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PURPOSE OF REVIEW: To update information about the relationship between metabolic dysfunction-associated steatotic liver disease (MASLD) and atherosclerosis. This review emphasizes the potential mechanisms linking MASLD with atherosclerosis and the possible causal relationships between these conditions. RECENT FINDINGS: An increased risk of cardiovascular disease is related to MASLD. Several molecular, cellular, and metabolic mechanisms have been described to explain the development of atherothrombosis in MASLD patients. These include atherogenic dyslipidemia, low-grade vascular inflammation, endothelial dysfunction, foam cell formation, proliferation of vascular smooth muscle cells, insulin resistance, gut microbiota dysbiosis, activation of renin-angiotensin and sympathetic nervous systems, hypercoagulability, and decreased fibrinolysis. Also, there is recent evidence suggesting an association between genetically driven liver fat and coronary heart disease mediated by the causal effect of apoB-containing lipoproteins. Several meta-analyses and systematic reviews have reported a strong association between MASLD and cardiovascular outcomes. MASLD is an important and independent risk factor for atherosclerosis development. Multiple mechanisms may be involved in this association. Further research is required to establish a causal association between MASLD and atherosclerosis.
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Aterosclerose , Humanos , Aterosclerose/etiologia , Aterosclerose/complicações , Fígado Gorduroso/complicações , Fígado Gorduroso/metabolismo , Fígado Gorduroso/etiologia , Fatores de Risco , Resistência à InsulinaRESUMO
OBJECTIVE: To build a model based on cardiometabolic indicators that allow the identification of overweight adolescents at higher risk of subclinical atherosclerotic disease (SAD). METHODS: Cross-sectional study involving 161 adolescents with a body mass index ≥ +1 z-Score, aged 10 to 19 years. Carotid intima-media complex thickness (IMT) was evaluated using ultrasound to assess subclinical atherosclerotic disease. Cardiometabolic indicators evaluated included nutritional status, central adiposity, blood pressure, lipidic profile, glycemic profile, as well as age and sex. Data was presented using measures of central tendency and dispersion, as well as absolute and relative frequency. The relationship between IMT measurement (outcome variable) and other variables (independent variables) was assessed using Pearson or Spearman correlation, followed by multiple regression modeling with Gamma distribution to analyze predictors of IMT. Statistical analysis was performed using SPSS and R software, considering a significance level of 5 %. RESULTS: It was observed that 23.7 % had Carotid thickening, and the prevalence of abnormal fasting glucose was the lowest. Age and fasting glucose were identified as predictors of IMT increase, with IMT decreasing with age by approximately 1 % per year and increasing with glucose by around 0.24 % per mg/dL. CONCLUSION: The adolescent at higher risk is younger with higher fasting glycemia levels.
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Aterosclerose , Glicemia , Espessura Intima-Media Carotídea , Jejum , Humanos , Adolescente , Feminino , Masculino , Estudos Transversais , Glicemia/análise , Aterosclerose/sangue , Aterosclerose/etiologia , Criança , Jejum/sangue , Adulto Jovem , Índice de Massa Corporal , Fatores de Risco , Fatores Etários , Sobrepeso/sangue , Sobrepeso/complicaçõesRESUMO
In the modern world, cardiovascular diseases have a special place among the most common causes of death. Naturally, this widespread problem cannot escape the attention of scientists and researchers. One of the main conditions preceding the development of fatal cardiovascular diseases is atherosclerosis. Despite extensive research into its pathogenesis and possible prevention and treatment strategies, many gaps remain in our understanding of this disease. For example, the concept of multiple low-density lipoprotein modifications was recently stated, in which desialylation is of special importance. Apart from this, sialic acids are known to be important contributors to processes such as endothelial dysfunction and inflammation, which in turn are major components of atherogenesis. In this review, we have collected information on sialic acid metabolism, analyzed various aspects of its implication in atherosclerosis at different stages, and provided an overview of the role of particular groups of enzymes responsible for sialic acid metabolism in the context of atherosclerosis.
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Aterosclerose , Doenças Cardiovasculares , Humanos , Ácido N-Acetilneuramínico/metabolismo , Metabolismo dos Lipídeos , Aterosclerose/etiologia , Aterosclerose/metabolismo , Ácidos Siálicos/metabolismo , InflamaçãoRESUMO
BACKGROUND AND AIMS: Systemic inflammatory diseases could act as an unfavorable condition in which epicardial adipose tissue (EAT) becomes harmful to cardiovascular health. The objectives were: (a) to quantitatively compare the presence of EAT between patients with systemic inflammatory diseases and controls; (b) to analyze the association between EAT and subclinical atheromatosis in individuals with systemic inflammatory diseases. METHODS: Studies that have quantified EAT in a population with systemic inflammatory diseases compared to a control group, or that describe the association between EAT and the presence of subclinical atheromatosis in patients with systemic inflammatory diseases were included. A quantitative analysis was performed for the first objective. This systematic review was performed according to PRISMA guidelines. RESULTS: Twenty-one studies including 1448 patients with systemic inflammatory diseases, were considered eligible for this study. Patients with systemic inflammatory disease have a higher volume (MD: 10.4cm3 [1.8-19.1]; p<0.01), higher thickness (MD: 1.0mm [0.8-1.2]; p<0.01), and a statistically non-significant higher area (MD: 3.1cm2 [1.0-5.2]; p=0.46) of EAT compared to the control group. Most studies reported a significant association between EAT and subclinical atheromatosis in patients with different systemic inflammatory diseases. CONCLUSION: This study demonstrated that EAT is increased in patients with systemic inflammatory diseases compared with healthy controls, and that EAT measurement is closely correlated with subclinical atherosclerosis in these patients. The causality of this association should be tested in prospective studies.
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Aterosclerose , Pericárdio , Humanos , Estudos Prospectivos , Pericárdio/diagnóstico por imagem , Aterosclerose/etiologia , Tecido Adiposo/diagnóstico por imagemRESUMO
Dyslipidemia presents high levels of serum cholesterol and is characterized as a risk factor for cardiovascular diseases, especially for the development of atherosclerosis. E. oleracea oil (OFEO), A. esculentus oil (OFAE), B. orellana oil (OFBO), and Chronic SM® granules (CHR) are rich in bioactive compounds with the potential to treat changes in lipid metabolism. This study investigated the effects of treatments with oils from A. esculentus, E. oleracea, B. orellana, and Chronic SM® on Cocos nucifera L. saturated-fat-induced dyslipidemia. The chromatographic profile showed the majority presence of unsaturated fatty acids in the tested oils. The quantification of tocotrienols and geranylgeraniol in OFBO and CHR was obtained. Treatments with OFEO, OFAE, OFBO, and CHR were able to significantly reduce glycemia, as well as hypertriglyceridemia, total cholesterol, and LDL-cholesterol, besides increasing HDL-cholesterol. The treatments inhibited the formation of atheromatous plaques in the vascular endothelium of the treated rats. The obtained results suggest that the OFEO, OFAE, OFBO, and CHR exhibit antidyslipidemic effects and antiatherogenic activity.
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Abelmoschus , Aterosclerose , Dislipidemias , Euterpe , Ratos , Animais , Ratos Wistar , Bixaceae , Aterosclerose/tratamento farmacológico , Aterosclerose/etiologia , Dislipidemias/tratamento farmacológico , Dislipidemias/etiologia , HDL-Colesterol , ÓleosRESUMO
Objective: In this study, we aimed to evaluate subclinical atherosclerosis in patients with obesity who had cardiovascular disease risk indicators such as arterial stiffness, which is evaluated using pulse wave velocity (PWV), carotid intima-media thickness (CIMT), and biomarkers of endothelial dysfunction such as endocan, ADAMTS97, and ADAMTS9. Subjects and methods: Sixty obese subjects, including 23 subjects with body mass index (BMI) ≥ 40, 37 subjects with BMI ≥ 30 but < 40, and 60 age-and sex-matched control subjects, were included in our study. Serum endocan, ADAMTS97, and ADAMTS9 levels as well as PWV and CIMT measurements of the subjects in the obese and control groups were performed. Results: In the obesity group, PWV levels were significantly higher than they were in the control group and endocan levels were significantly lower than they were in the control group. When we compared the obese group with BMI ≥ 40 and the control group, the BMI ≥ 40 group had significantly higher PWV and CIMT levels than the control group had, whereas endocan, ADAMTS7, and ADAMTS9 levels were similar to those of the control group. When we compared the obese group with BMI ≥ 30 < 40 to the control group, endocan levels were lower in the group with BMI ≥30 < 40, and PWV and CIMT levels were similar to the control group. Conclusion: We found that arterial stiffness and CIMT increased in obese patients with BMI ≥ 40 and that increased arterial stiffness was associated with age, systolic blood pressure, and HBA1C. In addition, we found that the endocan levels were lower in obese patients than they were in nonobese control individuals.
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Aterosclerose , Rigidez Vascular , Humanos , Espessura Intima-Media Carotídea , Análise de Onda de Pulso , Aterosclerose/etiologia , Obesidade/complicações , Biomarcadores , Fatores de RiscoRESUMO
In individuals with very low high-density lipoprotein (HDL-C) cholesterol, such as Tangier disease, LCAT deficiency, and familial hypoalphalipoproteinemia, there is an increased risk of premature atherosclerosis. However, analyzes based on comparisons of populations with small variations in HDL-C mediated by polygenic alterations do not confirm these findings, suggesting that there is an indirect association or heterogeneity in the pathophysiological mechanisms related to the reduction of HDL-C. Trials that evaluated some of the HDL functions demonstrate a more robust degree of association between the HDL system and atherosclerotic risk, but as they were not designed to modify lipoprotein functionality, there is insufficient data to establish a causal relationship. We currently have randomized clinical trials of therapies that increase HDL-C concentration by various mechanisms, and this HDL-C elevation has not independently demonstrated a reduction in the risk of cardiovascular events. Therefore, this evidence shows that (a) measuring HDL-C as a way of estimating HDL-related atheroprotective system function is insufficient and (b) we still do not know how to increase cardiovascular protection with therapies aimed at modifying HDL metabolism. This leads us to a greater effort to understand the mechanisms of molecular action and cellular interaction of HDL, completely abandoning the traditional view focused on the plasma concentration of HDL-C. In this review, we will detail this new understanding and the new horizon for using the HDL system to mitigate residual atherosclerotic risk.
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Aterosclerose , Lipoproteínas HDL , Humanos , HDL-Colesterol , Aterosclerose/etiologia , Aterosclerose/terapiaRESUMO
OBJECTIVE: To identify childhood and parental factors associated with initiation of statin therapy in children with heterozygous familial hypercholesterolemia (HeFH), including underlying genetic diagnosis or parental premature atherosclerotic cardiovascular disease (ASCVD). STUDY DESIGN: This multicenter cohort study included 245 HeFH child-parent pairs from the REFERCHOL national register (2014-2020). Demographic and clinical characteristics at the last visit were collected. Vascular disease in parents was defined as a history of ASCVD, and/or a coronary artery calcium score >100, and/or stenosis of >50% in at least carotid artery. Statistical analyses included descriptive analysis, logistic regression for univariate and multivariate effects of statins, and a sensitivity analysis combining the characteristics of children and parents. RESULTS: Among the 245 children in the study cohort, 135 (58%), with a mean age of 14 ± 3 years, were treated with a statin. In multivariable analysis, the predictive childhood factors associated with statin treatment were genetic diagnosis (OR, 2.5; 95% CI, 1.3 to 4.9; P = .01), older age (OR, 4.4; 95% CI, 1.8-10.6; P = .01), more than 2 visits (OR, 2.36; 95% CI, 1.18-4.73; P = .015), and longer duration of follow-up (OR, 1.3; 95% CI, 1.1-1.6; P < .001). The predictive parental factor associated with childhood treatment was the presence of vascular disease (OR, 2.4; 95% CI, 1.0-5.7; P = .04). CONCLUSIONS: HeFH confirmed by DNA testing during childhood and a history of vascular disease in parents were independently associated with statin treatment in children with HeFH. Genetic diagnosis may be useful for cardiovascular prevention in children.
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Aterosclerose , Inibidores de Hidroximetilglutaril-CoA Redutases , Hipercolesterolemia , Hiperlipoproteinemia Tipo II , Humanos , Criança , Adolescente , Inibidores de Hidroximetilglutaril-CoA Redutases/uso terapêutico , Estudos de Coortes , LDL-Colesterol , Hiperlipoproteinemia Tipo II/diagnóstico , Hiperlipoproteinemia Tipo II/tratamento farmacológico , Hiperlipoproteinemia Tipo II/genética , Hipercolesterolemia/complicações , Aterosclerose/etiologia , Aterosclerose/genéticaRESUMO
Stroke is the second leading cause of death worldwide and the vast majority can be attributed to modifiable risk factors, mainly behavioral and metabolic. The top six risk factors responsible for cardiovascular mortality in Brazil in 2019 were high systolic blood pressure, inadequate dietary exposure, high body mass index, high LDL cholesterol, high fasting blood glucose levels, and tobacco. We intend to discuss in this paper the evidence and recommendations in the approach of three essential risk factors for patients with a history of stroke: dyslipidemia, hypertension and diabetes.
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Aterosclerose , Hipertensão , Acidente Vascular Cerebral , Aterosclerose/etiologia , Humanos , Hipertensão/complicações , Neurologistas , Fatores de Risco , Acidente Vascular Cerebral/etiologiaRESUMO
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.
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Humanos , Feminino , Adulto , Adulto Jovem , Anticoncepcionais Orais Combinados/efeitos adversos , Aterosclerose/prevenção & controle , Treinamento Intervalado de Alta Intensidade , Estudos Transversais , Aterosclerose/etiologia , Fatores de Risco de Doenças CardíacasRESUMO
Oxidized low-density lipoprotein (ox-LDL) is the most harmful form of cholesterol associated with vascular atherosclerosis and hepatic injury, mainly due to inflammatory cell infiltration and subsequent severe tissue injury. Lox-1 is the central ox-LDL receptor expressed in endothelial and immune cells, its activation regulating inflammatory cytokines and chemotactic factor secretion. Recently, a Lox-1 truncated protein isoform lacking the ox-LDL binding domain named LOXIN has been described. We have previously shown that LOXIN overexpression blocked Lox-1-mediated ox-LDL internalization in human endothelial progenitor cells in vitro. However, the functional role of LOXIN in targeting inflammation or tissue injury in vivo remains unknown. In this study, we investigate whether LOXIN modulated the expression of Lox-1 and reduced the inflammatory response in a high-fat-diet mice model. Results indicate that human LOXIN blocks Lox-1 mediated uptake of ox-LDL in H4-II-E-C3 cells. Furthermore, in vivo experiments showed that overexpression of LOXIN reduced both fatty streak lesions in the aorta and inflammation and fibrosis in the liver. These findings were associated with the down-regulation of Lox-1 in endothelial cells. Then, LOXIN prevents hepatic and aortic tissue damage in vivo associated with reduced Lox-1 expression in endothelial cells. We encourage future research to understand better the underlying molecular mechanisms and potential therapeutic use of LOXIN.
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Aterosclerose , Células Progenitoras Endoteliais , Ftalazinas , Animais , Aorta/metabolismo , Aorta/patologia , Aterosclerose/tratamento farmacológico , Aterosclerose/etiologia , Aterosclerose/metabolismo , Aterosclerose/patologia , Células Cultivadas , Dieta Hiperlipídica/efeitos adversos , Células Progenitoras Endoteliais/efeitos dos fármacos , Células Progenitoras Endoteliais/metabolismo , Células Progenitoras Endoteliais/patologia , Inflamação/tratamento farmacológico , Inflamação/genética , Inflamação/metabolismo , Inflamação/patologia , Lipoproteínas LDL/metabolismo , Fígado/metabolismo , Camundongos , Ftalazinas/farmacologia , Receptores Depuradores Classe E/genética , Receptores Depuradores Classe E/metabolismoAssuntos
Aterosclerose , Povos Indígenas , Aterosclerose/etiologia , Brasil/epidemiologia , Humanos , Fumar Cachimbo , RespiraçãoRESUMO
BACKGROUND: COVID-19 patients may develop atherosclerosis-related complications. Whether a proportion of these patients already had asymptomatic cervicocephalic atherosclerosis before SARS-CoV-2 infection is not known. This study assessed whether pre-existing cervicocephalic atherosclerosis increased the susceptibility to SARS-CoV-2 infection or resulted in more severe or fatal COVID-19. METHODS: Individuals enrolled in the Atahualpa Project cohort who received head CT (for assessing carotid siphon calcifications) and B-mode ultrasounds (for measurement of the carotid intima-media thickness) prior to the pandemic were eligible for this study. Among this cohort, those who also received serological tests for detection of SARS-CoV-2 antibodies and clinical evaluations for assessment of COVID-19 severity were enrolled. Multivariate logistic regression and exposure-effect models were fitted to assess the association between pre-existing atherosclerosis biomarkers, and SARS-CoV-2 seropositivity and COVID-19 severity. RESULTS: Overall, 154 of 519 study participants (30%) had evidence of cervicocephalic atherosclerosis. A total of 325 (63%) individuals became SARS-CoV-2 positive, and 65 (23.5%) of seropositive individuals had severe or fatal COVID-19. The risk of SARS-CoV-2 seropositive status did not differ across individuals with and without atherosclerosis biomarkers (P = .360). Likewise, seropositive individuals with pre-existing atherosclerosis were not more prone to develop severe or fatal COVID-19 than those without evidence of atherosclerosis (P = .274). Average estimated exposure effects of pre-existing cervicocephalic atherosclerosis versus no atherosclerosis over SARS-CoV-2 seropositivity and COVID-19 severity were not significant. CONCLUSIONS: Pre-existing cervicocephalic atherosclerosis does not increase the risk of acquiring SARS-CoV-2 infection nor the severity of COVID-19 among seropositive individuals.
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Aterosclerose , COVID-19 , Aterosclerose/epidemiologia , Aterosclerose/etiologia , Espessura Intima-Media Carotídea , Estudos de Coortes , Humanos , SARS-CoV-2RESUMO
OBJECTIVE: Cardiovascular (CV) disease is still a major cause of excessive morbidity and mortality in patients with active acromegaly, which may be attributed to a high prevalence of associated pro-atherosclerotic risk factors. However, a direct effect of GH/IGF-1 excess on the vasculature has been previously suggested, warranting further investigation. The present study was designed to investigate whether chronic GH/IGF-1 excess is associated with an increased prevalence of subclinical atherosclerosis in patients with acromegaly. DESIGN: We measured carotid intima-media thickness (cIMT) and assessed carotid plaques by ultrasonography along with classical CV risk factors in 54 acromegaly patients (34 females, 50 ± 12 years and compared those with 62 (42 females, 53 ± 13 years) age-, sex- and CV risk factors- matched controls. In order to compare cIMT measurements between patients and controls we analyzed common carotid artery far wall data as well as a combined measurement result, which consisted of the mean value of the six different measurements, three at each side. RESULTS: mean ± SD serum GH and IGF-1 levels were 2.76 ± 4.65 ng/mL and 1.7 ± 1.25 x ULN, respectively, in all acromegaly patients. Age, body mass index, blood pressure, lipid levels, fasting glucose and Framingham's global cardiovascular risk score classification were similar comparing patients and controls. Combined median [IQR] cIMT measurements were similar in acromegaly patients and matched controls (0.59 [0.52-0.66] mm vs. 0.59 [0.52-0.69] mm; P = 0.872) as well as in acromegaly patients with active and controlled disease (0.59 [0.51-0.68] mm vs. 0.60 [0.54-0.68] mm; P = 0.385). No significant correlations were observed between cIMT measurements and GH (Spearman r = 0.1, P = 0.49) or IGF-1 (Spearman r = 0.13, P = 0.37) levels in patients with acromegaly. Carotid atherosclerotic plaques prevalence was similar in patients and controls (26% vs. 32%; P = 0.54) as well as in patients with active and controlled acromegaly (22% vs. 30%; P = 0.537). CONCLUSIONS: Our data suggest that GH/IGF-1 excess itself is not one of the main drivers of subclinical morphological atherosclerosis changes in patients with acromegaly and that optimal control of acromegaly-associated CV risk factors may preserve vasculature structure even when strict biochemical control is not achieved.
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Acromegalia , Aterosclerose , Doenças Cardiovasculares , Aterosclerose/epidemiologia , Aterosclerose/etiologia , Doenças Cardiovasculares/epidemiologia , Doenças Cardiovasculares/etiologia , Espessura Intima-Media Carotídea , Feminino , Fatores de Risco de Doenças Cardíacas , Humanos , Fator de Crescimento Insulin-Like I , Masculino , Fatores de RiscoRESUMO
The term "triglyceride-rich lipoproteins" (TRLs) includes chylomicrons and their remnants, very low-density lipoproteins (VLDL), and intermediate-density lipoproteins (IDL). In this manuscript, the mechanisms by which atherogenic TRLs contribute to the formation of atheroma plaques are reviewed. Cholesterol from TRLs that can be retained in the subendothelial space (i.e., remnants, DLs, and small VLDLs) contributes to the genesis of atherosclerosis. Triglycerides of atherogenic TRLs induce inflammation of the arterial wall. Mechanisms that explain the involvement of TRLs in atherosclerosis are the generation of pro-atherogenic changes in high-density lipoproteins and low-density lipoproteins, accumulation of TRLs in plasma, and their passage to the subendothelial space where they cause endothelial dysfunction and inflammation of the vascular wall. Furthermore, plasma accumulation of TRLs causes hyperviscosity and a procoagulant state. Finally, this manuscript summarizes the controversial aspects of the clinical approach and the treatment of cases with dyslipidemia explained by atherogenic TRLs.
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Aterosclerose , Lipoproteínas , Aterosclerose/etiologia , Colesterol , Humanos , Lipoproteínas VLDL , TriglicerídeosRESUMO
INTRODUCTION: Patients with psoriasis have an increased prevalence of cardiovascular risk factors as well as cardiovascular disease. OBJECTIVE: To determine if patients with psoriasis and metabolic syndrome (MS) have a higher frequency of subclinical atherosclerosis compared with those with psoriasis without MS. MATERIALS AND METHODS: A cross-sectional study was conducted in patients with psoriasis; MS was defined according to ATP III criteria. Demographic, clinical, and anthropometric data were obtained. Blood chemistry, high sensitive C-reactive protein (hs-CRP), and insulin were measure. Subclinical atherosclerosis was defined as high carotid intima-media thickness (CIMT) by Mode B ultrasound. RESULTS: 92 patients with psoriasis were included, 67 (72.8%) with MS and 25 (27.2%) without MS. Subjects with psoriasis and MS had significantly higher weight, body mass index, waist circumference, systolic blood pressure, glucose, insulin, triglycerides, insulin resistance, hs-CRP, and lower level of high-density lipoprotein cholesterol, compared with subjects without MS. High CIMT was greater in patients with psoriasis and MS than in those without MS. Age and MS were independent predictors of increased CIMT after multiple linear regression analysis. CONCLUSIONS: MS is associated with greater inflammation and subclinical atherosclerosis in patients with psoriasis.
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Aterosclerose , Insulinas , Síndrome Metabólica , Psoríase , Aterosclerose/epidemiologia , Aterosclerose/etiologia , Proteína C-Reativa/análise , Proteína C-Reativa/metabolismo , Espessura Intima-Media Carotídea , Estudos Transversais , Humanos , Síndrome Metabólica/complicações , Síndrome Metabólica/epidemiologia , Psoríase/complicações , Psoríase/epidemiologia , Fatores de RiscoRESUMO
OBJECTIVE: To evaluate structural and functional carotid changes and inflammatory profiles in children with obstructive sleep apnea (OSA) and healthy controls. STUDY DESIGN: Patients with OSA and matched controls (ages 5-13 years) were recruited. Proinflammatory cytokines and acute phase reactants were measured at 6:00 p.m. Common carotid artery measures were determined using ultrasound. Confirmatory factor analysis was used to determine subgroups of cytokines and their effects on carotid measures. RESULTS: Ninety-six patients participated (53 healthy controls, 43 patients with OSA). OSA was associated with increased proinflammatory cytokines (cluster of differentiation-40 ligand [CD40-L], interleukin [IL]-6, and IL-8) and high sensitivity C-reactive protein (P < .05 for all). One cytokine subgroup (IL-6 and IL-8) was negatively associated with markers of carotid function, indicating reduced arterial distensibility and increased stiffness (P < .05 for 3 ultrasound measures); and tumor necrosis factor-α had an opposing effect on carotid function compared with this cytokine subgroup (P < .05 for 2 ultrasound measures). Linear regression demonstrated significant associations between and tumor necrosis factor- α and 2 measures of carotid function (P < .05 for each). Children with OSA did not have functional or structural carotid changes compared with controls. CONCLUSION: OSA was not directly associated with structural and functional carotid changes but was associated with upregulation of key proinflammatory cytokines (sCD40-L, IL-6, and IL-8). Together, IL-6 and IL-8 were associated with changes in carotid function. Longitudinal studies are needed to demonstrate that the inflammatory milieu observed in our population is a precursor of atherosclerosis in children.
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Proteínas de Fase Aguda/metabolismo , Aterosclerose/etiologia , Artéria Carótida Primitiva/fisiopatologia , Citocinas/sangue , Inflamação/etiologia , Apneia Obstrutiva do Sono/fisiopatologia , Adolescente , Aterosclerose/sangue , Aterosclerose/diagnóstico , Aterosclerose/fisiopatologia , Biomarcadores/sangue , Artéria Carótida Primitiva/diagnóstico por imagem , Artéria Carótida Primitiva/patologia , Estudos de Casos e Controles , Criança , Pré-Escolar , Estudos Transversais , Feminino , Humanos , Inflamação/sangue , Inflamação/diagnóstico , Inflamação/fisiopatologia , Modelos Lineares , Masculino , Estudos Prospectivos , Apneia Obstrutiva do Sono/sangue , Apneia Obstrutiva do Sono/complicações , UltrassonografiaRESUMO
Introducción: El sexo influye en la susceptibilidad de las personas de ambos géneros con relación a la mayoría de las enfermedades comunes, incluidas la diabetes mellitus y la aterosclerosis. Objetivo: Identificar si existen diferencias en la presentación de la enfermedad cardiovascular aterosclerótica entre hombres y mujeres de edad mediana con diabetes mellitus. Métodos: Se realizó un estudio descriptivo de corte transversal en 1449 pacientes con diabetes mellitus en edad mediana (40 a 59 años) que ingresaron en el Centro de Atención al Diabético de Bayamo, Granma, desde el año 2010 al 2019. Se empleó la prueba de Chi Cuadrado para comprobar la relación entre las variables cualitativas, y T de Student para comparar los valores promedio de las variables cuantitativas. Resultados: La proporción de enfermedad cardiovascular aterosclerótica en el sexo masculino fue similar a la del femenino (51,4 por ciento x 48,6 por ciento, p=0.2328). No hubo discrepancias importantes en el porcentaje de la enfermedad, entre ambos sexos, en los diferentes grupos etarios. El riesgo de enfermedad cardiovascular aterosclerótica en los hombres fue mayor que en las mujeres premenopausicas (OR=2,19, IC: 1,4-3,3 p=0,0002), pero inferior respecto a las posmenopáusicas. (OR=1.12, IC: 0.8-1.4, p=0.4129). El análisis multivariado mostró al tiempo de la diabetes >10 años y a la hipertensión arterial como riesgo de enfermedad cardiovascular aterosclerótica en ambos sexos. Asimismo, se evidenció en la edad mayor de 45 años en los hombres (OR=2.5, IC: 1.4-4.6) y la menopausia en las mujeres (OR=1.8, IC: 1.1-3.07). Conclusiones: La frecuencia de la enfermedad cardiovascular aterosclerótica en las personas de edad mediana con diabetes mellitus es similar en ambos sexos. El sexo masculino tiene mayor riesgo de enfermarse que las mujeres premenopausicas, pero menor que las posmenopáusicas. La hipertensión arterial y el tiempo de la diabetes son factores de riesgo comunes para uno y otro sexo(AU)
Introduction: Sex influences the susceptibility of people of both genders to most common diseases, including diabetes mellitus (DM) and atherosclerosis. Objective: Identify if there are differences in the presentation of atherosclerotic cardiovascular disease between middle-aged men and women with diabetes mellitus. Methods: A descriptive cross-sectional study was conducted in 1449 patients with DM in middle age (40 to 59 years) who were admitted to the Diabetic´s Care Center of Bayamo, Granma province, from 2010 to 2019. The Chi-Square test was used to check the relation between the qualitative variables, and the T Student test to compare the average values of the quantitative variables. Results: The proportion of atherosclerotic cardiovascular disease in males was similar to that of females (51.4 percent x 48.6 percent, p=0.2328). There were no major discrepancies in the percentage of atherosclerotic cardiovascular disease, between both sexes, in the different age groups. The risk of atherosclerotic cardiovascular disease in men was higher than in pre-menopausal women (OR=2.19, CI: 1.4-3.3 p=0.0002), but lower than in post-menopausal women. (OR=1.12, CI: 0.8-1.4, p=0.4129). Multivariate analysis showed diabetes >10 years and arterial hypertension as a risk of atherosclerotic cardiovascular disease in both sexes. It was also evidenced in ages over 45 years in men (OR=2.5, CI: 1.4-4.6) and menopause in women (OR=1.8, CI: 1.1-3.07). Conclusions: The frequency of atherosclerotic cardiovascular disease in middle-aged people with diabetes mellitus is similar in both sexes. Males have a higher risk of atherosclerotic cardiovascular disease than pre-menopausal women, but lower than post-menopausal women. High blood pressure and diabetes time are common risk factors for both sexes(AU)
Assuntos
Humanos , Masculino , Feminino , Pessoa de Meia-Idade , Menopausa , Doenças Cardiovasculares/mortalidade , Diabetes Mellitus/etiologia , Aterosclerose/etiologia , Fatores de Risco de Doenças Cardíacas , Distribuição de Qui-Quadrado , Epidemiologia Descritiva , Estudos Transversais , Análise MultivariadaRESUMO
CONTEXT: Chronic kidney disease (CKD) and diabetes are associated with dyslipidemia, metabolic abnormalities, and atherosclerotic risk. Nuclear magnetic resonance (NMR) spectroscopy provides much more detail on lipoproteins than traditional assays. METHODS: In about 38 000 participants from the Mexico City Prospective Study, aged 35 to 84 years and not using lipid-lowering medication, NMR spectroscopy quantified plasma concentrations of lipoprotein particles, their lipidic compositions, and other metabolic measures. Linear regression related low estimated glomerular filtration rate (eGFR; <60 mL/min/1.73 m2) to each NMR measure after adjustment for confounders and for multiplicity. Analyses were done separately for those with and without diabetes. RESULTS: Among the 38 081 participants (mean age 52 years, 64% women), low eGFR was present for 4.8% (306/6403) of those with diabetes and 1.2% (365/31 678) of those without diabetes. Among both those with and without diabetes, low eGFR was significantly associated with higher levels of 58 NMR measures, including apolipoprotein B (Apo-B), the particle numbers of most Apo-B containing lipoproteins, the cholesterol and triglycerides carried in these lipoproteins, several fatty acids, total cholines and phosphatidylcholine, citrate, glutamine, phenylalanine, ß-OH-butyrate, and the inflammatory measure glycoprotein-A, and significantly lower levels of 13 NMR measures, including medium and small high-density lipoprotein particle measures, very low-density lipoprotein particle size, the ratio of saturated:total fatty acids, valine, tyrosine, and aceto-acetate. CONCLUSIONS: In this Mexican population with high levels of adiposity and diabetes, low kidney function was associated with widespread alterations in lipidic and metabolic profiles, both in those with and without diabetes. These alterations may help explain the higher atherosclerotic risk experienced by people with CKD.