{"title":"Association between Dietary Vitamin E Intake and the Risk of Hypertension in US Adults","authors":"Chang Liu, Dan Liang","doi":"10.2174/0115701611297956240425115501","DOIUrl":"https://doi.org/10.2174/0115701611297956240425115501","url":null,"abstract":"Background:: Many studies have shown that Vitamin E (VitE) intake has beneficial effects on human health, but the relationship between VitE intake and Blood Pressure (BP) is not well understood. Thus, our present study aimed to assess the relationship between VitE intake and hypertension, systolic and diastolic BP in US (United States) adults. Method:: We used data from the 2003-2018 National Health and Nutrition Examination Survey (NHANES). Weighted multivariate regression analysis, subgroup analysis, and Restricted Cubic Splines (RCS) were used to explore the independent associations between VitE intake and hypertension, systolic and diastolic BP. A total of 32,371 participants were included in this study. The mean VitE intake of participants was 8.50 ± 0.08 mg/d. The prevalence of hypertension in subjects was 37.76% and it decreased with increasing VitE intake quartiles (quartile 1: 40.97%, quartile 2: 37.60%, quartile 3: 37.47%, quartile 4: 35.66%). A significant negative correlation was found between VitE intake and hypertension. Result:: We also observed a significant negative association between VitE intake and systolic BP (model 1: β = -0.11, 95% CI: -0.15 ~ -0.07; model 2: β = -0.09, 95% CI: -0.12 ~ -0.05; and model 3: β = -0.05, 95% CI: -0.10 ~ -0.01). Quartile 2 of dietary VitE intake significantly correlated to a lower diastolic BP compared to the lowest quartile of VitE intake (model 3: β = -0.72, 95%CI: -1.26~-0.18). Conclusion:: In US adults, VitE intake has not been significantly found to be associated with hypertension, but it has been found to exhibit a negative association with both systolic and diastolic BP in US adults.","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":"125 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140834674","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification of Critical Genes Differentiating Stable and Unstable Atherosclerotic Plaques: A Bioinformatic and Computational Analysis","authors":"Maryam Mahjoubin-Tehran, Raul D. Santos, Wael Almahmeed, Khalid Al-Rasadi, Amirhossein Sahebkar","doi":"10.2174/0115701611282362240409035233","DOIUrl":"https://doi.org/10.2174/0115701611282362240409035233","url":null,"abstract":"Background: Identification of biomarkers to distinguish between stable and unstable plaque formation would be very useful to predict plaque vulnerability. Methods: We downloaded microarray profiles of gene set enrichment (GSE) accession numbers including GSE71226 and GSE20680 (group A: containing healthy vs stable plaque samples) and GSE62646 and GSE34822 (group B: containing stable vs unstable plaque samples) from Gene expression omnibus (GEO) database. Differentially expressed genes were compared in both data sets of each group. Results: Ten and 12 key genes were screened in groups A and B, respectively. Gene Ontology (GO) enrichment was applied by the plugin “BiNGO” (Biological networks gene ontology tool) of the Cytoscape. The key genes were mostly enriched in the biological process of positive regulation of the cellular process. The protein-protein interaction and co-expression network were analyzed by the STRING (search tool for the retrieval of interacting genes/proteins) and GeneMANIA (gene multiple association network integration algorithm) plugin of Cytoscape, respectively, which showed that Epidermal growth factor (EGF), Heparin-binding EGF like growth factor (HBEGF), and Matrix metalloproteinase 9 (MMP9) were at the core of the network. Further validation of key genes using two datasets showed that Phosphodiesterase 5A (PDE5A) and Protein S (PROS1) were decreased in unstable plaques, while Suppressor of cytokine signaling (SOCS3), HBEGF, and Leukocyte immunoglobulin-like receptor B4 (LILRB4) were increased. Conclusion: The present study used several datasets to identify key genes associated with stable and unstable atherosclerotic plaque.","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":"5 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-04-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140624036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
María Fernanda Castillo, Daniela Salgado-Canales, Marco Arrese, Francisco Barrera, Dimitri P Mikhailidis
{"title":"Effect of Intermittent Fasting on Lipid Profile, Anthropometric and Hepatic Markers in Non-Alcoholic Fatty Liver Disease (NAFLD): A Systematic Review","authors":"María Fernanda Castillo, Daniela Salgado-Canales, Marco Arrese, Francisco Barrera, Dimitri P Mikhailidis","doi":"10.2174/0115701611285401240110074530","DOIUrl":"https://doi.org/10.2174/0115701611285401240110074530","url":null,"abstract":"Background: The first-line treatment for non-alcoholic fatty liver disease (NAFLD) is lifestyle modification; this should accompany any pharmacological intervention. Intermittent fasting (IF) has shown benefits over metabolic and cardiovascular parameters. Non-religious IF includes Time-Restricted Feeding (TRF), Alternate-Day Fasting (ADF), and 5:2 IF interventions. Objective: To evaluate the effects of IF on anthropometric, liver damage, and lipid profile markers in subjects with NAFLD. Methods: A bibliographic search was carried out according to the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines using PubMed and Scopus databases. Results: Five studies involving 470 patients with NAFLD were included. In relation to anthropometric markers, all the articles reported body weight reduction (2.48-7.63%), but only ADF and 5:2 IF reported a body weight reduction >5%; also, all the articles reported fat mass reduction. Concerning hepatic markers, all the articles reported a reduction in hepatic steatosis and alanine aminotransferase activity, but no changes in fat-free mass and high-density lipoprotein cholesterol levels. There were variable results on fibrosis, other liver enzymes, waist circumference and body mass index, as well as the levels of triglycerides, total cholesterol, and low-density lipoprotein cholesterol. Conclusion: Any form of IF could be potentially beneficial for NAFLD treatment and some associated cardiometabolic parameters. However, it is necessary to evaluate the effects and safety of IF in long-term studies involving a higher number of participants with different stages of NAFLD. The effect of IF on NAFLD-associated vascular risk also needs evaluation.","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":"167 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139689103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pier Luigi Antignani, Mateja K Jezovnik, Ales Blinc, Dimitri P Mikhailidis, Panagiotis Anagnostis, Gerit-Holger Schernthaner, Mojca Jensterle, Katica Bajuk Studen, Miso Sabovic, Pavel Poredos
{"title":"Hyperparathyroidism and Peripheral Arterial Disease.","authors":"Pier Luigi Antignani, Mateja K Jezovnik, Ales Blinc, Dimitri P Mikhailidis, Panagiotis Anagnostis, Gerit-Holger Schernthaner, Mojca Jensterle, Katica Bajuk Studen, Miso Sabovic, Pavel Poredos","doi":"10.2174/0115701611280905231227045826","DOIUrl":"10.2174/0115701611280905231227045826","url":null,"abstract":"<p><p>Primary hyperparathyroidism (PHPT) is presented in various forms, including classic PHPT, characterised by increased parathyroid hormone (PTH) secretion, normohormonal PHPT, and normocalcaemic PHPT. Secondary hyperparathyroidism is characterised by increased PTH secretion triggered by factors such as vitamin D deficiency and kidney failure. This review aims to discuss the involvement of hyperparathyroidism (HPT) in atherosclerosis, including peripheral arterial disease (PAD). The increased level of PTH is involved in developing subclinical and overt vascular diseases, encompassing endothelial dysfunction, vascular stiffness, hypertension, and coronary and peripheral arterial diseases. It has been consistently associated with an augmented risk of cardiovascular morbidity and mortality, independent of classical risk factors for atherosclerosis. Chronic hypercalcemia associated with increased levels of PTH contributes to the development of calcification of vessel walls and atherosclerotic plaques. Vascular calcification can occur in the intima or media of the arterial wall and is associated with stiffness of peripheral arteries, which the formation of atherosclerotic plaques and narrowing of the vessel lumen can follow. For treating hyperparathyroidism, particularly SHPT, calcimimetics, novel phosphorus binders and novel vitamin D receptor activators are used. However, they are ineffective in severe PHPT. Therefore, parathyroidectomy remains the primary therapeutic option of PHPT.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"88-94"},"PeriodicalIF":4.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139570216","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Saeed Abughazaleh, Omar Obeidat, Mohammad Tarawneh, Hashim Al-Ani, Ahmad Al Nawaiseh, Mohamed F Ismail
{"title":"Burden of Ischemic Heart Diseases among US States from 1990-2019.","authors":"Saeed Abughazaleh, Omar Obeidat, Mohammad Tarawneh, Hashim Al-Ani, Ahmad Al Nawaiseh, Mohamed F Ismail","doi":"10.2174/0115701611305792240426120709","DOIUrl":"10.2174/0115701611305792240426120709","url":null,"abstract":"<p><strong>Background: </strong>Ischemic Heart Disease (IHD) is a leading cause of global mortality, including in the United States. Understanding the burden of IHD in the United States is crucial for informed decision-making and targeted interventions aimed at reducing morbidity and mortality associated with this leading cause of death. This study aimed to understand the burden of IHD, identify gender disparities and risk factors, explore the relationship between socioeconomic growth and IHD, and analyze risk factor distribution across the states of the United States.</p><p><strong>Methods: </strong>This study utilized data from the Global Burden of Diseases Study 2019, which provided comprehensive information on IHD from 1990 to 2019. Data related to IHD from these years were extracted using a query tool from the Institute for Health Metrics and Evaluation (IHME) website. The study assessed the relationship between IHD and socioeconomic development using the Socio-demographic Index (SDI) and measured the overall impact of IHD using Disability-adjusted Life Years (DALYs), considering premature death and disability. Additionally, the study analyzed the burden of IHD attributed to six main risk factors. Data analysis involved comparing prevalence, mortality, SDI, DALYs, attributable burden, and risk estimation among the states.</p><p><strong>Results: </strong>Between 1990 and 2019, there was an improvement in socioeconomic development in all states. Age-standardized rates of disease burden for IHD decreased by 50% [ASDR 3278.3 to 1629.4 (95% UI: 1539.9-1712.3) per 100,000] with the most significant decline observed in Minnesota. Males had higher burden rates than females in all states, and the southeast region had the highest mortality rates. The prevalence of IHD showed a declining trend, with approximately 8.9 million cases (95% UI: 8.0 million to 9.8 million) in 2019, representing a 37.1% decrease in the Age-standardized Prevalence Rate (ASPR) from 1990. Metabolic risks were the leading contributors to the disease burden, accounting for 50% of cases, with Mississippi having the highest attributable risk. Arkansas had the highest attributable risk for high cholesterol and smoking. Conversely, Minnesota had the lowest burden of IHD among all the states.</p><p><strong>Conclusion: </strong>This study highlights variations in the burden of IHD across US states and emphasizes the need for tailored prevention programs to address specific risk factors and gender differences. Understanding the trend in IHD may inform policymakers and healthcare professionals in effectively allocating resources to reduce the burden of IHD and improve national health outcomes.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"426-436"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140860246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cardiovascular Protection of Aspirin in Chronic Kidney Disease Patients: An Updated Systematic Review and Meta-Analysis.","authors":"Ting Chen, Yunlei Deng, Rong Gong","doi":"10.2174/1570161121666230530154647","DOIUrl":"10.2174/1570161121666230530154647","url":null,"abstract":"<p><strong>Purpose: </strong>To evaluate aspirin's cardiovascular (CV) protective effect in chronic kidney disease (CKD) patients.</p><p><strong>Methods: </strong>We searched PubMed, Embase, Cochrane Library, and Web of Science (up to December 2022) for randomized controlled trials (RCTs) and observational studies comparing aspirin with placebo in CKD patients for the prevention of CV disease (CVD). Efficacy outcomes included CVD, heart failure, myocardial infarction, stroke, CV and all-cause mortality; safety outcomes included major bleeding, minor bleeding, and renal events.</p><p><strong>Results: </strong>Six RCTs and 6 observational studies, including 35,640 participants, met the inclusion criteria and reported relevant CV outcomes, with a mean follow-up of 46.83 months. The pooled data showed aspirin had no significant preventive effect on CVD events (RR=1.03; 95% CI, 0.84-1.27). However, CV mortality was significantly reduced in the aspirin group (RR=0.74; 95% CI, 0.58-0.95). Furthermore, aspirin use did not increase the risk of major bleeding and renal events but significantly increased minor bleeding events (RR=2.11; 95% CI, 1.30-3.44). Renal events were significantly increased after sensitivity analysis (RR=1.10; 95% CI, 1.04-1.16).</p><p><strong>Conclusion: </strong>Aspirin did not prevent CV events, with a significantly increased risk of minor bleeding and renal events. Besides, aspirin use had no statistically significant reduction in the risk of all-cause mortality but had a statistically significant reduction in the risk of CV mortality.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"287-296"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9545736","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cytoplasmic Polyadenylation Element Binding Protein 1 and Atherosclerosis: Prospective Target and New Insights.","authors":"Jing Zhou, Chao-Ke Tang","doi":"10.2174/0115701611258090231221082502","DOIUrl":"10.2174/0115701611258090231221082502","url":null,"abstract":"<p><p>The ribonucleic acid (RNA)-binding protein Cytoplasmic Polyadenylation Element Binding Protein 1 (CPEB1), a key member of the CPEB family, is essential in controlling gene expression involved in both healthy physiological and pathological processes. CPEB1 can bind to the 3'- untranslated regions (UTR) of substrate messenger ribonucleic acid (mRNA) and regulate its translation. There is increasing evidence that CPEB1 is closely related to the pathological basis of atherosclerosis. According to recent investigations, many pathological processes, including inflammation, lipid metabolism, endothelial dysfunction, angiogenesis, oxidative stress, cellular senescence, apoptosis, and insulin resistance, are regulated by CPEB1. This review considers the prevention and treatment of atherosclerotic heart disease in relation to the evolution of the physiological function of CPEB1, recent research breakthroughs, and the potential participation of CPEB1 in atherosclerosis.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"95-105"},"PeriodicalIF":4.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139570211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
R Herman, A Janez, D P Mikhailidis, P Poredos, A Blinc, M Sabovic, K Bajuk Studen, G H Schernthaner, P Anagnostis, P L Antignani, M Jensterle
{"title":"Growth Hormone, Atherosclerosis and Peripheral Arterial Disease: Exploring the Spectrum from Acromegaly to Growth Hormone Deficiency.","authors":"R Herman, A Janez, D P Mikhailidis, P Poredos, A Blinc, M Sabovic, K Bajuk Studen, G H Schernthaner, P Anagnostis, P L Antignani, M Jensterle","doi":"10.2174/0115701611269162231106042956","DOIUrl":"10.2174/0115701611269162231106042956","url":null,"abstract":"<p><p>Growth hormone (GH) and insulin-like growth factor 1 (IGF-1) are increasingly recognised for their role in cardiovascular (CV) physiology. The GH-IGF-1 axis plays an essential role in the development of the CV system as well as in the complex molecular network that regulates cardiac and endothelial structure and function. A considerable correlation between GH levels and CV mortality exists even among individuals in the general population without a notable deviation in the GHIGF- 1 axis functioning. In addition, over the last decades, evidence has demonstrated that pathologic conditions involving the GH-IGF-1 axis, as seen in GH excess to GH deficiency, are associated with an increased risk for CV morbidity and mortality. A significant part of that risk can be attributed to several accompanying comorbidities. In both conditions, disease control is associated with a consistent improvement of CV risk factors, reduction of CV mortality, and achievement of standardised mortality ratio similar to that of the general population. Data on the prevalence of peripheral arterial disease in patients with acromegaly or growth hormone deficiency and the effects of GH and IGF-1 levels on the disease progression is limited. In this review, we will consider the pivotal role of the GH-IGF-1 axis on CV system function, as well as the far-reaching consequences that arise when disorders within this axis occur, particularly in relation to the atherosclerosis process.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"28-35"},"PeriodicalIF":4.5,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"92153238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Efficacy and Safety of Bempedoic Acid in Patients with High Cardiovascular Risk: An Update.","authors":"Ozge Telci Caklili, Manfredi Rizzo, Mustafa Cesur","doi":"10.2174/0115701611290763240126045433","DOIUrl":"10.2174/0115701611290763240126045433","url":null,"abstract":"<p><p>Statins play a significant role in the prevention of cardiovascular (CV) diseases (CVDs); however, non-adherence with statin treatment or statin intolerance (mainly attributed to muscleassociated side effects) is not uncommon. New agents such as bempedoic acid (BA) can provide more treatment options. BA is administered orally, once daily, at a dose of 180 mg in current clinical practice. It can decrease circulating low-density lipoprotein cholesterol (LDL-C) levels by nearly 30% as monotherapy or by 20% as an add-on to statins. CV outcome studies have shown that BA decreases major adverse CV event risk in patients with established CVD or high CV risk by 13%. When patients with high CV risk were analyzed alone, the risk reduction was 30%. Its side effects include a rise in serum uric acid levels and liver enzyme activity, whereas it does not increase diabetes risk as statins do. BA can be used as adjunctive therapy to statins in patients at high CV risk in whom lipid targets cannot be achieved or as an alternative to statins in patients with statin intolerance.</p>","PeriodicalId":11278,"journal":{"name":"Current vascular pharmacology","volume":" ","pages":"242-250"},"PeriodicalIF":2.8,"publicationDate":"2024-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139697136","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}