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The Triggering Receptor Expressed on Myeloid cells 2 (TREM-2) has been widely known by its anti-inflammatory activity. It can be activated in response to microbes and tissue damage, leading to phagocytosis, autophagy, cell polarization and migration, counter inflammation, and tissue repair. So far, the receptor has been largely explored in neurodegenerative disorders, however, a growing number of studies have been investigating its contribution in different pathological conditions, including metabolic diseases, in which (resident) macrophages play a crucial role. In this regard, TREM-2 + macrophages have been implicated in the onset and development of obesity, atherosclerosis, and fibrotic liver disease. These macrophages can be detected in the brain, white adipose tissue, liver, and vascular endothelium. In this review we discuss how different murine models have been demonstrating the ability of such cells to contribute to tissue and body homeostasis by phagocytosing cellular debris and lipid structures, besides contributing to lipid homeostasis in metabolic diseases. Therefore, understanding the role of TREM-2 in metabolic disorders is crucial to expand our current knowledge concerning their immunopathology as well as to foster the development of more targeted therapies to treat such conditions.
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PURPOSE: Understanding the relationship between antithyroperoxidase antibodies (TPOAb) and carotid intima-media thickness (cIMT) could provide insights into the mechanisms linking thyroid autoimmunity and cardiovascular disease. We aimed to explore the association of multiple categories of TPOAb with the increased cIMT at baseline and at follow-up in participants from the ELSA-Brasil Study. METHODS: This prospective cohort study analyzed data from 9,264 participants (51.5 ± 8.9 years old, 55.9% women) without a history of cardiovascular disease. Fasting serum TPOAb levels were determined. Values of cIMT equal to or above one deviation standard of the sample's mean were classified as increased cIMT at baseline. The increased cIMT after the 8-year follow-up was calculated after excluding participants with increased cIMT at baseline. Multivariate analyses were done using binary logistic and Poisson regression models. RESULTS: The increased cIMT was prevalent in 14.3% of the participants at baseline and its development occurred in 16.8% participants during the cohort. After adjustment for all confounder variables, TPOAb detectability (OR = 1.84, 95%CI = 1.21-2.79), and low detectable (OR = 1.81, 95%CI = 1.18-2.75), high detectable (OR = 2.01, 95%CI = 1.29-3.11) and positive (OR = 1.70, 95%CI = 1.07-2.70) TPOAb were positively associated with increased cIMT at baseline. The associations of low and high detectable TPOAb and increased cIMT at baseline were consistent when excluding those with thyroid dysfunction. There was no statistically significant association between TPOAb levels and increased cIMT at follow-up (p > 0.05), neither for all sample nor for euthyroid individuals. CONCLUSION: Different levels of TPOAb, including its detectability, were associated with increased cIMT at baseline in the studied sample. We highlight that may be relevant to consider the levels of TPOAb detectability as possible marker of increased cardiovascular risk.
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Photobiomodulation (PBM) has been shown to be promising for the promotion of angiogenesis. The present study investigated the effects of PBM on vascularization in an animal model of peripheral artery disease. Wistar rats were divided into three groups. The control group received no procedures. The ischemia group was submitted to ligation of the femoral artery of the hindleg. The ischemia + PBM group was submitted to ligation of the femoral artery followed by PBM (660 and 808 nm, 100 mW, 4 J) over the site. Animals with ischemia treated with PBM exhibited comparable results to the control group with regards to the diameter of the α-SMA+ vessels, cross-sectional area of muscle fibers, percentage of collagen and serum concentration of IL-17A, as well as similarities in terms of vertical mobility, temperature of the hindleg, number of acts of grooming, and percentage of movement, indicating a condition like that of limbs unaffected by ischemia.
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Objective: Assessing subclinical atherosclerosis (sAT) is crucial for preventing cardiovascular disease. The Mediterranean diet is considered the gold standard for cardiovascular protection, but cultural and economic barriers can hinder adherence to it. The prudent dietary pattern (DP) has been associated with protective effects against chronic diseases. However, its impact on primary cardiovascular prevention remains uncertain. This study examined adherence to various DPs and their effect on sAT, measured by total carotid plaque area (TPA). Methods: This cross-sectional study included 116 adults enrolled in a cardiovascular prevention program. Demographic, clinical, laboratory, and TPA data were collected. Adherence to DPs was assessed using a food frequency questionnaire. Participants were categorized according to their adherence to 4 mutually exclusive DPs: prudent, traditional, sweet, and mixed. Generalized linear models were used to assess the effect of DPs on TPA, adjusting for relevant cardiovascular variables. Results: The traditional, sweet, and mixed DPs were associated with higher TPA values than the prudent DP, with medians (interquartile range) of 27 (99), 39 (49), 27.5 (58), and 0 (36) mm2, respectively. Gamma regression analysis found that the beta exponents for the traditional, sweet, and mixed DPs versus the prudent DP were 3.78 (p=0.046); 3.73 (p=0.013), and 2.20 (p=0.072), respectively. Systolic blood pressure values were higher for the sweet and mixed DPs than for the prudent DP (133.9±11.7; 132.5±13.9 and 122.7±8.8 mmHg, respectively; p<0.05). Conclusion: These findings underscore the importance of additional research and targeted interventions to promote healthier DPs to promote improvements in cardiovascular health.
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Aterosclerosis , Humanos , Medición de Riesgo , Aterosclerosis/complicaciones , Aterosclerosis/diagnóstico , Masculino , Factores de Riesgo , Femenino , Persona de Mediana Edad , Progresión de la Enfermedad , Hígado Graso/complicaciones , Factores de Tiempo , Enfermedad del Hígado Graso no Alcohólico/complicacionesRESUMEN
Atherosclerosis (AS) is a chronic inflammatory vascular disease. Dysregulated lipid metabolism, oxidative stress, and inflammation are the major mechanisms implicated in the development of AS. In addition, evidence suggests that gut dysbiosis plays an important role in atherogenesis, and modulation of the gut microbiota with probiotics and phenolic compounds has emerged as a promising strategy for preventing and treating AS. It has been shown that probiotics and phenolic compounds can improve atherosclerosis-related parameters by improving lipid profile, oxidative stress, and inflammation. In addition, these compounds may modulate the diversity and composition of the gut microbiota and improve atherosclerosis. The studies evaluated in the present review showed that probiotics and phenolic compounds, when consumed individually, improved atherosclerosis by modulating the gut microbiota in various ways, such as decreasing gut permeability, decreasing TMAO and LPS levels, altering alpha and beta diversity, and increasing fecal bile acid loss. However, no study was found that evaluated the combined use of probiotics and phenolic compounds to improve atherosclerosis. The available literature highlights the synergistic potential between phenolic compounds and probiotics to improve their health-promoting properties and functionalities. This review aims to summarize the available evidence on the individual effects of probiotics and phenolic compounds on AS, while providing insights into the potential benefits of nutraceutical approaches using probiotic strains, quercetin, and resveratrol as potential adjuvant therapies for AS treatment through modulation of the gut microbiota.
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Objective: To determine subclinical cardiovascular disease (sCVD) in middle-aged women with clinically manifested hand osteoarthritis (HOA) and to improve the characterization of cardiovascular risk in this population. Design: We cross-sectionally evaluated the relationship between HOA and sCVD in 1,803 volunteers from the Mexican Teachers' Cohort. From 2012 to 2016, a subsample from Mexico City, the Northern state Nuevo León, and the Southern states Chiapas and Yucatán was invited for clinical evaluations, during which neurologists examined carotid arteries using ultrasound, and a standardized HOA questionnaire was also administered. HOA was defined as age ≥45 years, hand joint pain, and morning stiffness that lasted no longer than 30 minutes. sCVD was assessed using the intima-media thickness (IMT) and atherosclerotic plaques. Results: Among participants with a mean age of 51 years (±4), 18.4% met the criteria for HOA, and the prevalence of carotid atherosclerosis was 23.1%. After multivariable adjustment, women diagnosed with HOA had a 1.8% (95% confidence interval [CI] 0.3, 3.3) greater mean IMT than those without this joint disease. Similarly, women with HOA had 36% (95% CI 1.01, 1.84) higher odds of carotid atherosclerosis. Conclusions: HOA is associated with sCVD in middle-aged women. This relationship might be due to low-grade chronic inflammation; however, further research is required to clarify the underlying mechanisms.
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Acute coronary syndrome (ACS) represents an important clinical manifestation of coronary artery disease (CAD) and is characterized by a particularly poor prognosis. Myocardial reperfusion through primary percutaneous coronary intervention (PPCI) is imperative in the event of acute ST elevation myocardial infarction (STEMI). Interleukin-22 (IL-22) regulates immune and inflammatory responses. This interleukin has been described in the scenario of the CAD, but there are no data in patients with STEMI undergoing PPCI. Objectives: The goals of this study were to investigate the differences in circulating IL-22 levels between patients with STEMI undergoing PPCI and healthy controls and to determine whether these differences were associated with the culprit coronary artery, door-to-balloon time (DBT), final angiographic result, CAD classification, and presence of diabetes mellitus (DM). Methods: A total of 280 participants were recruited, comprising 210 STEMI cases and 70 healthy controls. Participants underwent clinical and angiographic evaluations, and serum IL-22 levels were measured using an enzyme-linked immunosorbent assay (ELISA). Data analysis was performed using the Mann-Whitney and Fisher tests, with p < 0.05 indicating significance. Results: Serum IL-22 levels were lower in cases (149.63, 84.99-294.56) than in the controls (482.67, 344.33-641.00); p < 0.001. Lower IL-22 levels were associated with the right coronary artery (RCA) (144.57, 70.84-242.43; 146.00, 63.60-279.67; 191.71, 121.80-388.97); p = 0.033. IL-22 was lower with shorter DBT (≤60 min, 106.00, 49.60-171.71; >60 min, 153.00, 88.86-313.60); p = 0.043. Conclusions: IL-22 levels were significantly lower in patients with STEMI than in healthy controls.
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The role of ferroptosis and iron metabolism dysregulation in the pathophysiology of cardiovascular diseases is increasingly recognized. Conditions such as hypertension, cardiomyopathy, atherosclerosis, myocardial ischemia/reperfusion injury, heart failure, and cardiovascular complications associated with COVID-19 have been linked to these processes. Inflammation is central to these conditions, prompting exploration into the inflammatory and immunoregulatory molecular pathways that mediate ferroptosis and its contribution to cardiovascular disease progression. Notably, emerging evidence highlights interleukin-37 as a protective cytokine with the ability to activate the nuclear factor erythroid 2-related factor 2 pathway, inhibit macrophage ferroptosis, and attenuate atherosclerosis progression in murine models. However, a comprehensive review focusing on interleukin-37 and its protective role against ferroptosis in CVD is currently lacking. This review aims to fill this gap by summarizing existing knowledge on interleukin-37, including its regulatory functions and impact on ferroptosis in conditions such as atherosclerosis and myocardial infarction. We also explore experimental strategies and propose that targeting interleukin-37 to modulate ferroptosis presents a promising therapeutic approach for the prevention and treatment of cardiovascular diseases.
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Enfermedades Cardiovasculares , Ferroptosis , Interleucina-1 , Humanos , Interleucina-1/metabolismo , Enfermedades Cardiovasculares/metabolismo , Animales , COVID-19/metabolismo , COVID-19/inmunología , Aterosclerosis/metabolismo , Aterosclerosis/patología , SARS-CoV-2/metabolismoRESUMEN
BACKGROUND: Capsaicin, a bioactive compound found in peppers, is recognized for its anti-inflammatory, antioxidant, and anti-lipidemic properties. This study aimed to evaluate the effects of capsaicin on atherosclerosis progression. METHODS: Apolipoprotein E knockout mice and their C57BL/6 controls were utilized to assess blood lipid profile, inflammatory status, and atherosclerotic lesions. We also examined the influence of capsaicin on cholesterol influx and efflux, and the role of TRPV1 and PPARγ signaling pathways in bone marrow-derived macrophages. RESULTS: Capsaicin treatment reduced weight gain, visceral adiposity, blood triglycerides, and total and non-HDL cholesterol. These improvements were associated with a reduction in atherosclerotic lesions in the aorta and carotid. Capsaicin also improved hepatic oxidative and inflammatory status. Systemic inflammation was also reduced, as indicated by reduced leukocyte rolling and adhesion on the mesenteric plexus. Capsaicin decreased foam cell formation by reducing cholesterol influx through scavenger receptor A and increasing cholesterol efflux via ATP-binding cassette transporter A1, an effect primarily linked to TRPV1 activation. CONCLUSIONS: These findings underscore the potential of capsaicin as a promising agent for atherosclerosis prevention, highlighting its comprehensive role in modulating lipid metabolism, foam cell formation, and inflammatory responses.
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Aterosclerosis , Capsaicina , Células Espumosas , Inflamación , PPAR gamma , Canales Catiónicos TRPV , Animales , Masculino , Ratones , Antiinflamatorios/farmacología , Aterosclerosis/prevención & control , Aterosclerosis/tratamiento farmacológico , Transportador 1 de Casete de Unión a ATP/metabolismo , Capsaicina/farmacología , Colesterol/sangre , Colesterol/metabolismo , Células Espumosas/efectos de los fármacos , Células Espumosas/metabolismo , Inflamación/tratamiento farmacológico , Metabolismo de los Lípidos/efectos de los fármacos , Macrófagos/efectos de los fármacos , Macrófagos/metabolismo , Ratones Endogámicos C57BL , Ratones Noqueados , Ratones Noqueados para ApoE , PPAR gamma/metabolismo , Transducción de Señal/efectos de los fármacos , Canales Catiónicos TRPV/metabolismoRESUMEN
BACKGROUND: Different types of exercise, performed acutely or chronically, have different repercussions on central hemodynamics, arterial stiffness, and cardiac function. In this study, we aim to compare the effects of acute elbow flexion (EFlex) and knee extension (KExt) exercises on vascular and hemodynamic parameters and arterial stiffness indices in healthy young adults. METHODS: Young adults (20 to 39 years) underwent randomized muscle strength tests to obtain 1 repetition maximum (1RM) for elbow flexion (EFlex) and knee extension (KExt). After a minimum interval of 48 h, cardiovascular parameters were assessed using Mobil-O-Graph® (Mobil-O-Graph, IEM, Germany) at three-time points: at baseline (before exercise), immediately after elbow flexion or knee extension exercises with a load corresponding to 50% of 1RM (T0) and after 15 min of rest (T15). RESULTS: Immediately after exercise (T0), peripheral systolic blood pressure, peripheral pulse pressure, central systolic blood pressure, and central pulse pressure were significantly higher in KExt than EFlex (Δ 3.13; Δ 3.06; Δ 5.65; Δ 5.61 mmHg, respectively). Systolic volume, cardiac output, and cardiac index were significantly higher immediately after KExt when compared with EFlex (Δ 4.2 ml; Δ 0.27 ml/min and 0.14 l/min*1/m2, respectively). The reflection coefficient and the pulse wave velocity were also significantly higher at T0 in KExt compared to EFlex ( Δ 8.59 and Δ 0.12 m/sec, respectively). CONCLUSION: Our results show differential contribution of muscle mass in vascular and hemodynamic parameters evaluated immediately after EFlex and KExt. In addition, our study showed for the first time that the reflection coefficient, an index that evaluates the magnitude of the reflected waves from the periphery, was only affected by KExt.
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Background: Some clinical dyslipidemia cases do not respond to statins, known as statin-resistant familial hypercholesterolemia (SR-FH), in which patients are under a high cardiovascular risk despite statin therapy. Therefore, novel therapeutic alternatives are required. Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) reduce cholesterol levels and cardiovascular disease risk, particularly in patients with SR-FH, where PCSK9i may differentially affect pro- and anti-inflammatory mediators depending on the clinical setting. Aim: To evaluate the effect of PCSK9i treatment on pro- and anti-inflammatory cytokines in patients with SR-FH. Methods: Before-after comparison, quasi-experimental, single-center study in patients with SR-FH. Blood samples were processed to obtain complete blood counts of glycated hemoglobin and serum lipid levels. Flow cytometry was performed to characterize baseline circulating M1- and M2-macrophages and monocytes. Multiplexing of plasma samples was used to compare plasma fraktaline, interleukins (ILs), monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factor (TNF)-alpha. The endpoints were lower serum lipid levels and pro-inflammatory mediator modification. Results: Twenty patients with SR-FH, aged 58 years and most of them males, were included, with a mean body-mass index of 26.4 and showing ischemic heart disease and similar values of baseline M1- and M2-macrophages and monocytes. Six-month iPSCK-9 therapy considerably reduced LDLc, increased anti-inflammatory cytokine (IL-4), and modified pro-inflammatory cytokine (TNF-alpha and MCP-1) levels. No notable effects were observed for the other markers. Conclusion: PCSK9i therapy exerted subclinical anti-inflammatory and anti-atherogenic effects, indicating potential benefits for clinical outcomes.
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OBJECTIVE: To explore the potential associations between high-density lipoprotein (HDL) levels and inflammasome components in the context of systemic lupus erythematosus (SLE). METHODS: A cross-sectional study was conducted. A group of 50 patients with SLE and 50 healthy controls matched by sex and similar age ranges were enrolled. Serum HDL cholesterol (HDL-C) and C reactive protein (CRP) levels were quantified. Serum cytokine levels, including IL-1ß and IL-6, were determined by ELISA. The gene expression of inflammasome-related genes in peripheral blood mononuclear cells was measured by quantitative real-time PCR. RESULTS: HDL-C levels were lower in the patients with SLE (p<0.05), and on segregation according to disease activity, those with active SLE had the lowest HDL-C levels. Patients with SLE presented higher concentrations of the serum inflammatory cytokines IL-1ß and IL-6 (p<0.0001) but similar levels of CRP to those in controls. A similar scenario was observed for the gene expression of inflammasome components, where all the evaluated markers were significantly upregulated in the SLE population. These results revealed significant negative correlations between HDL levels and disease activity, serum IL-6 and IL-1ß levels and the mRNA expression of NLRP3, IL-1ß and IL-18. In addition, significant positive correlations were found between disease activity and serum IL-1ß and between disease activity and the mRNA expression of IL-18, and interestingly, significant positive correlations were also observed between active SLE and serum IL-1ß and the mRNA expression of NLRP3. CONCLUSION: Our results suggest that HDL is essential for SLE beyond atherosclerosis and is related to inflammation regulation, possibly mediated by inflammasome immunomodulation.
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Proteína C-Reactiva , Inflamasomas , Interleucina-1beta , Lupus Eritematoso Sistémico , Humanos , Lupus Eritematoso Sistémico/inmunología , Lupus Eritematoso Sistémico/sangre , Femenino , Masculino , Estudios Transversales , Adulto , Inflamasomas/inmunología , Persona de Mediana Edad , Interleucina-1beta/sangre , Proteína C-Reactiva/análisis , Lipoproteínas HDL/sangre , Leucocitos Mononucleares/inmunología , Leucocitos Mononucleares/metabolismo , Estudios de Casos y Controles , Interleucina-6/sangre , HDL-Colesterol/sangre , Proteína con Dominio Pirina 3 de la Familia NLR/metabolismo , Citocinas/sangreRESUMEN
OBJECTIVE: Atherosclerosis (AS) is a common pathogenesis of cardiovascular diseases. Puerarin (Pue) is a Chinese herbal remedy used to prevent and treat AS. Here, this research investigated the effect of Pue on AS progression. METHODS: ApoE-/- mice were induced with acrolein. Body weight, blood lipid index, inflammatory factors, mitochondrial oxidative stress, and lipid deposition were detected. IL-6 and TNF-α were detected by ELISA. Oil red staining and H&E staining were used to observe the aortic sinus plaque lesions. Serum expressions of inflammatory factors IL-6, TNF-a, SOD, GSH and MDA were detected by ELISA, the mRNA expression levels of HDAC1 in the aorta were detected by RT-qPCR, and IL-6 and TNF-α in the aorta were detected by immunohistochemistry. JNK, p-JNK, OPA-1, and HDAC1 were detected by Western blotting. RESULTS: Pue administration can effectively reduce lipid accumulation in AS mice induced by acrolein. Pue promoted the activity of SOD, GSH and MDA, and inhibited the formation of atherosclerotic plaques and the process of aortic histological changes. Pue reduced IL-6 and TNF-α. HDAC1 expression was down-regulated and p-JNK-1 and JNK protein expression was up-regulated. CONCLUSION: Pue reduces inflammation and alleviates AS induced by acrolein by mediating the JNK pathway to inhibit HDAC1-mediated oxidative stress disorder.
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Acroleína , Aterosclerosis , Histona Desacetilasa 1 , Isoflavonas , Estrés Oxidativo , Animales , Aterosclerosis/inducido químicamente , Aterosclerosis/metabolismo , Aterosclerosis/tratamiento farmacológico , Estrés Oxidativo/efectos de los fármacos , Histona Desacetilasa 1/metabolismo , Isoflavonas/farmacología , Isoflavonas/uso terapéutico , Acroleína/farmacología , Masculino , Factor de Necrosis Tumoral alfa/metabolismo , Interleucina-6/metabolismo , Sistema de Señalización de MAP Quinasas/efectos de los fármacos , Ratones , Modelos Animales de Enfermedad , Ensayo de Inmunoadsorción Enzimática , Western Blotting , Aorta/efectos de los fármacos , Aorta/patologíaRESUMEN
Resumo Fundamento Alcançar as metas nutricionais estabelecidas pelas sociedades científicas é um desafio constante e nem sempre alcançado. Objetivo Investigar a adequação alimentar de indivíduos com doença cardiovascular (DCV), participantes do Programa Alimentar Brasileiro Cardioprotetor residentes da região Nordeste do Brasil, segundo as recomendações da Sociedade Brasileira de Cardiologia (SBC). Métodos Análise transversal com dados do estudo de implementação da Dieta Cardioprotetora Brasileira (DICA BR) que avaliou indivíduos com DCV, atendidos em centros especializados em saúde cardiovascular em oito estados do Nordeste. O consumo alimentar foi obtido por recordatório alimentar de 24 horas e a adequação da dieta seguiu as recomendações da SBC. Foram considerados significantes valores de p < 0,05. Resultados Foram estudados 647 pacientes, com média (desvio padrão) de idade de 63,1 (9,4) anos, sendo 50,2% do sexo feminino. Na avaliação da ingestão alimentar, observou-se baixa adequação de carboidratos (52,3%), proteínas (70,9%), lipídios (38,8%) e fibras (22,4%). Observou-se que a maioria das mulheres consumia dieta hipoproteica (59,2%) e idosos tinham maior inadequação no consumo de carboidratos (52,6%). Em relação a ingestão de sódio, os homens apresentaram maior ingestão (72,9%), enquanto os idosos apresentaram redução de 13%. Além disso, foi demonstrado que os homens ingeriam mais fibras (28,1%) e indivíduos com maior escolaridade tinham um consumo elevado de ácidos graxos saturados (70,5%). Conclusões A maioria dos indivíduos não alcançou as metas dietoterápicas preconizadas para prevenção cardiovascular secundária. Os achados do presente estudo reforçam a necessidade de implementação de estratégias estruturadas, a fim de estimular hábitos alimentares saudáveis nesses indivíduos.
Abstract Background Achieving nutritional goals established by scientific societies is a constant challenge and not always achieved. Objective To investigate the dietary adequacy of individuals with cardiovascular disease (CVD), participants in the Cardioprotective Brazilian Food Program residing in the Northeast region of Brazil, according to the recommendations of the Brazilian Society of Cardiology (SBC). Methods Cross-sectional analysis with data from the study implementing the Brazilian Cardioprotective Diet (DICA BR), which evaluated individuals with CVD treated in specialized cardiovascular health centers in eight states in the Northeast region. Food consumption was obtained by 24-hour dietary records and dietary adequacy followed SBC recommendations. Values of p < 0.05 were considered significant. Results 647 patients were studied, with a mean (standard deviation) age of 63.1 (9.4) years, 50.2% of whom were female. When evaluating food intake, a low adequacy of carbohydrates (52.3%), proteins (70.9%), lipids (38.8%), and fiber (22.4%) was observed. It was observed that the majority of women consumed a low-protein diet (59.2%) and the elderly had a greater inadequacy in carbohydrate consumption (52.6%). Regarding sodium intake, men had a higher intake (72.9%), while the elderly showed a 13% reduction. Furthermore, it was shown that men ate more fiber (28.1%) and individuals with higher education had a high consumption of saturated fatty acids (70.5%). Conclusions Most individuals did not achieve the recommended dietary therapy goals for secondary cardiovascular prevention. The findings of the present study reinforce the need to implement structured strategies to encourage healthy eating habits in these individuals.
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Atherosclerosis (AS) has become the leading cause of cardiovascular disease worldwide. Our previous study had observed that Nippostrongylus brasiliensis (Nb) infection or its derived products could inhibit AS development by inducing an anti-inflammatory response. We performed a metabolic analysis to screen Nb-derived metabolites with anti-inflammation activity and evaluated the AS-prevention effect. We observed that the metabolite uridine had higher expression levels in mice infected with the Nb and ES (excretory-secretory) products and could be selected as a key metabolite. ES and uridine interventions could reduce the pro-inflammatory responses and increase the anti-inflammatory responses in vitro and in vivo. The apolipoprotein E gene knockout (ApoE-/-) mice were fed with a high-fat diet for the AS modeling. Following the in vivo intervention, ES products or uridine significantly reduced serum and liver lipid levels, alleviated the formation of atherosclerosis, and reduced the pro-inflammatory responses in serum or plaques, while the anti-inflammatory responses showed opposite trends. After blocking with 5-HD (5-hydroxydecanoate sodium) in vitro, the mRNA levels of M2 markers were significantly reduced. When blocked with 5-HD in vivo, the degree of atherosclerosis was worsened, the pro-inflammatory responses were increased compared to the uridine group, while the anti-inflammatory responses decreased accordingly. Uridine, a key metabolite from Nippostrongylus brasiliensis, showed anti-inflammatory and anti-atherosclerotic effects in vitro and in vivo, which depend on the activation of the mitochondrial ATP-sensitive potassium channel.
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Antiinflamatorios , Aterosclerosis , Nippostrongylus , Uridina , Animales , Masculino , Ratones , Antiinflamatorios/farmacología , Apolipoproteínas E/genética , Apolipoproteínas E/deficiencia , Aterosclerosis/metabolismo , Aterosclerosis/genética , Modelos Animales de Enfermedad , Canales KATP/metabolismo , Canales KATP/genética , Ratones Noqueados , Mitocondrias/metabolismo , Mitocondrias/efectos de los fármacos , Uridina/farmacologíaRESUMEN
Fundamento: la aterosclerosis es una enfermedad de origen multifactorial que se agrava a consecuencia de un medio ambiente adverso y de estilos de vida no saludables. Las evidencias confirman su inicio desde las etapas más tempranas de la vida. Objetivo: describir la presencia de lesiones ateroscleróticas tempranas en las aortas de fetos y neonatos fallecidos hijos de madres hipertensas. Método: se realizó un estudio descriptivo de tipo transversal que incluyó a los fetos mayores de 22 semanas y neonatos fallecidos hijos de madres hipertensas, a quienes se les realizó autopsia en el departamento de anatomía patológica, del Hospital Universitario Ginecobstétrico Eusebio Hernández Pérez, en el período comprendido entre enero del 2021 hasta diciembre 2022, con un total de 18. Se recogieron los siguientes datos en las historias clínicas: sexo del fallecido, edad gestacional en el momento del parto, peso postparto, edad materna y antecedentes de hipertensión arterial (crónica o gestacional). Se analizaron las 18 aortas (torácicas y abdominales) de los fallecidos seleccionados. Resultados: del total de fallecidos estudiados el 70,6 % presentó lesiones ateroscleróticas tempranas, caracterizadas por engrosamiento de la íntima a modo de cojinete, presencia de linfocitos en la íntima o en la pared arterial cercana a ella y/o macrófagos. En algunos casos se observó una de estas variantes histológicas y en otros la combinación de dos o tres. Conclusiones: las lesiones ateroscleróticas tempranas están presentes en las aortas de la mayoría de los fetos y neonatos estudiados, con predominio en las que presentaban hipertensión gestacional.
Foundation: atherosclerosis is a disease of multifactorial origin that is aggravated as a result of an adverse environment and unhealthy lifestyles. Evidence confirms its onset from the earliest stages of life. Objective: to describe the presence of early atherosclerotic lesions in the aortas of deceased fetuses and neonates born to hypertensive mothers. Method: a descriptive cross-sectional study was carried out that included fetuses older than 22 weeks and deceased neonates born to hypertensive mothers, who underwent autopsy in the pathological anatomy department of the Eusebio Hernández Pérez Gynecobstetric University Hospital, in the period between January 2021 and December 2022, with a total of 18. The following data were collected in the medical records: sex of the deceased, gestational age at the time of delivery, postpartum weight, maternal age, and history of arterial hypertension (chronic or gestational). The 18 aortas (thoracic and abdominal) of the selected deceased were analyzed. Results: of the total number of deceased studied, 70.6 % presented early atherosclerotic lesions, characterized by thickening of the intima as a cushion, presence of lymphocytes in the intima or in the arterial wall close to it and/or macrophages. In some cases, one of these histological variants was observed and in others a combination of two or three. Conclusions: early atherosclerotic lesions are present in the aortas of the majority of the fetuses and neonates studied, with a predominance in those with gestational hypertension.
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LOX-1, ORL-1, or lectin-like oxidized low-density lipoprotein receptor 1 is a transmembrane glycoprotein that binds and internalizes ox-LDL in foam cells. LOX-1 is the main receptor for oxidized low-density lipoproteins (ox-LDL). The LDL comes from food intake and circulates through the bloodstream. LOX-1 belongs to scavenger receptors (SR), which are associated with various cardiovascular diseases. The most important and severe of these is the formation of atherosclerotic plaques in the intimal layer of the endothelium. These plaques can evolve into complicated thrombi with the participation of fibroblasts, activated platelets, apoptotic muscle cells, and macrophages transformed into foam cells. This process causes changes in vascular endothelial homeostasis, leading to partial or total obstruction in the lumen of blood vessels. This obstruction can result in oxygen deprivation to the heart. Recently, LOX-1 has been involved in other pathologies, such as obesity and diabetes mellitus. However, the development of atherosclerosis has been the most relevant due to its relationship with cerebrovascular accidents and heart attacks. In this review, we will summarize findings related to the physiologic and pathophysiological processes of LOX-1 to support the detection, diagnosis, and prevention of those diseases.
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Enfermedades Cardiovasculares , Receptores Depuradores de Clase E , Humanos , Receptores Depuradores de Clase E/metabolismo , Receptores Depuradores de Clase E/genética , Enfermedades Cardiovasculares/metabolismo , Enfermedades Cardiovasculares/etiología , Animales , Lipoproteínas LDL/metabolismo , Aterosclerosis/metabolismo , Aterosclerosis/patologíaRESUMEN
BACKGROUND: Endothelial dysfunction (ED) suspicion will allow to prevent accelerated atherosclerosis and premature death. OBJECTIVE: To establish the usefulness of thermography for endothelial function screening in adults with cardiovascular risk factors. MATERIAL AND METHODS: Cross-sectional, analytical diagnostic test. A brachial arterial diameter (BAD) increase < 11% at one-minute post-ischemia meant probable ED and was confirmed if BAD was ≥ 11% post-sublingual nitroglycerin. Thermographic photographs of the palmar region were obtained at one minute. Descriptive statistics, ROC curve, Mann-Whitney's U-test, chi-square test, or Fisher's exact test were used. RESULTS: Thirty-eight subjects with a median age of 50 years, and with 624 thermographic measurements were included. Nine had ED (flow-mediated vasodilation [FMV]: 2.5%). The best cutoff point for normal endothelial function in subjects with cardiovascular risk factors was ≥ 36 °C at one minute of ischemia, with 85% sensitivity, 70% specificity, positive and negative predictive values of 78 and 77%, area under the curve of 0.796, LR+ 2.82, LR- 0.22. CONCLUSION: An infrared thermography-measured temperature in the palmar region greater than or equal to 36 °C after one minute of ischemia is practical, non-invasive, and inexpensive for normal endothelial function screening in adults with cardiovascular risk factors.
ANTECEDENTES: La sospecha de disfunción endotelial (DE) permitirá prevenir la aterosclerosis acelerada y la muerte prematura. OBJETIVO: Establecer la utilidad de la termografía en el cribado de la función endotelial en adultos con factores de riesgo cardiovascular. MATERIAL Y MÉTODOS: Estudio transversal analítico de prueba diagnóstica. El incremento del diámetro de la arteria braquial < 11 % a un minuto posisquemia significó probable DE, confirmada si el diámetro fue ≥ 11 % posnitroglicerina sublingual. Se obtuvieron fotografías termográficas al minuto de la región palmar. Se aplicó estadística descriptiva, curva ROC, pruebas U de Mann-Whitney, chi cuadrada o exacta de Fisher. RESULTADOS: Se incluyeron 38 sujetos, mediana de edad de 50 años, con 624 mediciones termográficas; nueve presentaron DE (vasodilatación mediada por flujo de 2.5 %). El mejor punto de corte para la función endotelial normal en sujetos con factores de riesgo cardiovascular fue ≥ 36 °C al minuto de isquemia, con sensibilidad de 85%, especificidad de 70%, valores predictivos positivo y negativo de 78 y 77%, área bajo la curva de 0.796, razón de verisimilitud positiva de 2.82 y razón de verisimilitud negativa de 0.22. CONCLUSIÓN: La medición de la temperatura en la región palmar mediante termografía infrarroja ≥ 36 °C tras un minuto de isquemia es práctica, no invasiva y económica para el cribado de la función endotelial normal en adultos con factores de riesgo cardiovascular.
Asunto(s)
Endotelio Vascular , Termografía , Humanos , Termografía/métodos , Persona de Mediana Edad , Masculino , Femenino , Estudios Transversales , Endotelio Vascular/fisiopatología , Adulto , Anciano , Factores de Riesgo de Enfermedad Cardiaca , Sensibilidad y Especificidad , Rayos Infrarrojos , Arteria Braquial/fisiología , Enfermedades Cardiovasculares/diagnóstico , Enfermedades Cardiovasculares/fisiopatología , Vasodilatación/fisiología , Valor Predictivo de las PruebasRESUMEN
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.