Your browser doesn't support javascript.
Show: 20 | 50 | 100
Results 1 - 20 de 3.149
Int. j. cardiovasc. sci. (Impr.) ; 35(4): 500-510, July-Aug. 2022. tab, graf
Article in English | LILACS | ID: biblio-1385267


Abstract Background: The use of combined oral contraceptives (COC) is a risk factor for atherosclerotic disease, and physical exercise can minimize this condition. Objective: To verify if high intensity interval training (HIIT) promotes changes in the lipid and inflammatory profile of women using COC. Methods: Sequential crossover study with women aged 20-30 years, classified as irregularly active by the international physical activity questionnaire (IPAQ), when using COC. A physical-clinical assessment was performed with anthropometric measurements, VO2max, and analysis of lipid and inflammatory profile. Participants were divided into 2 groups: the initial intervention group (GII), which began practicing HIIT for 2 months, and the posterior intervention group (GIP), which remained inactive for the same period. The GII and GIP would then alternate their conditions. The collected data was divided into: Initial moment (IM), post-exercise moment (PEM) and post-inactivity (PIM). The statistical analyses were performed using the Statistical Package for the Social Sciences, adopting a significance level of p <0.05 . Results: Twelve women were evaluated. After crossing the GII and GIP data, there was a difference in the C-reactive protein values between the IM of 4 (1.6-6.3 mg/dL) vs. PEM 2 (1.5-5 mg/dL); as well as between the PEM vs. the PIM= 4 (1.5-5.8 mg/dL), with a p -value = 0.04 in the comparisons. There was no change between the "moments" of the lipid profile, although it was possible to notice a reduction in resting HR and an increase in indirect VO2max. Conclusion: The HIIT program was able to reduce the inflammatory profile, but it did not alter the lipid profile of irregularly active women using COC.

Humans , Female , Adult , Young Adult , Contraceptives, Oral, Combined/adverse effects , Atherosclerosis/prevention & control , High-Intensity Interval Training , Cross-Sectional Studies , Atherosclerosis/etiology , Heart Disease Risk Factors
Rev. cuba. med ; 61(1)mar. 2022.
Article in Spanish | LILACS-Express | LILACS, CUMED | ID: biblio-1408981


Introducción: La disbiosis conocida como la alteración de la relación simbiótica entre la microbiota intestinal y el huésped están implicados en la patogenia de la enfermedad cardiovascular aterosclerótica. Objetivo: Realizar una revisión documental sobre los mecanismos fisiopatológicos que relacionan los metabolitos bioactivos generados por la disbiosis intestinal con el desarrollo y progresión de la enfermedad cardiovascular aterosclerótica. Métodos: Se utilizó el motor de búsqueda Google Académico y se consultaron artículos de libre acceso en las bases de datos Pubmed, SciELO, Lilacs, Cumed y Hinari desde septiembre 2020 hasta el mes de marzo 2021. Las palabras clave utilizadas para esta revisión fueron:microbioma, microbiota intestinal, disbiosis, aterosclerosis, enfermedad cardiovascular y sus equivalentes en inglés, según el descriptor de Ciencias de la Salud (DeCS). Se consideraron artículos originales, de revisión, revisiones sistemáticas y metaanálisis posteriores al año 2015. Se revisaron un total de 73 artículos. Desarrollo: Las relaciones fisiopatológicas entre la disbiosis intestinal y las enfermedades cardiovasculares son complejas, ya que se influyen mutuamente a través de los sus toxinas endógenas (metabolitos bioactivos), el sistema circulatorio, las respuestas inmunitarias y los cambios metabólicos. Las investigaciones futuras deberían centrarse en dilucidar los actores moleculares subyacentes e identificar si las vías que interconectan la disbiosis intestinal con la ECA son causales, correlacionales o consecuentes. Conclusiones: La evidencia acumulada sostiene que la disbiosis de la microbiota intestinal está involucrada en la síntesis de metabolitos proaterogénicos los cuales modulan los mecanismos implicados en la fisiopatología de la ECA(AU)

Introduction: Dysbiosis is known as the alteration of the symbiotic relationship between the intestinal microbiota and the host is involved in the pathogenesis of atherosclerotic cardiovascular disease. Objective: To carry out a documentary review on the pathophysiological mechanisms that relate the bioactive metabolites generated by intestinal dysbiosis with the development and progression of atherosclerotic cardiovascular disease. Methods: The Google Scholar search engine was used and free access articles were consulted in Pubmed, SciELO, Lilacs, Cumed and Hinari databases from September 2020 to March 2021. The keywords used for this review were microbiome, gut microbiota, dysbiosis, atherosclerosis, cardiovascular disease and their English equivalents, according to the Health Sciences (DeCS) descriptor. Original articles, review articles, systematic reviews and meta-analyses after 2015 were considered. A total of 73 articles were reviewed. Findings: The pathophysiological relationships between intestinal dysbiosis and cardiovascular diseases are complex, since they influence each other through their endogenous toxins (bioactive metabolites), the circulatory system, immune responses and metabolic changes. Future research should focus on elucidating the underlying molecular players and on identifying whether the pathways that interconnect gut dysbiosis with ACE are causal, correlational, or consequential. Conclusions: The accumulated evidence supports that the dysbiosis of the intestinal microbiota is involved in the synthesis of proatherogenic metabolites which modulate the mechanisms involved in the pathophysiology of ACE(AU)

Humans , Male , Female , Cardiovascular Diseases/epidemiology , Metabolic Syndrome/epidemiology , Atherosclerosis/epidemiology , Dysbiosis , Gastrointestinal Microbiome/physiology
Int. j. cardiovasc. sci. (Impr.) ; 35(2): 243-252, Mar.-Apr. 2022. tab, graf
Article in English | LILACS | ID: biblio-1364985


Abstract Background: Atherosclerosis is a serious health problem, and several factors contribute to its occurrence. Longitudinal and qualified monitoring of primary health care (PHC) may contribute to the management of atherosclerosis and reduction of avoidable hospital admissions. Objectives: To estimate the trend in hospitalizations for atherosclerosis and the impact of PHC coverage on its evolution from 2008 to 2018 in Brazil. Methods: An ecological time series analytical study based on the outcomes of hospital admissions for atherosclerosis in Brazil. Time in years, PHC coverage, and Family Health Strategy (FHS) services were considered independent variables. A Prais-Winsten model was used to estimate the outcome trend, and α < 0.05 was adopted. Results: We observed a mean increase of 1.81 hospitalizations for atherosclerosis per 100 000 inhabitants annually (p = 0.002) in Brazil. This growth was evidenced in the Northeast (p < 0.001), Southeast (p = 0.003), and South (p < 0.001) regions, being stable in the North (p = 0.057) and Midwest (p = 0.62) regions. Men presented twice the growth in hospitalizations from the fifth decade of life on (p < 0.01). An inversely proportional relationship was observed for PHC coverage (B = -0.71; p < 0.001) and the proportion of FHS services (B = -0.59; p < 0.001) with the rate of admissions due to atherosclerosis in Brazil. Conclusions: Although hospitalizations for atherosclerotic complications are increasing in Brazil, they present regional and individual gender and age discrepancies, as well as a mitigating effect exerted by PHC coverage.

Humans , Primary Health Care/methods , Atherosclerosis/complications , Atherosclerosis/prevention & control , Brazil/epidemiology , Time Series Studies , Environmental Health , Ecological Studies , Atherosclerosis/epidemiology
Rev. méd. Chile ; 150(2): 261-265, feb. 2022. ilus
Article in Spanish | LILACS-Express | LILACS | ID: biblio-1389634


Atherosclerosis is the main cause of late saphenous vein graft (SVG) failure. Intracoronary images using optical coherence tomography (OCT) in addition to angiography allow a detailed analysis of the lesion beyond the degree of stenosis. We report a 67 years old diabetic male who underwent coronary surgery in 2009, consulting for an acute coronary syndrome. Angiography showed two different lesions on one aortocoronary venous grafts. OCT demonstrates atherosclerosis in different stages identifying the culprit lesion. Stent placement were successfully carried out.

Humans , Male , Aged , Tomography, Optical Coherence/methods , Atherosclerosis , Saphenous Vein/pathology , Saphenous Vein/diagnostic imaging , Coronary Artery Bypass/adverse effects , Treatment Outcome , Coronary Angiography/methods
Acta sci., Health sci ; 44: e58558, Jan. 14, 2022.
Article in English | LILACS | ID: biblio-1367771


Cardiovascular disease(CVD) remains the major cause of mortality in the world, typically claiming a third of all deaths. The primary cause of CVD is atherosclerosis. Therefore, timely prevention and therapy of atherosclerosis are able to reduce the risk of the development of its clinical manifestations. Anti-atherosclerotic activity of medicinal plants mainly appears in their multiple effects.This study was carried out to evaluate the hypolipidemic activity of virgin olive oil in experimentally induced hyperlipemic Wistar. A total of 24 rats were randomly allocated to 4 equal groups and treated as follows for 50 days: (1) Normal control (NC); that were fed with a standart diet; (2) High Cholesterol Diet Control (HCD); which received high cholesterol diet for 50 days; (3) Animals receiving high cholesterol diet for 50 days, after this period the animals are fed for eight days by the standard foodand receiving by gavage virgin olive oil (HCD+VOO) and(4) Animals fed for eight days with the standard food and receiving by gavage olive oil (VOO). High Cholesterol Diet containing yolk egg and coconut oil. Results showed that olive oil caused a significant (p < 0.01) reduction in serum levels of Total Cholesterol (TC), Triglycerides (TG), Low­Density Lipoprotein Cholesterol (LDL) and Atherogenic Index Serum (AIS). The results also demonstrated a significant (p < 0.01) increase in High­Density Lipoprotein Cholesterol (HDL). Moreover, virgin olive oil induced a significant reduction in liver lipid content. On the other hand, a High cholesterol diet induced oxidative stress was measured by estimating reduced glutathione level and amount of thiobarbituric acid reactive substances (TBARS) formed as an index of lipid peroxidation in a liver and a heart. Virgin olive oil supplementation attenuated all these variations. Our observations of the study indicate that the virgin olive oil has a significant antihyperlipidemic potential.

Animals , Rats , Oxidative Stress/immunology , Atherosclerosis/diet therapy , Diet, High-Fat/methods , Olive Oil/pharmacology , Triglycerides/pharmacology , Lipid Peroxidation/immunology , Cholesterol/pharmacology , Rats, Wistar/immunology , Diet, Atherogenic/methods , Glutathione/pharmacology , Hypercholesterolemia/immunology , Lipoproteins/immunology
São Paulo; s.n; s.n; 2022. 136 p. tab, graf.
Thesis in Portuguese | LILACS | ID: biblio-1392190


Introdução: A aterosclerose é uma doença inflamatória crônica decorrente de alterações na parede das artérias de médio e grande calibre e associadas a diversos fatores de risco, dentre os quais destaca-se as hiperlipidemias, ou seja, o aumento plasmático das lipoproteínas, mas também outras comorbidades, como a Síndrome Metabólica. Entre as lipoproteínas, a lipoproteína de baixa densidade (LDL) é de grande relevância na aterosclerose. Diferentes espécies de LDL modificada (LDLm) são originadas através de lipólise, glicação e proteólise, além da oxidação, variando em densidade e eletronegatividade, sendo melhor denominada LDL eletronegativa [LDL (-)]. Considerando as diferenças conformacionais entre a estrutura da ApoB-100 da LDL nativa e da LDL (-), em um estudo inicial, nosso grupo desenvolveu um anticorpo monoclonal (2C7) a partir da imunização de camundongos Balb/c com a LDL (-) humana. Em uma etapa seguinte foi mapeado o epítopo reconhecido pelo anticorpo monoclonal anti-LDL (-) através de phage display. O peptídeo ligante do anticorpo monoclonal anti-LDL (-) foi nomeado p2C7. Esse peptídeo não representa regiões da sequência linear da ApoB-100 humana, mas microdomínios conformacionais de epítopos da ApoB-100 da LDL (-), tornando-os candidatos para a imunomodulação da aterogênese. Portanto, investigar a imunomodulação induzida pelos peptídeo p2C7 miméticos da LDL (-), por representar um epítopo imunodominante da LDL (-), poderá abrir novas perspectivas terapêuticas futuras para a imunomodulação da aterosclerose. Objetivo: Avaliar a imunomodulação promovida pelo p2C7 in vivo, utilizando camundongos C57BL/6 LDLr -/- e amostras de plasma humano. Adicionalmente, no estágio (BEPE) realizado no Instituto Karolinska (dezembro de 2019 a março de 2021), investigou-se o imunometabolismo como mediador nas doenças cardiovasculares. Na parte II-A, estão descritos os resultados do estudo inicialmente proposto. Na parte II-B, apresenta-se os resultados que foram desenvolvidos posteriormente, com ampliação do escopo do projeto, abordando-se a inflamação vascular envolvida no aneurisma de aorta abdominal através de ferramentas de bioinformática. Na parte II-C, são apresentados os resultados do estudo do envolvimento da enzima indolamina 2,3 dioxigenase (IDO) na esteatohepatite não-alcoólica (NASH) e aterosclerose em camundongos ApoE-/- and ApoE/IDO/double-knockout. Metodologia: Foi avaliada a presença de anticorpos anti-p2C7 em amostras de plasma humano de indivíduos com ou sem síndrome metabólica. Realizamos a determinação de TNF circulante nas mesmas amostras e prosseguimos com regressões lineares associando os parâmetros inflamatórios com os níveis de anticorpos anti-p2C7. Camundongos C57BL/6 LDLr -/- foram imunizados com p2C7 e os adjuvantes Alum ou Montanide ISA 720, analisando-se os títulos de anticorpos contra p2C7 e LDL (-), a produção de citocinas (IL-10, IL-4, IL-2, IL-6, IFNγ, IL-17, TNFα) e células secretoras de anticorpos. Camundongos C57BL/6 LDLr -/- foram tolerizados contra os peptídeos mimotopos, com injeções intravenosas (veia caudal) e desafiados com a imunização contendo LDL (-) + Alum. Avaliou-se os títulos de anticorpos contra p2C7 e LDL (-) e a produção de citocinas (TNF-α, IFNγ, IL-12, IL-6, IL-10 e MCP-1). Os camundongos foram mantidos em dieta hipercolesterolêmica por 3 meses para formação da placa aterosclerótica. Após este período, os camundongos foram eutanasiados, avaliando-se a formação de placa aterosclerótica na artéria abdominal e arco aórtico, assim como a produção de citocinas (TNF-α, IFNγ, IL-12, IL-6, IL-10 e MCP-1). Camundongos C57BL/6 LDLr -/- foram imunizados com OVA-p2C7 e, após dieta hipercolesterolêmica de 3 meses para formação de placa aterosclerótica, foram avaliados os parâmetros inflamatórios e avaliada a captação de 18F-FDG no arco aórtico através de PET/CT. Resultados: A imunização com o p2C7 (livre) não foi capaz de induzir resposta humoral, não se observando títulos detectáveis de anticorpos reativos à p2C7 ou LDL (-) em nenhum camundongo imunizado, assim como não foram detectadas células secretoras de anticorpos específicos para a LDL (-). O grupo imunizado com Alum ou Montanide + p2C7 teve aumento significativo na produção de TNF- quando comparado com os demais grupos. O protocolo de tolerização foi realizado com sucesso, visto que os camundongos tolerizados apresentaram títulos de anticorpos inferiores aos controles para o epítopo utilizado. Apenas os camundongos tolerizados com o p2C7 apresentaram aumento significativo na produção de IL-6, IL-12, IL-10, TNF-α, IFNγ e MCP 1 após dieta hipercolesterolêmica. A imunização ativa com OVA-p2C7 foi capaz de reduzir a produção de TNF induzida pela dieta hipercolesterolêmica, assim como reduzir a captação de 18F-FDG. Conclusão: o epítopo p2C7 é altamente expresso na LDL (-) de pacientes com maior risco cardiovascular. Além disso, a imunização ativa com p2C7 também se mostra uma ferramenta promissora para prevenir e regular a inflamação causada pela LDL (-) no curso da aterosclerose

Introduction: Atherosclerosis is a chronic inflammatory disease resulting from changes in the wall of medium and large-caliber arteries and associated with several risk factors, among which hyperlipidemias stand out, ie, the increase in plasma lipoproteins, but also other comorbidities, such as Metabolic Syndrome. Among the lipoproteins, low-density lipoprotein (LDL) is of great relevance in atherosclerosis. Different isoforms of modified LDL (LDLm) are originated through lipolysis, glycation and proteolysis, in addition to oxidation, varying in density and electronegativity, being better called electronegative LDL [LDL (-)]. Considering the conformational differences between the ApoB-100 structure of native LDL and LDL (-), in an initial study, our group developed a monoclonal antibody (2C7) from the immunization of Balb/c mice with human LDL (-). In a next step, the epitope recognized by the anti-LDL monoclonal antibody (-) was mapped using phage display. The binding peptide of anti-LDL monoclonal antibodies (-) was named p2C7. This peptide does not represent linear sequence regions of human ApoB-100, but conformational microdomains of LDL (-) ApoB-100 epitopes, making them candidates for the immunomodulation of atherogenesis. Therefore, investigating the immunomodulation induced by p2C7 peptide mimetics of LDL (-) as it represents an immunodominant epitope of LDL (-) could open new future therapeutic perspectives for the immunomodulation of atherosclerosis. Objective: To evaluate the immunomodulation promoted by p2C7 in vivo, using C57BL/6 LDLr -/- mice, and human plasma samples. In addition, in the internship (BEPE), held at the Karolinska Institute (December 2019 to March 2021), immunometabolism as a mediator of Cardiovascular Diseases was studied. In part II-A, the results of the initially proposed study are described. In part II-B, the results that were developed later are presented, expanding the scope of the project, approaching the vascular inflammation involved in the abdominal aortic aneurysm through bioinformatics tools. In part II-C, the results of the study of the involvement of the enzyme indoleamine 2,3 dioxygenase (IDO) in non-alcoholic steatohepatitis (NASH) and atherosclerosis in ApoE-/- and ApoE/IDO/double mice are presented -knockout. Methodology: The presence of anti-p2C7 antibodies in human plasma samples with or without Metabolic Syndrome was evaluated. We measured circulating TNF in the same samples and proceeded with linear regressions associating inflammatory parameters with levels of anti-p2C7 antibodies. C57BL/6 LDLr -/- mice were immunized with p2C7 and the adjuvants Alum or Montanide ISA 720, analyzing the antibody titers against p2C7 and LDL (-), the production of cytokines (IL-10, IL-4, IL -2, IL-6, IFNγ, IL-17, TNFα) and antibody-secreting cells. C57BL/6 LDLr -/- mice were tolerized against mimotope peptides with intravenous injections (caudal vein) and challenged with immunization containing LDL (-) + Alum. Antibody titers against p2C7 and LDL (-) and cytokine production (TNF-α, IFNγ, IL-12, IL-6, IL-10 and MCP-1) were evaluated. The mice were kept on a hypercholesterolemic diet for 3 months for atherosclerotic plaque formation. After this period, the mice were euthanized, evaluating the formation of atherosclerotic plaque in the abdominal artery and aortic arch, as well as the production of cytokines (TNF-α, IFNγ, IL-12, IL-6, IL-10 and MCP -1). C57BL/6 LDLr -/- mice were immunized with OVA-p2C7 and, after a 3-month hypercholesterolemic diet for atherosclerotic plaque formation, inflammatory parameters were evaluated and 18F-FDG uptake was evaluated by PET/CT. Results: Immunization with p2C7 (free) was not able to induce a humoral response, with no detectable titers of antibodies reactive to p2C7 or LDL (-) being observed in any immunized mouse, as well as no detectable antibody-secreting cells for the LDL (-). The group immunized with Alum or Montanide + p2C7 had a significant increase in TNF-α production when compared to the other groups. The tolerance protocol was successfully performed, as the tolerized mice had lower antibody titers than controls for the epitope used. Only mice tolerated with p2C7 showed a significant increase in the production of IL-6, IL-12, IL-10, TNF-α, IFNγ and MCP 1 after a hypercholesterolemic diet. Active immunization with OVA-p2C7 was able to reduce TNF production induced by the hypercholesterolemic diet, as well as to reduce 18F-FDG uptake. Conclusion: the p2C7 epitope is highly expressed in LDL (-) of patients with higher cardiovascular risk. Furthermore, active immunization with p2C7 is also a promising tool to prevent and regulate inflammation caused by LDL (-) in the course of atherosclerosis

Animals , Male , Female , Mice , Immunization/instrumentation , Atherosclerosis/pathology , Immunomodulation , Arteries/abnormalities , Cardiovascular Diseases/pathology , Risk Factors , Diet/classification , Indoleamine-Pyrrole 2,3,-Dioxygenase/administration & dosage , Antibodies, Monoclonal/adverse effects , Antibody-Producing Cells/classification
Int. j. morphol ; 40(5): 1236-1241, 2022. ilus, tab
Article in English | LILACS-Express | LILACS | ID: biblio-1405279


SUMMARY: Statins inhibit cholesterol synthesis, but also have other pleiotropic effects. There are indications that they affect macrophage survival trough the regulation of apoptosis. We analyzed 50 samples of aortic wall, selected based on statins in patients' therapy (n=25, Th-S group) or statin-free therapy (n=25, Th-nonS group). Each group had 5 samples of healthy aortic tissue, 10 samples of mild and 10 samples of severe atherosclerotic changes in aortic wall. Tissue was stained with hematoxylin-eosin and immunohistochemical methods (anti-Bcl-2 antibody). Presence of Bcl2-positive macrophages (Bcl-2+ MP) was determined semiquantitatively, and data were processed in Microsoft Excell and IMB SPSS 23 Statistics. 60 % of patients in the Th-S group had a mild increase of Bcl-2+ MP The use of statins leads to a significantly more frequent increase in Bcl2+ macrophages in the intima of the healthy aortic tissue. Analysis of all aortic samples with pathohistological diagnosis showed that statin therapy was statistically significantly more often leading to a markedly increased presence of Bcl-2+ MP. In the media, all samples of the Th-S group have a mild increase of Bcl-2+ MP, and in adventitia 40 % of patients. The use of statins more often leads to a markedly increased presence of Bcl-2+ MP in aortic tissue with diagnosed mild and severe atherosclerosis. In samples of severe atherosclerosis, statins lead to a markedly increased presence of Bcl-2+ MP in the parts of the plaque towards the intima and towards the media. Statins lead to an increased presence of Bcl-2+ macrophages, prolong their life, both in healthy and atherosclerotic altered aortic tissue. This indicates potentiation of inflammation and damage to the aortic wall, and calls into question the positive effect of statins on the aortic wall with atherosclerosis.

RESUMEN: Las estatinas inhiben la síntesis de colesterol, pero también tienen otros efectos pleiotrópicos. Hay indicios de que afectan la supervivencia de los macrófagos a través de la regulación de la apoptosis.Se analizaron 50 muestras de pared aórtica, seleccionadas en base a estatinas en tratamiento de pacientes (n=25, grupo Th-S) o en tratamiento libre de estatinas (n=25, grupo Th- nonS). Cada grupo tenía 5 muestras de tejido aórtico sano, 10 muestras de cambios ateroscleróticos leves y 10 muestras de cambios ateroscleróticos severos en la pared aórtica. El tejido se tiñó con hematoxilina-eosina y métodos inmunohistoquímicos (anticuerpo anti-Bcl-2). La presencia de macrófagos positivos para Bcl2 (Bcl- 2+ MP) se determinó semicuantitativamente y los datos se procesaron en Microsoft Excell e IMB SPSS 23 Statistics. El 60 % de los pacientes del grupo Th-S tuvo un aumento leve de Bcl-2+ MP. El uso de estatinas conduce a un aumento significativamente más frecuente de macrófagos Bcl2+ en la íntima del tejido aórtico sano. El análisis de todas las muestras aórticas con diagnóstico anatomopatológico mostró que la terapia con estatinas fue significativamente más frecuente desde el punto de vista estadístico, lo que condujo a una presencia marcadamente mayor de Bcl-2+ MP. En los medios, todas las muestras del grupo Th-S tienen un leve aumento de Bcl-2+ MP, y en adventicia en el 40 % de los pacientes. El uso de estatinas con mayor frecuencia conduce a una presencia marcadamente mayor de MP Bcl-2+ en el tejido aórtico con aterosclerosis leve y grave diagnosticada. En muestras de aterosclerosis severa, las estatinas conducen a una presencia aumentada de Bcl-2+ MP en las partes de la placa hacia la íntima y hacia la media. Las estatinas conducen a una mayor presencia de macrófagos Bcl-2+, prolongan su vida, tanto en tejido aórtico sano como aterosclerótico alterado. Esto indica la potenciación de la inflamación y el daño a la pared aórtica y pone en duda el efecto positivo de las estatinas en la pared aórtica con aterosclerosis.

Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/administration & dosage , Atherosclerosis/metabolism , Aorta/drug effects , Risk Factors , Apoptosis/drug effects , Risk Assessment , Genes, bcl-2/physiology , Atherosclerosis/drug therapy , bcl-X Protein/metabolism , Plaque, Atherosclerotic , Macrophages/drug effects
urol. colomb. (Bogotá. En línea) ; 31(3): 21-29, 2022. ilus
Article in Spanish | LILACS, COLNAL | ID: biblio-1412083


La enfermedad cardiovascular aterosclerótica es la primera causa de muerte en todo el mundo, y la principal causa de años de vida perdidos por discapacidad (AVADs) en los adultos. Sus factores de riesgo son muy prevalentes en la población, y su ocurrencia se ha asociado con disfunción sexual tanto en hombres como en mujeres, debido a que comparten un mecanismo fisiopatológico similar en el caso de la disfunción eréctil en los hombres y potencialmente en la disfunción sexual femenina. Además, los trastornos mentales asociados (principalmente ansiedad y depresión) y los efectos adversos de los medicamentos antihipertensivos y antidepresivos también contribuyen a las disfunciones sexuales. Por otro lado, los inhibidores de la fosfodiesterasa 5 (iFDE5s) han demostrado seguridad y beneficios cardiovasculares en los hombres, y en las mujeres hay evidencia creciente de su utilidad en las disfunciones sexuales. En esta revisión, se presentan las implicaciones de la enfermedad cardiovascular aterosclerótica y su tratamiento en la vida sexual de hombres y mujeres, los efectos cardiovasculares de los tratamientos de las disfunciones sexuales, y la consejería a los pacientes.

Atherosclerotic cardiovascular disease is the leading cause of death worldwide and the leading cause of disability-adjusted life years (DALYs). Its risk factors are very prevalent in the population, and its occurrence has been associated with sexual dysfunction in both men and women, because they share a similar pathophysiological mechanism in the case of erectile dysfunction in men and potentially in female sexual dysfunction. Furthermore, associated mental disorders (mainly anxiety and depression) and the adverse effects of antihypertensive drugs and antidepressants also contribute to sexual dysfunction. On the other hand, phosphodiesterase 5 inhibitors (PDE5is) have shown safety and cardiovascular benefits in men, and in women there is growing evidence of their usefulness in female sexual dysfunctions. The present review describes the implications of atherosclerotic cardiovascular disease and its treatment on the sexual lives of men and women, the cardiovascular effects of the treatments for sexual dysfunctions, and patient counseling.

Humans , Male , Female , Sexuality , Atherosclerosis , Phosphodiesterase 5 Inhibitors , Anxiety , Therapeutics , Cardiovascular Diseases , Phosphoric Diester Hydrolases , Depression , Disability-Adjusted Life Years , Erectile Dysfunction , Mental Disorders , Antidepressive Agents , Antihypertensive Agents
Arq. bras. cardiol ; 118(2): 400-408, 2022. tab, graf
Article in English, Portuguese | LILACS | ID: biblio-1364332


Resumo Fundamento Foi demonstrado que as subunidades de interleucina-35 (IL-35) estão fortemente expressas nas placas ateroscleróticas em humanos. Assim, considera-se que elas têm um papel na aterosclerose. Objetivos Neste estudo, os níveis de IL-35 foram comparados com o grupo controle em pacientes com doença arterial coronariana (DAC) estável, e a associação entre os níveis de IL-35 e o tipo, gravidade e extensão da lesão foram investigadas com o escore Gensini (GS) e o escore Syntax (SS) no grupo de pacientes Métodos Sessenta pacientes (18 mulheres e 42 homens) com DAC, diagnosticados por meio da angiografia coronária, que apresentaram dor no peito típica e teste de esforço não invasivo positivo, e 46 pacientes (18 mulheres e 28 homens) com luminograma normal, foram incluídos no estudo. Tanto o GS quanto o SS foram calculados para o grupo de pacientes, e esses valores foram comparados com os níveis de IL-35. Variáveis com distribuição não normal foram avaliadas com o teste U de Mann-Whitney, enquanto os parâmetros com distribuição normal foram analisados com o teste t de Student. A diferença entre as variáveis categóricas foi avaliada pelo teste de qui-quadrado ou de Fisher. Os valores de p<0,05 foram considerados como estatisticamente sinificativos. Resultados Não foram observadas diferenças significativas entre pacientes e o grupo controle em termos de características demográficas e achados laboratoriais. Em comparação ao grupo controle, os níveis de IL-35 no grupo com DAC foram consideravalmente menores (36,9±63,9 ng/ml vs. 33,2±13,2 ng/ml, p<0,008). Embora não tenha sido estatisticamente significativo, os níveis de IL-35 foram maiores em pacientes com SS mais baixo do que nos com SS mais alto (33,2±13,7 vs. 31,8±8,9, p=0,51). Os valores de IL-35 em pacientes com GS alto foram significativamente mais baixos do que em pacientes com GS baixo (35±17,4 vs. 30,7±8,6, p=0,043). Conclusão Demonstrou-se que os níveis de IL-35 podem ser um novo biomarcador para a DAC estável, e que a IL-35 está associada à extensão da DAC.

Abstract Background It has been shown that interleukin-35 (IL-35) subunits are strongly expressed in atherosclerotic plaques in humans. Therefore, it is considered to play a role in atherosclerosis. Objectives In this study, IL-35 levels were compared with the control group in patients with stable coronary artery disease (CAD), and the association between IL-35 levels and the lesion type, lesion severity and extension was investigated with the Gensini score (GS) and the Syntax score (SS) in the patient group. Methods Sixty patients (18 female and 42 male) with CAD diagnosed by coronary angiography, who presented with typical chest pain and positive noninvasive cardiac stress test, and 46 patients (18 female and 28 male) with normal coronary lumenogram, were included in this study. Gensini and Syntax scores were calculated in the patient group, and these values were compared with IL-35 levels. Non-normally distributed variables were analyzed by the Mann-Whitney U test, whereas normally distributed parameters were assessed by Student's t-test. The difference between categorical variables were evaluated by the Chi-square or Fisher test. P-values<0.05 were considered as statistically significant. Results No significant differences were observed between patients and the control group in terms of demographic characteristics and laboratory findings. Compared to the control group, IL-35 levels of the CAD group were considerably lower (36.9±63.9 ng/ml vs. 33.2±13.2 ng/ml, p<0.008). Although not statistically significant, IL-35 levels were higher in patients with low SS than among those with high SS (33.2±13.7 vs. 31.8±8.9, p=0.51). The IL-35 values of the patients with high GS were significantly lower than in patients with low GS (35±17.4 vs. 30.7±8.6, p=0.043). Conclusion It has been shown that IL-35 levels can be a new biomarker for stable CAD, and IL-35 is associated with the extension of CAD.

Humans , Male , Female , Coronary Artery Disease/diagnosis , Interleukins/blood , Atherosclerosis/diagnosis , Severity of Illness Index , Biomarkers , Coronary Angiography
In. Soeiro, Alexandre de Matos; Leal, Tatiana de Carvalho Andreucci Torres; Accorsi, Tarso Augusto Duenhas; Gualandro, Danielle Menosi; Oliveira Junior, Múcio Tavares de; Caramelli, Bruno; Kalil Filho, Roberto. Manual da residência em cardiologia / Manual residence in cardiology. Santana de Parnaíba, Manole, 2 ed; 2022. p.788-792, tab.
Monography in Portuguese | LILACS | ID: biblio-1353341
Article in Chinese | WPRIM | ID: wpr-936296


OBJECTIVE@#To explore the expression of microRNA-132 (miR-132) and its potential role in the development of atherosclerosis (AS).@*METHODS@#Thirty AS samples and 30 samples of normal peripheral vessels were collected from atherosclerotic patients undergoing peripheral angiostomy in our hospital for detecting the expression level of miR-132 using RT-qPCR. The expression of miR-132 in human umbilical vein endothelial cells (HUVEC) was up-regulated by liposome transfection, and intracellular reactive oxygen species (ROS), localization relationship between ROS and mitochondria, functional changes of mitochondrial reactive oxygen superoxide species (mtROS), mitochondrial membrane potential (MMP) and opening of mitochondrial permeability transition pore (mPTP) were analyzed by flow cytometry and laser confocal microscopy. The activity of mitochondrial redox respiratory chain complex (type I, II, III, IV and V) in HUVECs was detected using ELISA, and the expression levels of key iron death proteins were detected with Western blotting.@*RESULTS@#RT-qPCR results showed that miR-132 was significantly up-regulated in atherosclerotic plaques compared with normal vascular samples (P < 0.001). Compared with control HUVECs, HUVECs overexpressing miR-132 showed a significantly increased level of intracellular ROS (P < 0.001), and most of ROS was colocalized with mitochondria. HUVECs overexpressing miR-132 also showed significantly decreased MMP (P < 0.001) and obviously increased mtROS (P < 0.001) and opening of mPTP (P < 0.001), which led to mitochondrial REDOX respiratory chain stress disorder. The key iron death protein GPX4 was significantly down-regulated and the oxidized protein NOX4 was significantly increased in miR-132-overexpressing HUVECs (P < 0.001).@*CONCLUSION@#MiR-132 promotes atherosclerosis by inducing mitochondrial oxidative stress-mediated ferroptosis, which may serve as a promising therapeutic target for AS.

Apoptosis , Atherosclerosis/genetics , Ferroptosis , Human Umbilical Vein Endothelial Cells/metabolism , Humans , Membrane Potential, Mitochondrial , MicroRNAs/metabolism , Mitochondria/metabolism , Oxidation-Reduction , Oxidative Stress , Reactive Oxygen Species/metabolism
Article in English | WPRIM | ID: wpr-939770


OBJECTIVE@#To detect whether Danlou Tablet (DLT) regulates the hypoxia-induced factor (HIF)-1α-angiopoietin-like 4 (Angptl4) mRNA signaling pathway and explore the role of DLT in treating chronic intermittent hypoxia (CIH)-induced dyslipidemia and arteriosclerosis.@*METHODS@#The mature adipocytes were obtained from 3T3-L1 cell culturation and allocated into 8 groups including control groups (Groups 1 and 5, 0.1 mL of cell culture grade water); DLT groups (Groups 2 and 6, 0.1 mL of 1,000 µg/mL DLT submicron powder solution); dimethyloxalylglycine (DMOG) groups (Groups 3 and 7, DMOG and 0.1 mL of cell culture grade water); DMOG plus DLT groups (Groups 4 and 8, DMOG and 0.1 mL of 1,000 µg/mL DLT submicron powder solution). Groups 1-4 used mature adipocytes and groups 5-8 used HIF-1 α-siRNA lentivirus-transfected mature adipocytes. After 24-h treatment, real-time polymerase chain reaction and Western blot were employed to determine the mRNA and protein expression levels of HIF-1 α and Angptl4. In animal experiments, the CIH model in ApoE-/- mice was established. Sixteen mice were complete randomly divided into 4 groups including sham group, CIH model group [intermittent hypoxia and normal saline (2 mL/time) gavage once a day]; Angptl4 Ab group [intermittent hypoxia and Angptl4 antibody (30 mg/kg) intraperitoneally injected every week]; DLT group [intermittent hypoxia and DLT (250 mg/kg) once a day], 4 mice in each group. After 4-week treatment, enzyme linked immunosorbent assay was used to detect the expression levels of serum total cholesterol (TC) and triglyceride (TG). Hematoxylin-eosin and CD68 staining were used to observe the morphological properties of arterial plaques.@*RESULTS@#Angptl4 expression was dependent on HIF-1 α, with a reduction in mRNA expression and no response in protein level to DMOG or DLT treatment in relation to siHIF-1 α -transfected cells. DLT inhibited HIF-1 α and Angptl4 mRNA expression (P<0.05 or P<0.01) and reduced HIF-1 α and Angptl4 protein expressions with DMOG in mature adipocytes (all P<0.01), as the effect on HIF-1 α protein also existed in the presence of siHIF-1 α (P<0.01). ApoE-/- mice treated with CIH had increased TG and TC levels (all P<0.01) and atherosclerotic plaque. Angptl4 antibody and DLT both reduce TG and TC levels (all P<0.01), as well as reducing atherosclerotic plaque areas, narrowing arterial wall thickness and alleviating atherosclerotic lesion symptoms to some extent.@*CONCLUSION@#DLT had positive effects in improving dyslipidemia and arteriosclerosis by inhibiting Angptl4 protein level through HIF-1 α-Angptl4 mRNA signaling pathway.

Angiopoietin-Like Protein 4/genetics , Animals , Apolipoproteins E , Atherosclerosis/metabolism , Drugs, Chinese Herbal , Dyslipidemias/genetics , Hypoxia/metabolism , Hypoxia-Inducible Factor 1, alpha Subunit/metabolism , Mice , Plaque, Atherosclerotic , Powders , RNA, Messenger/genetics , Signal Transduction , Triglycerides , Water
Article in Chinese | WPRIM | ID: wpr-939719


Exosomes are subtypes of extracellur vesicles containing a variety of cell-specific proteins, lipids and nucleic acids released during cell activation or apoptosis, and play the role of intercellur communication mediators in different physiological and pathological processes. With the development of research in recent years, the role of platelet-derived exosomes in cardiovascular diseases has attracted extensive attention. This paper reviews the role of platelet-derived exosomes in atherosclerotic thrombosis and the potential role of platelet-derived exosomes as biomarkers for the diagnosis and treatment of atherosclerotic thrombotic disease and the problems to be solved.

Apoptosis , Atherosclerosis/pathology , Blood Platelets/pathology , Exosomes/pathology , Humans , Thrombosis
Chinese Journal of Surgery ; (12): 117-121, 2022.
Article in Chinese | WPRIM | ID: wpr-935588


Aortoiliac occlusive disease (AIOD) refers to the stenosis and occlusion of the distal abdominal aorta and(or) bifurcation of the aortoiliac artery,which is mainly caused by atherosclerosis,leading to pelvic and lower limb ischemia.Open surgery has always been the main treatment for complex AIOD.However,in recent years,with the development of endovascular surgery technologies and medical instruments,its treatment concept has been greatly changed.More and more clinical evidence has proved that the long-term efficacy of endovascular therapy is not inferior to that of traditional open surgery,so minimally invasive endovascular therapy has become the preferred treatment for AIOD.

Aortic Diseases/surgery , Arterial Occlusive Diseases/surgery , Atherosclerosis , Endovascular Procedures , Humans , Iliac Artery/surgery , Treatment Outcome , Vascular Patency
Article in English | WPRIM | ID: wpr-928660


Cellular senescence is a biological process associated with the degeneration of cell structure and function, which contribute to age-related diseases. Atherosclerosis is a chronic inflammatory disease that can cause a variety of cardiovascular disorders. In this article, we review the effects of cellular senescence on the development of atherosclerosis through diverse physiopathological changes, focusing on the alterations in senescent organelles and the increased senescence-associated secretory phenotype (SASP), and exploring the relevant therapeutic strategies for atherosclerosis by clearing senescent cells and reducing SASP, to provide new insights for the treatment of atherosclerosis.

Aging , Atherosclerosis , Cardiovascular Diseases , Cellular Senescence , Chronic Disease , Humans , Senescence-Associated Secretory Phenotype
Article in Chinese | WPRIM | ID: wpr-927994


This study explores the regulatory effect of astragaloside Ⅳ on miR-17-5 p and its downstream proprotein convertase subtillisin/kexin type 9(PCSK9)/very low density lipoprotein receptor(VLDLR) signal pathway, aiming at elucidating the mechanism of astragaloside Ⅳ against atherosclerosis(AS). In cell experiment, oxidized low-density lipoprotein(ox-LDL) was used for endothelial cell injury modeling with vascular smooth muscle cells(VSMCs). Then cells were classified into the model group, miR-17-5 p inhibitor group, blank serum group, and astragaloside Ⅳ-containing serum group based on the invention. Afterward, cell viability and the expression of miR-17-5 p, VLDLR, and PCSK9 mRNA and protein in cells in each group were detected. In animal experiment, 15 C57 BL/6 mice were used as the control group, and 45 ApoE~(-/-) mice were classified into the model group, miR-17-5 p inhibitor group, and astragaloside Ⅳ group, with 15 mice in each group. After 8 weeks of intervention, the peripheral serum levels of interleukin-6(IL-6), interleukin-10(IL-10), and tumor necrosis factor-α(TNF-α), and the expression of miR-17-5 p, VLDLR, and PCSK9 mRNA in the aorta of mice were detected. The pathological changes of mice in each group were observed. According to the cell experiment, VSMC viability in the miR-17-5 p inhibitor group and the astragaloside Ⅳ-containing serum group was higher than that in the model group(P<0.05). The mRNA and protein expression of miR-17-5 p and VLDLR in VSMCs in the miR-17-5 p inhibitor group and the astragaloside Ⅳ-containing serum group was lower than that in the model group(P<0.05), but the mRNA and protein expression of PCSK9 was higher than that in the model group(P<0.05). As for the animal experiment, the levels of IL-6 and TNF-α in the peripheral serum of the miR-17-5 p inhibitor group and the astragaloside Ⅳ group were lower(P<0.05) and the serum level of IL-10 was higher(P<0.05) than that of the model group. The mRNA expression of miR-17-5 p and VLDLR in the aorta in the miR-17-5 p inhibitor group and the astragaloside Ⅳ group was lower(P<0.05), and PCSK9 mRNA expression was higher(P<0.05) than that in the model group. Pathological observation showed mild AS in the miR-17-5 p inhibitor group and the astragaloside Ⅳ group. In summary, astragaloside Ⅳ can prevent the occurrence and development of AS. The mechanism is that it performs targeted regulation of miR-17-5 p, further affecting the PCSK9/VLDLR signal pathway, inhibiting vascular inflammation, and thus alleviating endothelial cell injury.

Animals , Atherosclerosis/genetics , Lipoproteins, LDL/metabolism , Mice , MicroRNAs/metabolism , Proprotein Convertase 9/metabolism , Receptors, LDL/metabolism , Saponins , Signal Transduction , Triterpenes
Article in Chinese | WPRIM | ID: wpr-927321


Atherosclerotic cardiovascular disease is the general name of a series of diseases based on atherosclerosis. With the development of the social economy and the progress of population aging in China, the burden of atherosclerotic cardiovascular disease is increasing. However, in recent years some clinical studies have proved that the traditional blood lipid indicators, including low-density lipoprotein cholesterol, have some limitations in the risk control of atherosclerotic cardiovascular disease, and the blood lipid indicators need to be further supplemented and improved. This consensus expounds non-traditional blood lipid indexes from the perspectives of test and clinic, mainly including apolipoprotein B and lipoprotein a, non-high density lipoprotein cholesterol and lipoprotein residue, and non-fasting blood lipid. This consensus systematically expounds the pathophysiological mechanism of non-traditional blood lipid indexes, the relationship with cardiovascular disease, detection methods and performance, intervention, control and application in the state of cardiovascular disease, and gives the corresponding clinical expert suggestion.

Atherosclerosis/prevention & control , Cardiovascular Diseases/prevention & control , Consensus , Humans , Lipids , Lipoproteins , Risk Factors
Rev. Investig. Salud. Univ. Boyacá ; 8(2): 18-31, 20211201. tab, fig
Article in Spanish | LILACS, COLNAL | ID: biblio-1369435


Introducción: El signo de Frank o signo del lóbulo hendido se ha asociado con la existencia de una desorganización de las fibras elásticas y un espesamiento de las arteriolas que provoca una esclerosis vascular y una isquemia crónica local del lóbulo de la oreja.Objetivo: Determinar la relación del signo de lóbulo hendido con las enfermedades cardiovasculares en pacientes del servicio de Medicina Interna del Instituto Autónomo Hospital Universitario de los Andes, entre diciembre de 2017 y julio de2018. Materiales y métodos: Estudio observacional descriptivo y transversal de casos y controles, para establecer la relación entre el signo del lóbulo hendido y la enfermedad cardiovascular. Resultados: Se observa que el tabaquismo es un factor de riesgo asociado directamente con la presencia del signo del lóbulo hendido (p = 0,047), dado que existe una mayor tendencia a su aparición mientras mayor es la intensidad del tabaquismo. La presencia del signo del lóbulo genera un riesgo relativo de 2,062 veces, en cuanto a eventos cardiovasculares en comparación con aquellos quienes no lo presentan. Conclusiones: Se considera que la asociación encontrada entre el signo del lóbulo hendido, el tabaquismo y las enfermedades cardiovasculares ofrecen una herramienta fácilmente identificable de una población de riesgo mayor para el desarrollo de estas patologías.

Introduction: The sign of Frank or sign of the cleft lobe has been associated with the existence of a disorganization of the elastic fibers and a thickening of the arterioles that causes a vascular sclerosis and a chronic local ischemia of the lobe of the ear. Objectives: To determine the relationship of the split lobe sign with cardiovascular diseases in patients of the Internal Medicine service of the Autono-mous University Hospital of the Andes, December-2017 to July-2018. Methodology: A descriptive and cross-sectional observational study of cases and controls to establish a relationship between the sign of the diseased lobe and cardiovascular disease. Results: We observed Smoking is a risk factor directly associated with the presence of the cleft lobe sign p (0.047), there being a greater tendency to appear when the intensity of smoking is higher. The presence of the lobe sign generates a relative risk of 2.062 times in terms of cardiovascular events compared to those who do not. Conclusions: We consider that the association found between the sign of the cleft lobe, smoking and cardiovascular diseases, give us an easily identifiable tool for a population at higher risk for the deve-lopment of these pathologies.

Introdução: O sinal de Frank ou sinal de lóbulo fendido tem sido associado com desorganização das fibras elásticas e espessamento das arteríolas, levando à esclerose vascular e isquemia local crônica do lóbulo da orelha. Objetivo: Determinar a relação entre o sinal do lóbulo fendido e as doenças cardiovasculares em pacientes do Departamento de Medicina Interna do Instituto Autónomo Hospital Universitário dos Andes, entre dezembro de 2017 e julho de 2018. Materiais e métodos: Estudo observacional, descritivo, transversal, caso-controle para estabelecer a relação entre o sinal do lóbulo fendido e a doença cardiovascular. Resultado: Fumar é um fator de risco diretamente associado à presença do sinal do lóbulo fendido (p = 0,047), pois há uma tendência maior para que ele apareça quanto maior a intensidade do fumo. A presença do sinal do lóbulo gera um risco relativo 2.062 vezes maior para eventos cardiovasculares do que para aqueles sem ele. Conclusão: A associação encontrada entre o sinal do lóbulo fendido, o tabagismo e a doença cardio-vascular é considerada como uma ferramenta facilmente identificável de uma população com maior risco para o desenvolvimento dessas patologias.

Hypertension , Risk , Atherosclerosis
Int. j. cardiovasc. sci. (Impr.) ; 34(5,supl.1): 121-127, Nov. 2021. tab, graf
Article in English | LILACS | ID: biblio-1346340


Abstract The association between periodontitis and myocardial infarction remains unclear in the literature. Few studies have addressed periodontitis exposure as a predisposing factor for the development of myocardial infarction. Therefore, the present systematic review aims to analyze the association between periodontitis and myocardial infarction. This meta-analysis systematically searched MEDLINE, EMBASE, The Cochrane Controlled Trials Register, SCIELO, LILACS, CINAHL, Scopus, Web of Science and grey literature for studies estimating the association between periodontitis and myocardial infarction. Quality of evidence was assessed for all studies. The meta-analysis was conducted using random-effects models. Four of the six studies selected were included in the meta-analysis, including 1,035,703 subjects. The association between periodontitis and myocardial infarction was: RR: 5.99 (95% CI: 1.17-30.68), but with high heterogeneity (I2 = 100%; p <0.01). The results including only the highest quality articles, was lower: RR: 2.62 (95% CI: 1.47-4.70 3.83), but with lower heterogeneity (I2 = 85.5%; p < 0.01).The present systematic review with meta-analysis showed an association between periodontitis and acute myocardial infarction, but with a high level of heterogeneity.

Humans , Periodontitis/complications , Myocardial Infarction/complications , Pulpitis/complications , Atherosclerosis/complications , Lipoproteins/analysis , Myocardial Infarction/etiology , Myocardial Infarction/mortality