Cardiovascular Therapeutics最新文献

{"title":"DUSP22 Ameliorates Endothelial-to-Mesenchymal Transition in HUVECs through Smad2/3 and MAPK Signaling Pathways","authors":"Lu Chen,&nbsp;Hongyu Su,&nbsp;Zekai Tao,&nbsp;Cui Liang,&nbsp;Zhongzhao Liu,&nbsp;Yiming Dong,&nbsp;Peipei Zheng,&nbsp;Yuan Liu","doi":"10.1155/2024/5583961","DOIUrl":"10.1155/2024/5583961","url":null,"abstract":"<p>Endothelial-to-mesenchymal transition (EndMT) is the process by which endothelial cells lose their endothelial properties and acquire mesenchymal characteristics. Dual-specific protein phosphatase 22 (DUSP22) inactivates various protein kinases and transcription factors by dephosphorylating serine/threonine residues: hence, it plays a key role in many diseases. The aim of this study was to explore the functional role of DUSP22 in EndMT. In the transforming growth factor-<i>β</i>-induced EndMT model in human umbilical vein endothelial cells (HUVECs), we observed a downregulation of DUSP22 expression. This DUSP22 deficiency could aggravate EndMT. Conversely, the overexpression of DUSP22 could ameliorate EndMT. We used signaling pathway inhibitors to verify our results and found that DUSP22 could regulate EndMT through the smad2/3 and the mitogen-activated protein kinase (MAPK) signaling pathways. In summary, DUSP22 ameliorates EndMT in HUVECs in vitro through the smad2/3 and MAPK signaling pathways.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/5583961","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140075165","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Major Limitations of Cardiovascular Risk Scores","authors":"Ibtissam Talha,&nbsp;Noureddine Elkhoudri,&nbsp;Abderraouf Hilali","doi":"10.1155/2024/4133365","DOIUrl":"10.1155/2024/4133365","url":null,"abstract":"<p><i>Background</i>. Epidemiological studies conducted in extensive population cohorts have led to the creation of numerous cardiovascular risk predictor models. However, these tools have certain limitations that restrict its applicability. The aim behind the following work is to summarize today’s best-known limitations of cardiovascular risk assessment models through presenting the critical analyses conducted in this area, with the intention of offering practitioners a comprehensive understanding of these restrictions. Critical analyses revealed that these scales exhibit numerous limitations that could impact their performance. Most of these models evaluate cardiovascular risk based on classic risk factors and other restrictions, thereby negatively affecting their sensitivity. Scientists have made significant advancements in improving cardiovascular risk models, tailoring them to accommodate a wide range of populations and devising scales for estimating cardiovascular risks that can account for all prevailing restrictions. Better understanding these limitations could improve the cardiovascular risk stratification.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/4133365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140001803","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Laminaria japonica Aresch-Derived Fucoidan Ameliorates Hyperlipidemia by Upregulating LXRs and Suppressing SREBPs","authors":"Yan Zhang,&nbsp;Tian Liu,&nbsp;Ze-Jie Qu,&nbsp;Xue Wang,&nbsp;Wen-Gang Song,&nbsp;Shou-Dong Guo","doi":"10.1155/2024/8649365","DOIUrl":"10.1155/2024/8649365","url":null,"abstract":"<p>Cardiovascular disease (CVD) is the leading cause of morbidity and mortality worldwide, and hyperlipidemia is one major inducing factor of CVD. It is worthy to note that fucoidans are reported to have hypolipidemic activity with species specificity; however, the underlying mechanisms of action are far from clarification. This study is aimed at investigating the plasma lipid-lowering mechanisms of the fucoidan from <i>L. japonica</i> Aresch by detecting the levels of hepatic genes that are involved in lipid metabolism. Our results demonstrated that the fucoidan F3 significantly lowered total cholesterol and triglyceride in C57BL/6J mice fed a high-fat diet. In the mouse liver, fucoidan F3 intervention significantly increased the gene expression of peroxisome proliferator-activated receptor (PPAR) <i>α</i>, liver X receptor (LXR) <i>α</i> and <i>β</i>, and ATP-binding cassette transporter (ABC) G1 and G8 and decreased the expression of proprotein convertase subtilisin/kexin type 9 (PCSK9), low-density lipoprotein receptor, cholesterol 7 alpha-hydroxylase A1, and sterol regulatory element-binding protein (SREBP) 1c and SREBP-2. These results demonstrated that the antihyperlipidemic effects of fucoidan F3 are related to its activation of PPAR<i>α</i> and LXR/ABC signaling pathways and inactivation of SREBPs. In conclusion, fucoidan F3 may be explored as a potential compound for prevention or treatment of lipid disorders.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/8649365","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139761752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment of Angiography-Based Renal Quantitative Flow Ratio Measurement in Patients with Atherosclerotic Renal Artery Stenosis","authors":"Xiang Huang,&nbsp;Xiao-Lan Li,&nbsp;Heng Zhou,&nbsp;Xiao-Mei Li","doi":"10.1155/2024/4618868","DOIUrl":"10.1155/2024/4618868","url":null,"abstract":"<p><i>Background</i>. Quantitative flow ratio (QFR) is an angiography-based fractional flow reserve measurement without pressure wire or induction of hyperemia. A recent innovation that uses combined geometrical data and hemodynamic boundary conditions to measure QFR from a single angiographic view has shown the potential to measure QFR of the renal artery-renal QFR (rQFR). <i>Objective</i>. The aim of this pilot study was to assess the feasibility of rQFR measurement and the contribution of rQFR in selecting patients with atherosclerotic renal artery stenosis (ARAS) undergoing revascularization. <i>Methods</i>. This retrospective trial enrolled patients who had ARAS (50-90%) and hypertension. The enrolled patients were treated by optimal antihypertensive medication or revascularization, respectively, and the therapeutic strategies were based on rFFR measurement and/or clinical feature. <i>Results</i>. A total of 55 patients underwent rQFR measurement. Among the enrolled patients, 18 underwent optimal antihypertensive medication and 37 underwent revascularization, 19 patients in whom rQFR and rFFR were both assessed. During the 180-day follow-up, 25 patients saw an improvement in their blood pressure among the 37 patients that underwent revascularization. ROC analysis revealed that rQFR had a high diagnostic accuracy for predicting blood pressure improvement (AUC_rQFR = 0.932, 95% CI 0.798-0.998). The ideal cut-off value of rQFR for predicting blood pressure improvement after revascularization is ≤0.72 (sensitivity: 72.00%, specificity: 100%). The paired <i>t</i> test and Bland–Altman analyses demonstrated good agreement between rQFR and rFFR (<i>t</i> = 1.887, 95% CI -0.021 to 0.001, 95% limits of agreement: -0.035 to 0.055, <i>p</i> = 0.075). The Spearman correlation test reveals that there was a significant positive correlation between rQFR and rFFR (<i>r</i> = 0.952, 95% CI 0.874 to 0.982, <i>p</i> &lt; 0.001). <i>Conclusion</i>. The rQFR has the potential to enhance the ability of angiography to detect functionally significant renal artery stenosis during angiography and to produce results that are comparable to invasive hemodynamic assessment.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2024 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2024-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1155/2024/4618868","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139413645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improving Health Outcomes in Coronary Artery Disease Patients with Short-Term Protocols of High-Intensity Interval Training and Moderate-Intensity Continuous Training: A Community-Based Randomized Controlled Trial","authors":"Catarina Gonçalves, Jorge Bravo, João Pais, Ana Abreu, Armando Raimundo","doi":"10.1155/2023/6297302","DOIUrl":"https://doi.org/10.1155/2023/6297302","url":null,"abstract":"Studies have shown that the higher the aerobic capacity, the lower the risk of cardiovascular mortality and morbidity. In the case of cardiac patients, high-intensity interval training (HIIT) seems to be more effective than moderate-intensity continuous training (MICT) in improving aerobic capacity. The aim of this study was to investigate the effects of two community-based exercise programs using two short-term protocols (HIIT and MICT) on physical fitness and physical activity (PA) levels in coronary artery disease (CAD) patients. <i>Methods.</i> In this randomized controlled trial, body composition, aerobic capacity, muscle strength, and daily PA levels were assessed before and after 6 weeks of intervention in 69 patients diagnosed with CAD. All patients were randomly (1 : 1 : 1) assigned to two exercise groups (HIIT or MICT) or a control group (no exercise). Both training programs consisted of 6 weeks of supervised treadmill exercise, three sessions per week. MICT targeted ≈70-75% of peak heart rate (HR), while HIIT aimed for ≈85-95% of peak HR. The control group only followed the medical recommendations. <i>Results.</i> Community-based exercise programs showed more positive effects on physical fitness variables and physical activity levels compared to control. HIIT could significantly improve waist circumference, body fat mass, VO₂peak, sedentary behavior, and moderate-to-vigorous PA compared to MICT. Moreover, the control group showed poorer results. <i>Conclusion.</i> HIIT can improve health outcomes more positively than MICT and control. These findings indicate that HIIT may be an alternative and effective training method in community-based exercise programs for CAD patients. This trial is registered with NCT03538119.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"31 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138716204","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ginkgolide B Blocks Vascular Remodeling after Vascular Injury via Regulating Tgfβ1/Smad Signaling Pathway","authors":"Quan Wang, Shuai Ni, Li Ling, Siqi Wang, Hanbin Xie, Zhanhong Ren","doi":"10.1155/2023/8848808","DOIUrl":"https://doi.org/10.1155/2023/8848808","url":null,"abstract":"Coronary artery disease (CAD) is the most prevalent cardiovascular disease worldwide, resulting in myocardial infarction (MI) and even sudden death. Following percutaneous coronary intervention (PCI), restenosis caused by vascular remodeling is always formed at the stent implantation site. Here, we show that Ginkgolide B (GB), a naturally occurring terpene lactone, effectively suppresses vascular remodeling and subsequent restenosis in wild-type mice following left carotid artery (LCA) injury. Additional experiments reveal that GB exerts a protective effect on vascular remodeling and further restenosis through modulation of the Tgf<i>β</i>1/Smad signaling pathway <i>in vivo</i> and in human vascular smooth muscle cells (HVSMAs) but not in human umbilical vein endothelial cells (HUVECs) <i>in vitro</i>. Moreover, the beneficial effect of GB is abolished after incubated with pirfenidone (PFD, a drug for idiopathic pulmonary fibrosis, IPF), which can inhibit Tgf<i>β</i>1. In Tgf<i>β</i>1^-/- mice, treatment with pirfenidone capsules and Yinxingneizhi Zhusheye (including Ginkgolide B) fails to improve vascular remodeling and restenosis. In conclusion, our data identify that GB could be a potential novel therapeutic agent to block vessel injury-associated vascular remodeling and further restenosis and show significant repression of Tgf<i>β</i>1/Smad signaling pathway.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"27 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138579501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Valsartan Attenuated Homocysteine-Induced Impaired Autophagy and ER Stress in Human Umbilical Vein Endothelial Cells","authors":"Xinyan Wu, Ani Wang, Long Xu, Meng Li, Qingxian Zhai, Weidong Wang, Chunling Li, Lizi Jin","doi":"10.1155/2023/8817431","DOIUrl":"https://doi.org/10.1155/2023/8817431","url":null,"abstract":"Hyperhomocysteinemia is a risk factor for various cardiovascular diseases. However, the mechanism underlying homocysteine- (Hcy-) induced vascular injury remains unclear. The purpose of the present study was to examine a potential mechanism by which Hcy induced injury in human umbilical vascular endothelial cells (HUVEC). The protein abundance of autophagy-related markers was markedly decreased after Hcy treatment, which was associated with endoplasmic reticulum (ER) stress and apoptosis in HUVECs. Protein expression level of angiotensin II type 1 receptor (AT1 receptor) was dramatically increased in response to Hcy. Valsartan, an AT1 receptor blocker, improved autophagy and prevented ER stress and apoptosis in HUVECs treated with Hcy. Consistent with this, silence of AT1 receptor with siRNA decreased the protein abundance of ER stress markers, prevented apoptosis, and promoted autophagy in HUVECs. Inhibition or knockdown of AT1 receptor was shown to be associated with suppression of p-GSK3<i>β</i>/GSK3<i>β</i>-p-mTOR/mTOR signaling pathway. Additionally, inhibition of autophagy by 3-MA aggravated Hcy-induced apoptosis, while amelioration of ER stress by 4-PBA prevented Hcy-induced injury in HUVECs. Hcy-induced HUVEC injury was likely attributed to AT1 receptor activation, leading to impaired autophagy, ER stress, and apoptosis.","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"10 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138579504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Relationship between β1-AA and AT1-AA and Cardiac Function in Patients with Hypertension Complicated with Left Ventricular Diastolic Function Limitation","authors":"Liang Wang, Xue-Bai Lv, Yu-Ting Yuan, Ning Wang, Hong-Ying Yao, Wen-Chao Zhang, Peng-Fei Yin, Xiao-Hui Liu","doi":"10.1155/2023/7611819","DOIUrl":"https://doi.org/10.1155/2023/7611819","url":null,"abstract":"&lt;i&gt;Objective&lt;/i&gt;. To investigate the association between &lt;i&gt;β&lt;/i&gt;1 adrenergic receptor autoantibodies (&lt;i&gt;β&lt;/i&gt;1-AA) and angiotensin II type-1 receptor autoantibodies (AT1-AA) and cardiac function in patients with hypertension complicated with left ventricular diastolic function limitation. &lt;i&gt;Methods&lt;/i&gt;. A total of 120 patients with essential hypertension who were not taking drug treatment and were hospitalised in the Department of Cardiology at the authors’ hospital from April 2018 to December 2018 were enrolled in this study and divided into a diastolic dysfunction group (65 cases) and a normal diastolic group (55 cases) according to their left ventricular diastolic function. The levels of cardiac parameters, &lt;i&gt;β&lt;/i&gt;1-AA, AT1-AA, and other indicators were compared. Logistic regression analysis was used to analyse the related factors affecting left ventricular diastolic dysfunction (LVDD). The diagnostic efficacy of related factors in the diagnosis of diastolic dysfunction was evaluated. &lt;i&gt;Results&lt;/i&gt;. Univariate analysis demonstrated that the left ventricular posterior wall diameter (&lt;span&gt;&lt;svg height=\"8.69875pt\" style=\"vertical-align:-0.3499298pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 38.462 8.69875\" width=\"38.462pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,0,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,6.24,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,12.48,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,15.444,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,21.684,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,30.831,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;/svg&gt;&lt;span&gt;&lt;/span&gt;&lt;svg height=\"8.69875pt\" style=\"vertical-align:-0.3499298pt\" version=\"1.1\" viewbox=\"41.317183799999995 -8.34882 21.997 8.69875\" width=\"21.997pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,41.367,0)\"&gt;&lt;use xlink:href=\"#g113-50\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,47.607,0)\"&gt;&lt;use xlink:href=\"#g113-47\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,50.571,0)\"&gt;&lt;use xlink:href=\"#g113-51\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,56.811,0)\"&gt;&lt;/path&gt;&lt;/g&gt;&lt;/svg&gt;&lt;/span&gt; vs. &lt;span&gt;&lt;svg height=\"8.69875pt\" style=\"vertical-align:-0.3499298pt\" version=\"1.1\" viewbox=\"-0.0498162 -8.34882 32.222 8.69875\" width=\"32.222pt\" xmlns=\"http://www.w3.org/2000/svg\" xmlns:xlink=\"http://www.w3.org/1999/xlink\"&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,0,0)\"&gt;&lt;use xlink:href=\"#g113-58\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,6.241,0)\"&gt;&lt;use xlink:href=\"#g113-47\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,9.205,0)\"&gt;&lt;use xlink:href=\"#g113-50\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,15.445,0)\"&gt;&lt;use xlink:href=\"#g113-51\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;g transform=\"matrix(.013,0,0,-0.013,24.591,0)\"&gt;&lt;use xlink:href=\"#g117-37\"&gt;&lt;/use&gt;&lt;/g&gt;&lt;/svg&gt;&lt;span&gt;&lt;/span&gt;&lt;span&gt;&lt;svg height=\"8.69875pt\" style=\"vertical-align:-0.3499298pt\" version=\"1.1\" viewbox=\"35.07718","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"283 1 1","pages":""},"PeriodicalIF":3.1,"publicationDate":"2023-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138579418","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frequencies of VKORC1-1639G>A and rs397509427 in Patients on Warfarin and Healthy Syrian Subjects.","authors":"Yara Altawil, Lama A Youssef","doi":"10.1155/2023/8898922","DOIUrl":"10.1155/2023/8898922","url":null,"abstract":"<p><strong>Background: </strong>Vitamin K epoxide reductase complex subunit 1 (<i>VKORC1</i>) gene encodes a key enzyme with multiple cellular activities, namely, the reduction of vitamin K to its active form. <i>VKORC1</i>-1639G>A (rs9923231) is a common single nucleotide polymorphism with a crucial impact on warfarin dosing and possibly other physiological functions. This study aimed at investigating the frequencies of <i>VKORC1</i>-1639G>A alleles and genotypes in Syrian healthy subjects and patients on warfarin for different indications.</p><p><strong>Methods: </strong>A total of 138 individuals were enrolled in this cross-sectional study. Genomic DNA was extracted from both patients on warfarin and healthy subjects, and polymerase chain reaction (PCR) specific amplicons were genotyped via standard sequencing which also allowed the detection of rs397509427. Comparisons of -1639G>A frequency with other populations were drawn.</p><p><strong>Results: </strong>Of 94 patients on warfarin, 53 (56.38%) were with idiopathic venous thromboembolism (VTE). Despite comparable frequencies of the -1639A allele (47% and 50%), the AA and GA genotypes were at disparate frequencies of 93.2% versus 79.8% in the healthy subjects (<i>n</i> = 44) versus patients on warfarin, respectively. Carriers of the GG genotype were at a four-fold increased risk of VTE in comparison with those of the AA and GA genotypes (odds ratio (OR) = 4, 95% CI = 1.105 - 13.6, <i>P</i> = 0.0469). All study subjects were wild-type for the rs397509427 variant.</p><p><strong>Conclusions: </strong>Our results prove a high -1639A prevalence in Syrian healthy subjects and patients on warfarin at frequencies comparable to other Mediterranean and Middle Eastern populations. The A allele carriers are at a lower VTE risk, whereas a global prevalence gradient of the G allele is suggested to be associated with VTE risk.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2023 ","pages":"8898922"},"PeriodicalIF":3.1,"publicationDate":"2023-11-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10689069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138476839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of Thrombolysis on Circulating Microparticles in Patients with ST-Segment Elevation Myocardial Infarction.","authors":"Zhe Li, Wei Zhang, Qun-Rang Wang, Yu-Juan Yang, Xin-Hong Liu, Gong Cheng, Feng-Jun Chang","doi":"10.1155/2023/5559368","DOIUrl":"https://doi.org/10.1155/2023/5559368","url":null,"abstract":"<p><strong>Objective: </strong>We demonstrated that circulating microparticles (MPs) are increased in patients with coronary heart disease (both chronic coronary syndrome (CCS) and acute coronary syndrome). Whether thrombolysis affects MPs in patients with ST-segment elevation myocardial infarction (STEMI) with or without percutaneous coronary intervention (PCI) is unknown.</p><p><strong>Methods: </strong>This study was divided into three groups: STEMI patients with thrombolysis (<i>n</i> = 18) were group T, patients with chronic coronary syndrome (<i>n</i> = 20) were group CCS, and healthy volunteers (<i>n</i> = 20) were the control group. Fasting venous blood was extracted from patients in the CCS and control groups, and venous blood was extracted from patients in the T group before (pre-T) and 2 hours after (post-T) thrombolysis. MPs from each group were obtained by centrifugation. After determining the concentration, the effects of MPs on endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in rat myocardial tissue in vitro were detected by immunohistochemistry and western blotting. Changes in nitric oxide (NO) and oxygen free radicals (O₂^•-) were also detected. The effect of MPs on vasodilation in isolated rat thoracic aortae was detected.</p><p><strong>Results: </strong>Compared with that in the control group (2.60 ± 0.38 mg/ml), the concentration of MPs was increased in patients with CCS (3.49 ± 0.72 mg/ml) and in STEMI patients before thrombolysis (4.17 ± 0.58 mg/ml). However, thrombolysis did not further increase MP levels (post-T, 4.23 ± 1.01 mg/ml) compared with those in STEMI patients before thrombolysis. Compared with those in the control group, MPs in both CCS and STEMI patients before thrombolysis inhibited the expression of eNOS (both immunohistochemistry and western blot analysis of phosphorylation at Ser1177), NO production in the isolated myocardium and vasodilation in vitro and stimulated the expression of iNOS (immunohistochemistry and western blot analysis of phosphorylation at Thr495), and the generation of O₂^•- in the isolated myocardium. The effects of MPs were further enhanced by MPs from STEMI patients 2 hours after thrombolysis.</p><p><strong>Conclusion: </strong>Changes in MP function after thrombolysis may be one of the mechanisms leading to ischemia-reperfusion after thrombolysis.</p>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2023 ","pages":"5559368"},"PeriodicalIF":3.1,"publicationDate":"2023-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10676276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138458096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}