Cardiovascular Therapeutics最新文献

{"title":"lncRNA NEAT1 Downregulation Ameliorates the Myocardial Infarction of Mice by Regulating the miR-582-5p/F2RL2 Axis","authors":"Zhenhua Wu,&nbsp;Yunpeng Bai,&nbsp;Yujuan Qi,&nbsp;Chao Chang,&nbsp;Yan Jiao,&nbsp;Yaobang Bai,&nbsp;Zhigang Guo","doi":"10.1155/2022/4481360","DOIUrl":"10.1155/2022/4481360","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. This study is aimed at effectively investigating the role of coagulation factor II thrombin receptor like 2 (F2RL2) in myocardial infarction (MI) as well as the upstream regulatory miRNA and lncRNA. <i>Methods</i>. Regulatory genes of F2RL2 were analyzed using StarBase and verified by dual-luciferase reporter assay. The MI mouse model was established. The left ventricular ejection fraction (EF) and fractional shortening (FS) were examined by echocardiography. The infarct area, pathological changes, and cell apoptosis in mouse myocardial tissue were evaluated using triphenyltetrazolium chloride and Evans blue, hematoxylin-eosin, and TUNEL staining assays. Oxygen-glucose deprivation- (OGD-) induced human cardiac myocytes (HCMs) were cultured and transfected. The cell viability, proliferation, and apoptosis were determined by CCK-8, EdU staining, and flow cytometry assays. The expressions of F2RL2, miR-582-5p, and nuclear paraspeckle assembly transcript 1 (NEAT1) in myocardial tissues and HCMs were quantified by qRT-PCR or Western blot. <i>Results</i>. NEAT1 sponged miR-582-5p which targeted F2RL2. NEAT1 and F2RL2 were highly expressed while miR-582-5p was lowly expressed in MI mice. F2RL2 downregulation prevented the reduction in EF and SF and the elevation in infarct area and cell apoptosis of MI mice. Both F2RL2 and NEAT1 downregulations reversely modulated the decreased viability and proliferation and the increased apoptosis of OGD-induced HCMs, while miR-582-5p inhibitor did oppositely. NEAT1 silencing upregulated miR-582-5p level but downregulated F2RL2 level. miR-582-5p inhibitor upregulated the F2RL2 level. The role of NEAT1 silencing in OGD-induced HCMs was reversed by miR-582-5p inhibitor whose effect was further offset by F2RL2 downregulation. <i>Conclusion</i>. NEAT1 downregulation ameliorates MI by regulating the miR-582-5p/F2RL2 axis, providing novel biomarkers for MI treatment.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9741539/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10414779","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":"A Study on Weight Loss Cause as per the Side Effect of Liraglutide","authors":"Jin Yu,&nbsp;Jeongmin Lee,&nbsp;Seung-Hwan Lee,&nbsp;Jae-Hyung Cho,&nbsp;Hun-Sung Kim","doi":"10.1155/2022/5201684","DOIUrl":"10.1155/2022/5201684","url":null,"abstract":"<div>\u0000 <p><i>Purpose</i>. Liraglutide is known to have much lower weight loss effects in real clinical fields than in randomized clinical trials because of its side effects (SE) and discomfort associated with injections. This study is aimed at determining whether the side effects of liraglutide affect weight reduction and its maintenance in real-world practice. <i>Methods</i>. Endocrinologists conducted a retrospective chart review of data from two tertiary university hospitals. All patients who had been prescribed liraglutide at least once between January 2014 and December 2019 were included. For an average of 3 and 6 months, weight changes due to the presence or absence of SE and discontinuation (MAIN or STOP) of liraglutide were checked. <i>Results</i>. Only 40.8% (64/157) of the patients remained on liraglutide for 6 months; 14.7% (23/157) maintained the drug despite SEs (MAIN_SE(+)), and 40.1% (63/157) discontinued the drug despite not having SEs (STOP_SE(-)). At 3 months, there was −5.9 ± 0.6<i>%</i>, −7.9 ± 0.9<i>%</i>, −4.5 ± 0.5<i>%</i>, and −3.4 ± 0.6<i>%</i> weight reduction in the MAIN_SE(-), MAIN_SE(+), STOP_SE(-), and STOP_SE(+) groups, respectively (all <i>p</i> &lt; 0.001 compared to the baseline). However, there were no significant differences in the weight loss between the MAIN (<i>p</i> = 0.062) and STOP (<i>p</i> = 0.204) groups. At 6 months, the weight reduction was −2.0 ± 0.5<i>%</i> (<i>p</i> &lt; 0.001) in MAIN_SE(-), −2.2 ± 0.7<i>%</i> (<i>p</i> &lt; 0.005) in MAIN_SE(+), −1.7 ± 0.7<i>%</i> (<i>p</i> &lt; 0.01) in STOP_SE(-), and −2.0 ± 0.6<i>%</i> (<i>p</i> = 0.01) in STOP_SE(+), compared to baseline. SEs also caused no significant differences in weight loss between the MAIN (<i>p</i> = 0.787) and STOP (<i>p</i> = 0.694) groups. <i>Conclusions</i>. Our study confirmed that the side effects of liraglutide did not affect weight reduction. Moreover, in the real world, the continuous rate of liraglutide use is not high, and the weight gradually increases after 3 months. Therefore, in addition to the side effects of liraglutide, the medical staff should consider various factors that affect drug adherence, consider ways to increase compliance, and continue to ensure management so that patients can maintain their weight.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-12-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9733986/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10846797","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":"Safety and Efficacy of Bivalirudin versus Unfractionated Heparin Monotherapy in Patients with CAD and DM Undergoing PCI: A Retrospective Observational Study","authors":"Jing Li,&nbsp;Sanbao Chen,&nbsp;Sicong Ma,&nbsp;Mingque Yang,&nbsp;Zizhao Qi,&nbsp;Kun Na,&nbsp;Miaohan Qiu,&nbsp;Yi Li,&nbsp;Yaling Han","doi":"10.1155/2022/5352087","DOIUrl":"10.1155/2022/5352087","url":null,"abstract":"<div>\u0000 <p><i>Introduction.</i> Optimal anticoagulants for patients with diabetes mellitus (DM) undergoing percutaneous coronary intervention (PCI) are unclear. This retrospective observational study is aimed at evaluating efficacy and safety of bivalirudin versus unfractionated heparin (UFH) monotherapy in patients with DM undergoing PCI. <i>Methods.</i> A total of 3890 diabetic patients receiving PCI in the General Hospital of Northern Theater Command were divided into the bivalirudin group (<i>n</i> = 869) and the UFH group (<i>n</i> = 3021) according to different anticoagulant therapy regimens. Indication for PCI was in accordance with current guidelines including national cardiovascular data registry. The primary endpoint was 30-day net adverse clinical events (NACEs). The secondary endpoints included 30-day major adverse cardiac and cerebral events (MACCEs), bleeding events defined according to the Bleeding Academic Research Consortium (BARC) definition, and stent thrombosis (ST). Patients were matched by propensity score at a ratio of 1 : 1. <i>Results.</i> After propensity score matching, the bivalirudin group was associated with a lower incidence of NACEs (3.0% vs. 6.0%, <i>P</i> = 0.003) than the UFH group. The incidence of MACCE (1.7% vs. 3.3%, <i>P</i> = 0.033) was significantly lower in the bivalirudin group, mainly due to a lower mortality rate (0.6% vs. 2.0%, <i>P</i> = 0.010). In addition, patients in the bivalirudin group had less bleeding (1.4% vs. 3.0%, <i>P</i> = 0.022) than those in the UFH group, although BARC 2, 3, and 5 bleeding (0.1% vs. 0.6%, <i>P</i> = 0.218) was numerically lower. <i>Conclusion.</i> In diabetic patients undergoing PCI, bivalirudin was significantly associated with reduced risks of 30-day NACE and MACCE, mainly driven by the lower rates of bleeding and mortality, compared with heparin monotherapy.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9729030/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10391557","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":"Knockdown of lncRNA XIST Ameliorates IL-1β-Induced Apoptosis of HUVECs and Change of Tissue Factor Level via miR-103a-3p/HMGB1 Axis in Deep Venous Thrombosis by Regulating the ROS/NF-κB Signaling Pathway","authors":"Guangxin Cao,&nbsp;Hua Zhou,&nbsp;Dong Wang,&nbsp;Lei Xu","doi":"10.1155/2022/6256384","DOIUrl":"10.1155/2022/6256384","url":null,"abstract":"<div>\u0000 <p><i>Background</i>. The effect of lncRNA X inactive-specific transcript (XIST) inducing cardiovascular diseases on deep vein thrombosis (DVT) and its mechanism has not been reported. In this study, we uncovered the mystery that lncRNA XIST causes DVT with HUVEC dysfunction. <i>Method</i>. The expression levels of lncRNA XIST and miR-103a-3p were detected by qRT-PCR, and HMGB1 expression was determined by qRT-PCR and western blot. The correlations among the expression levels of lncRNA XIST, miR-103a-3p, and HMGB1 were determined by Spearman’s rank-order correlation test. XIST siRNA (si-XIST) was transfected into HUVECs to knock down the intrinsic expression of lncRNA XIST. The influences of si-XIST on interleukin-1 beta- (IL-1<i>β-</i>) treated HUVEC viability and apoptosis and the level of tissue factor (TF) were detected by MTT, flow cytometry, and ELISA kit, respectively. The relationships between lncRNA XIST, miR-103a-3p, and HMGB1 were predicted by the Encyclopedia of RNA Interactomes (ENCORI) database and verified by dual luciferase reporter assay. The effects of lncRNA XIST and miR-103a-3p on HMGB1 expression were detected by qRT-PCR, western blot, and immunofluorescence analysis. The levels of ROS/NF-<i>κ</i>B pathway-related proteins were detected to study the regulatory mechanism of lncRNA XIST/miR-103a-3p/HMGB1 on IL-1<i>β</i>-treated HUVECs apoptosis and change of TF level. <i>Results</i>. The upregulated expression levels of lncRNA XIST and HMGB1 and downregulated level of miR-103a-3p were found in the plasma of DVT patients and IL-1<i>β</i>-treated HUVECs. Si-XIST promoted cell viability and inhibited HUVEC apoptosis and ameliorated the change of TF level triggered by IL-1<i>β</i>. lncRNA XIST sponged miR-103a-3p and miR-103a-3p targeted HMGB1. Si-XIST inhibited the ROS/NF-<i>κ</i>B pathway to suppress HUVEC apoptosis and ameliorate the change of TF level induced by IL-1<i>β</i> via the miR-103a-3p/HMGB1 axis. <i>Conclusion</i>. lncRNA XIST sponged miR-103a-3p improving HMGB1 expression to exacerbate DVT by activating the ROS/NF-<i>κ</i>B signaling pathway. Our findings indicated that lncRNA XIST can be used as a potential therapeutic target in DVT.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349161","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":"Noncoding RNA in the Regulation of Acute Aortic Dissection: From Profile to Mechanism","authors":"Ruibin Wei,&nbsp;Yingqing Feng","doi":"10.1155/2022/2371401","DOIUrl":"10.1155/2022/2371401","url":null,"abstract":"<div>\u0000 <p>Aortic dissection is a life-threatening condition caused by a tear in the intimal layer of the aorta or bleeding within the aortic wall, resulting in the separation of the layers of the aortic wall. As Nienaber reported, aortic dissection is most common in people 65–75 years old and has an incidence of 35 cases per 100,000 people per year in this population. Many pathogenic factors are involved in aortic dissection, including hypertension, dyslipidemia, and abnormality of the aortic intima caused by genetic variation. However, with the development of gene sequencing and transgenic technology, genetic methods are being used for the diagnosis and treatment of diseases, including acute aortic dissection. Genetic research on acute aortic dissection began around 2006. Recently, research on acute aortic dissection has mainly focused on microRNA (miRNA). Studies have found that miRNA plays a critical regulatory role in the occurrence and development of acute aortic dissection. By regulating miRNA expression, acute aortic dissection can be prevented and treated.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9699736/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349159","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":"Potential Roles of Glucagon-Like Peptide 1 Receptor Agonists (GLP-1 RAs) in Nondiabetic Populations","authors":"Dan Xu,&nbsp;Ankith Nair,&nbsp;Charlie Sigston,&nbsp;Chau Ho,&nbsp;Jia Li,&nbsp;Daya Yang,&nbsp;Xinxue Liao,&nbsp;Wei Chen,&nbsp;Ming Kuang,&nbsp;Yanbing Li,&nbsp;Christopher Reid,&nbsp;Haipeng Xiao","doi":"10.1155/2022/6820377","DOIUrl":"10.1155/2022/6820377","url":null,"abstract":"<div>\u0000 <p>Glucagon-like peptide 1 receptor agonists (GLP-1 RAs) have been observed in several large cardiovascular outcome trials to significantly reduce the incidence of major cardiovascular event (MACE) with type 2 diabetic patients. The clinical trials of GLP-1 RAs, including lixisenatide, exenatide, liraglutide, semaglutide, albiglutide, and dulaglutide, are associated with a significantly 14% lower risk of MACE in patients with T2DM and a history of CV disease, and with a nonsignificantly 6% lower risk in patients without history of CV disease. Some of the interpretation with GLP-1 RA trials suggested the possible role of glucagon-like peptide-1 receptor agonists (GLP-1 RAs) in primary prevention of cardiovascular diseases in nondiabetic individual, echoed by a recent editorial redefining the role of GLP-1 RAs being beyond glycaemic control. The narrative review provides an in-depth insight into GLP-1 RA use guideline in different countries and regions of the world and examines the safety and concern of GLP-1 RA use. The narrative review draws the comparison of GLP-1 RA use between diabetic and nondiabetic individual in terms of cardiovascular and metabolic benefits and points out the direction of future clinical trials of GLP-1 RAs in nondiabetic individuals. The focus of the review is on GLP-1 RAs’ preventive roles in nondiabetic individuals with cardiovascular disease, chronic kidney diseases, obesity, dyslipidaemia, hypertension, nonalcoholic fatty liver diseases, polycystic ovarian syndrome (PCOS), and perioperative complications of bariatric surgery, albeit in small studies and subset analysis of clinical trials of diabetic patients.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9683988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349164","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":"Inflammatory Response and Immune Regulation in Brain-Heart Interaction after Stroke","authors":"Lihua Zou,&nbsp;Ruquan Han","doi":"10.1155/2022/2406122","DOIUrl":"10.1155/2022/2406122","url":null,"abstract":"<div>\u0000 <p>Cerebrocardiac syndrome (CCS) is one of the secondary myocardial injuries after stroke. Cerebrocardiac syndrome may result in a poor prognosis with high mortality. Understanding the mechanism of the brain-heart interaction may be crucial for clinical treatment of pathological changes in CCS. Accumulating evidence suggests that the inflammatory response is involved in the brain-heart interaction after stroke. Systemic inflammatory response syndrome (SIRS) evoked by stroke may injure myocardial cells directly, in which the interplay between inflammatory response, oxidative stress, cardiac sympathetic/parasympathetic dysfunction, and splenic immunoregulation may be also the key pathophysiology factor. This review article summarizes the current understanding of inflammatory response and immune regulation in brain-heart interaction after stroke.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9683992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349158","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":"HSPB1 Regulates Autophagy and Apoptosis in Vascular Smooth Muscle Cells in Arteriosclerosis Obliterans","authors":"Keqin Chen,&nbsp;Changmiao Hou,&nbsp;Lei Xu,&nbsp;Hanwu Peng,&nbsp;Chaogui He,&nbsp;Jing Liu,&nbsp;Guoqing Wang,&nbsp;Shaoshuai Huang,&nbsp;Xiehong Liu","doi":"10.1155/2022/3889419","DOIUrl":"10.1155/2022/3889419","url":null,"abstract":"<div>\u0000 <p><i>Objective</i>. Small heat shock protein-1 (HSPB1) is a small heat shock protein that participates in many cellular processes and alleviates stress-induced cell injury. Autophagy protects cells from many types of stress and plays a key role in preventing stress in arteriosclerosis obliterans (ASO). However, the roles of HSPB1 in autophagy and apoptosis in the context of ASO pathogenesis remain unclear. <i>Methods</i>. In vivo and in vitro studies were used to determine whether HSPB1 is associated with ASO progression. The expression of HSPB1 was measured in normal and sclerotic blood vessels. The role of HSPB1 and its potential downstream signaling pathway were determined in VSMCs by overexpressing and silencing HSPB1. <i>Results</i>. A total of 91 ASO patients admitted to and treated at our hospital from Sep. 2020 to Sep. 2021 were selected, and plasma HSPB1 expression was assessed. We divided the patients with ASO into the grade I (<i>n</i> = 39), II (<i>n</i> = 29), III (<i>n</i> = 10), and IV (<i>n</i> = 13) groups according to Fontaine’s classification. Plasma HSPB1 levels were markedly decreased in patients with grade III (<i>n</i> = 10) and IV (<i>n</i> = 13) ASO compared with patients with grade I ASO. Furthermore, HSPB1 expression was significantly decreased, and p62 and cleaved caspase-3 were increased in the sclerotic vasculature compared to the normal vasculature (<i>p</i> &lt; 0.05). Overexpression of HSPB1 promoted apoptosis of VSMCs following ox-LDL treatment. Knockdown of HSPB1 led to a marked increase in the expression of LC3II and Beclin-1 in ox-LDL-stimulated VSMCs, whereas knockdown of HSPB1 attenuated these changes (<i>p</i> &lt; 0.05). Importantly, overexpression of HSPB1 promoted the dephosphorylation of JNK in ox-LDL-stimulated VSMCs. Conversely, downregulation of HSPB1 induced the opposite change. <i>Conclusion</i>. Loss of HSPB1 promotes VSMC autophagy and inhibits VSMC apoptosis, which are associated with ASO. HSPB1 and its downstream signaling pathways could be potential therapeutic targets for ASO treatment.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9678445/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10349163","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":"Positive Association of Plasma Trimethylamine-N-Oxide and Atherosclerosis in Patient with Acute Coronary Syndrome","authors":"Wanwen Kong,&nbsp;Junyi Ma,&nbsp;Ying Lin,&nbsp;Weiyu Chen","doi":"10.1155/2022/2484018","DOIUrl":"10.1155/2022/2484018","url":null,"abstract":"&lt;div&gt;\u0000 &lt;p&gt;&lt;i&gt;Aim&lt;/i&gt;. Atherosclerosis is the major cause of acute coronary syndrome (ACS) which is a significant contributor to both morbidity and mortality in the world. The microbiome-derived metabolite trimethylamine-N-oxide (TMAO) has aroused great interest and controversy as a risk factor of atherosclerosis. Therefore, in this study, we aimed at investigating whether plasma TMAO can be a risk factor of atherosclerosis in coronary artery of patients with ACS and how this relates to lipids and proinflammatory cytokines in plasma. &lt;i&gt;Methods&lt;/i&gt;. We enrolled consecutive patients with ACS who underwent percutaneous coronary intervention (PCI). Gensini scoring was used to evaluate angiographic atherosclerosis in the coronary artery of the patients. 13 patients were divided into low (Gensini score &lt; 25), 33 into intermediate (Gensini score 25-50), and 81 into severe atherosclerosis (Gensini score ≥50). Plasma TMAO, vasculitis factors, and cardiovascular biomarkers were measured by clinical biochemistry, intima-media thickness (IMT) of carotid artery was determined by the Color Doppler ultrasound, and the atherosclerotic lesion in coronary artery was assessed in PCI. &lt;i&gt;Results&lt;/i&gt;. Plasma TMAO concentrations were positively associated with Gensini score (OR = 0.629, &lt;i&gt;p&lt;/i&gt; &lt; 0.001) and Gensini subgroup (R = 0.604, &lt;i&gt;p&lt;/i&gt; &lt; 0.001). Plasma TMAO concentrations in patients with severe coronary atherosclerosis were higher than those of patients with moderate coronary atherosclerosis, and the plasma TMAO concentrations of patients with moderate coronary atherosclerosis were higher than those of patients with mild coronary atherosclerosis, the difference was statistically significant [4.73 (3.13, 4.62) versus 1.13 (0.63, 3.34) versus 0.79 (0.20, 1.29), &lt;i&gt;p&lt;/i&gt; &lt; 0.001], respectively. Furthermore, ROC analysis showed that plasma TMAO could identify the severity of atherosclerosis (&lt;i&gt;p&lt;/i&gt; &lt; 0.001). The AUC of TMAO for severe atherosclerosis was 0.852 (95&lt;i&gt;%&lt;/i&gt;CI = 0.779 − 0.925). The sensitivity and specificity of TMAO for identifying severe atherosclerosis are 96.3% and 63.0% when the cut-off value of TMAO was set at 1.2715 pg/ml. Furthermore, logistic regression analysis showed plasma TMAO concentrations were positively associated with severity of atherosclerosis in coronary artery (OR = 1.934, 95&lt;i&gt;%&lt;/i&gt;CI = 1.522 − 2.459, &lt;i&gt;p&lt;/i&gt; &lt; 0.001). For all that, negatively association was observed between TMAO and age (OR = −0.224, &lt;i&gt;p&lt;/i&gt; &lt; 0.05), B-type natriuretic peptide (BNP) (OR = −0.175, &lt;i&gt;p&lt;/i&gt; &lt; 0.05), and interleukin-8 (IL-8) (OR = −0.324, &lt;i&gt;p&lt;/i&gt; &lt; 0.001), while positive association was observed between TMAO and nitric oxide (NO) (OR = 0.234, &lt;i&gt;p&lt;/i&gt; &lt; 0.01). However, there is no obvious association was observed between Gensini score and cardiovascular biomarkers, vasculitis factors, and carotid IMT, respectively. &lt;i&gt;Conclusion&lt;/i&gt;. Our cross-sectional observation suggested that plasma TMAO conce","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-11-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9649308/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40483745","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":"A Clinical Nomogram Based on the Triglyceride-Glucose Index to Predict Contrast-Induced Acute Kidney Injury after Percutaneous Intervention in Patients with Acute Coronary Syndrome with Diabetes Mellitus","authors":"Yue Hu,&nbsp;Xiaotong Wang,&nbsp;Shengjue Xiao,&nbsp;Na Sun,&nbsp;Chunyan Huan,&nbsp;Huimin Wu,&nbsp;Minjia Guo,&nbsp;Tao Xu,&nbsp;Defeng Pan","doi":"10.1155/2022/5443880","DOIUrl":"10.1155/2022/5443880","url":null,"abstract":"<div>\u0000 <p>The aim of the study was to investigate the factors influencing contrast-induced acute kidney injury (CI-AKI) after percutaneous intervention (PCI) in patients with acute coronary syndrome (ACS) with diabetes mellitus (DM). A total of 1073 patients with ACS combined with DM who underwent PCI at the Affiliated Hospital of Xuzhou Medical University were included in this study. We divided the patients into the CI-AKI and non-CI-AKI groups according to whether CI-AKI occurred or not. The patients were then randomly assigned to the training and validation sets at a proportion of 7 : 3. Based on the results of the LASSO regression and multivariate analyses, we determined that the subtypes of ACS, age, multivessel coronary artery disease, hyperuricemia, low-density lipoprotein cholesterol, triglyceride-glucose index, and estimated glomerular filtration rate were independent predictors on CI-AKI after PCI in patients with ACS combined with DM. Using the above indicators to develop the nomogram, the AUC-ROC of the training and validation sets were calculated to be 0.811 (95% confidence interval (CI): 0.766-0.844) and 0.773 (95% CI: 0.712-0.829), respectively, indicating high prediction efficiency. After verification by the Bootstrap internal verification, we found that the calibration curves showed good agreement between the nomogram predicted and observed values. And the DCA results showed that the nomogram had a high clinical application. In conclusion, we constructed and validated the nomogram to predict CI-AKI risk after PCI in patients with ACS and DM. The model can provide a scientific reference for predicting the occurrence of CI-AKI and improving the prognosis of patients.</p>\u0000 </div>","PeriodicalId":9582,"journal":{"name":"Cardiovascular Therapeutics","volume":"2022 1","pages":""},"PeriodicalIF":3.4,"publicationDate":"2022-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9633196/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40673518","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}