIN-ASSOCIATED AUTOIMMUNE MYOPATHY: A CASE REPORT
    (2019) BRIGIDO, Alexandra Regia Dantas; ROCHA, Viviane Z.; MINAME, Marcio H.; SANTOS, Raul D.
  • conferenceObject
    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.
  • conferenceObject
    Cardiovascular Disease in Elderly Familial Hypercholesterolemia Individuals Attending a Cascade Screening Program
    (2020) COUTINHO, Elaine; MINAME, Marcio H.; ROCHA, Viviane Z.; BITTENCOURT, Marcio S.; JANNES, Cinthia; PEREIRA, Alexandre; KRIEGER, Jose E.; SANTOS, Raul D.