Navegando por Palavras-chave "Coronary Calcification"

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    Estudo da relação entre a densidade do osso cortical e a progressão da calcificação coronariana em pacientes com doença renal crônica.
    (Universidade Federal de São Paulo (UNIFESP), 2019-04-25) Rodrigues, Larissa Dias Biolcati [UNIFESP]; Canziani, Maria Eugenia Fernandes [UNIFESP]; http://lattes.cnpq.br/8616590420890318; http://lattes.cnpq.br/5061000066270610; Universidade Federal de São Paulo (UNIFESP)
    Background: Loss of trabecular bone has been associated with vascular calcification progression in chronic kidney disease (CKD) patients. There are few data evaluating the relationship between cortical bone and vascular calcification in this population. Objectives: The aim of this study was to prospectively evaluate the association between changes of cortical bone density and coronary artery calcification progression in non-dialyzed CKD patients. Methods: Post hoc analysis of changes of cortical and trabecular bone, and changes of calcium score, using vertebral tomographic images, during 24 months. Cortical and trabecular bone layer were evaluated by Image J® and Vitrea 2® software, respectively. Cortical and trabecular bone density (BD) were expressed in Hounsfield Units (HU), and coronary artery calcium score in Agatston Units (AU). Results: 70 asymptomatic patients [57.8 ± 10.2 years, 63% males, 20% diabetic, estimated glomerular filtration rate (eGFR) = 37.3 (24.8 – 51.3) mL/min/1.73m2 ] were evaluated. The mean cortical and trabecular BD did not change over time. While 49 patients lost either bone, 29 (41%) patients lost cortical [-4.4%/year (ranging from -7.15 to -0.5)] and 39 (56%) lost trabecular bone [-3.15%/year (-13.7 to -0.25)]. There was no association between cortical and trabecular BD changes (p=0.12). Coronary artery calcification was observed in 33 (46%) patients at baseline, and 30 (91%) of them showed progression. While an inverse correlation between trabecular bone and calcium score changes was observed (p=0.001), there was no correlation between cortical bone and calcium score changes (p=0.34). Conclusion: CKD patients experience either cortical or trabecular bone loss over time, but these changes do not take place simultaneously in all patients. Cortical unlike trabecular bone loss is not associated to vascular calcification progression in these patients.
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    Papel da Resposta Imune Inata e Adaptativa na Doença Coronária Aterosclerótica em Portadores de Hipercolesterolemia Familiar
    (Universidade Federal de São Paulo (UNIFESP), 2019-08-29) Lopes, Waleria Simone Toledo Fonzar [UNIFESP]; Izar, Maria Cristina De Oliveira [UNIFESP]; Universidade Federal de São Paulo (UNIFESP)
    BACKGROUND: For hundreds of thousands of years, part of our genomic heritage was primarily developed to combat infectious agents. However, the participation of our immune system modulating the progression of atherosclerosis was only recently recognized in the differential role of lymphocyte subtypes,with B1 lymphocytes with an important antiatherogenic role, due to the production of IgM antibodies that interact with oxidized epitopes of apolipoprotein B, and B2 lymphocytes contributing to atherosclerosis progression favoring interactions of oxidized LDL with dendritic cells, thus contributing for the immune complex deposition in the intima layer and plaque instabilization. Familial Hypercholesterolemia (FH) is an inherited condition characterized by lifetime exposure to high LDL-c, premature atherosclerotic cardiovascular disease (ASCVD) and cutaneous stigmata. However, in spite of LDL-c burden and exposure to aggressive lipid-lowering therapy, there is heterogeneity on atherosclerosis presentation that cannot be explained by classical risk factors. Though, we postulated that the imune-inflammatory system could modulate the burden of atherosclerosis in FH patients. OBJECTIVES:Evaluate if the imune-inflammatory system can modulate the development of coronary atherosclerosis in FH patients under high-intensity lipidlowering therapy. METHODS: One-hundred and two patients with definite or probable diagnosis of FH (Dutch Lipid Clinic Network) were selected. Blood samples for laboratory tests (lipids, biochemistry, apolipoproteins A1, B and Lp(a), immune profile (absolute count and %of lymphocytes TCD4+, TCD8+, B memory cells, B naive, B1, ELISPOT assays, quantification of cytokines TNF-α, IFN-, IL-10, IL-6, IL-4, and IL-2 produced by B memory, B naive and T cells), quantification of monocitic, endothelial and platelet microparticles (flow citometry), and titers of autoantibodies of IgG and IgM isotype anti-oxLDL and anti-Apo B-D (ELISA) were assayed. Genetic study used NGS and a gene pannel with LDLR, APOB, PCSK9, LDLRAP1, APOL1andLIPAgenes. Coronary angiotomography and coronary calcium score (CCS) were performed for the evaluation of the extent and severity of coronary atherosclerosis. Data was compared among individuals with CCS = 0 vs. > 0, among categories of CCS (0; 1-99; 100-399; xxiv 400-999; > 1000 UA), CCS percentiles ( P75) and CAD-RADS categories (0-5). Statistical analysis used parametric and non-parametric tests, as appropriate, with significance set at a P-value < 0,05. RESULTS: CCS> 0 was more prevalent in males (P=0.015), smokers (P=0.016), in those with higher CAD-RADS score (P<0.001), but did not differ among intensities of treatment, presence of cardiovascular risk factors or clinical manifestations of ASCVD. Lipid parameters were similar among participants with CCS = 0 vs. CCS >0 (LDL-c 149 + 61 vs. 158 + 63, respectively; P=0.471). There was heterogeneity in the presentation of ASCVD, with mean and maximal CCS of 173 and 2139 UA, respectively. Immune profile variables, autoantibodies of IgG and IgM isotypes anti- LDLox and anti-Apo B-D, and microparticles did not differ among CCS and CADRADS score categories, although there were trends for diferences for some variables. CONCLUSION: Although there is a clear role of the immune-adaptive system in the development, progression and complications of ASCVD, it does not seem to significantly influence the expression of coronary atherosclerosis evaluated by angiotomography, in subjects with familial hypercholesterolemia under high-intensity lipid-lowering therapy. The expression of ASCVD in those individuals seems to result fromthe balance between long-term exposure to very high levels of LDL-c and highintensity lipid-lowering treatment.