Anatolian Journal of Cardiology最新文献

{"title":"Reply to Letter to the Editor: \"Is Right Ventricle- to-Left Ventricle Diameter Ratio, A Static Parameter Measured by Computed Tomography Pulmonary Angiography, An Effective Index of Right Ventricular Function?''.","authors":"Serhat Erol, Aslıhan Gürün Kaya, Fatma Arslan, Sümeyye Ayöz, Ayşegül Gürsoy Çoruh, Melahat Kul, Evren Özçınar, Aydın Çiledağ, Zeynep Pınar Önen, Akın Kaya, Özlem Özdemir Kumbasar, Stavros V Konstantinides","doi":"10.14744/AnatolJCardiol.2024.4938","DOIUrl":"10.14744/AnatolJCardiol.2024.4938","url":null,"abstract":"","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863120","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":"Impact of Thrombomodulin Polymorphism -33G>A on Acute Myocardial Infarction Risk and Circulating Inflammatory Markers.","authors":"Sounira Mehri, Raja Chaaba, Josef Finsterer, Wided Khamlaoui, Sonia Hammami, Mohamed Hammami","doi":"10.14744/AnatolJCardiol.2024.4534","DOIUrl":"10.14744/AnatolJCardiol.2024.4534","url":null,"abstract":"<p><strong>Background: </strong>There is increasing evidence that thrombomodulin (THBD) polymorphisms, along with inflammatory markers [i.e., C-reactive protein (CRP), fibrinogen, albumin], may increase the risk of acute myocardial infarction (AMI). The aim of the study was to investigate the role of the THBD -33G>A polymorphism (rs1042579) as a marker of AMI risk and to correlate it with serum levels of inflammatory markers.</p><p><strong>Methods: </strong>Case-control study of 277 AMI patients and 329 healthy controls. A binary logistic regression analysis was performed to evaluate the association between the parameters studied and AMI risk.</p><p><strong>Results: </strong>The frequencies of genotypes AA, GA, and GG of the THBD -33G>A polymorphism were 31.4%, 45.5%, and 23.1% in patients and 21.6%, 44.1%, and 34.3% in controls. A significant association was found between the AA genotype of the THBD -33G>A polymorphism (AA: OR = 2.011, 95% CI 1.561-3.074, P < .001) or A allele (A: OR = 1.725, 95% CI 1.493-2.510, P < .001) and AMI risk. A backward stepwise logistic regression method combining AMI status as the dependent variable and conventional risk factors (age, smoking, arterial hypertension (HTA), diabetes, dyslipidemia, CRP, albumin, fibrinogen, serum angiotensin converting enzyme (ACE) activity, serum malondialdehyde, conjugated dienes, glutathione peroxidase, cardiac troponin-I (cTnI) and THBD AA genotype) as independent variables showed that the most predictive risk factors for AMI were smoking, HTA, albumin, fibrinogen, CRP, ACE activity, cTnI, and the THBD AA-genotype with odds ratios of 2.942, 2.203, 2.352, 1.323, 1.652, 1.014, 2.105, and 3.781 respectively. The AA genotype was associated with increased diastolic blood pressure, CRP, ACE activity, and albumin levels.</p><p><strong>Conclusions: </strong>The study shows that the THBD -33G>A polymorphism should be included in the stratification of AMI risk.</p>","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11793801/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863108","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":"An Echocardiographic Study of a Rare Cause of Mitral Regurgitation: Hypoplastic Posterior Mitral Valve Leaflet.","authors":"Ahmet Karaduman, Cemalettin Yılmaz, İsmail Balaban, Mehmet Aytürk, Münevver Sarı, Zübeyde Bayram, Alev Kılıçgedik, Gökhan Kahveci","doi":"10.14744/AnatolJCardiol.2024.4710","DOIUrl":"https://doi.org/10.14744/AnatolJCardiol.2024.4710","url":null,"abstract":"<p><strong>Background: </strong>The precise etiology of hypoplasia of the posterior mitral valve leaflet (PMVL) remains incompletely elucidated; however, it has been hypothesized to stem from genetic mutations occurring during fetal development. Herein, we present the anatomical characteristics of the mitral valve and associated cardiac pathologies in patients with hypoplastic PMVL.</p><p><strong>Methods: </strong>This single-center retrospective study involved patients who presented between 2015 and 2021 at a tertiary healthcare facility. Among the cohort, 44 individuals had hypoplastic PMVL and were divided into 2 groups: those with severe mitral regurgitation (MR) and those with non-severe MR.</p><p><strong>Results: </strong>Among the patients, 11 (25%) had severe MR. The median lengths for the PMVL was 5 mm (5-6). Moreover, 10 patients had concomitant muscular formation. We found that 13 patients had bicuspid aortic valve (BAV), while the second most common concomitant cardiac congenital pathology was secundum atrial septal defect (ASD) in 7 patients. The anterior mitral leaflet (AML) length (P = .007), AML prolapse (P < .001), and A2P2 distance (P = .008) were higher in the group with severe MR. In addition, muscular formation was more common in patients with hypoplastic PMVL with severe MR (P < .001).</p><p><strong>Conclusion: </strong>Hypoplastic PMVL is a rare but significant anomaly that causes MR. While it can coexist with numerous congenital conditions, the most frequent associations include BAV and, secondly, ASD. Severe MR is particularly observed in cases accompanied by dilated mitral annulus, AML prolapse, and muscular formation.</p>","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863107","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":"Is Right Ventricle-to-Left Ventricle Diameter Ratio, A Static Parameter Measured by Computed Tomography Pulmonary Angiography, An Effective Index of Right Ventricular Function?","authors":"Abdulrahman Naser","doi":"10.14744/AnatolJCardiol.2024.4937","DOIUrl":"10.14744/AnatolJCardiol.2024.4937","url":null,"abstract":"","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863109","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":"Relaxin Inhibits Angiotensin II-Induced Cardiac Fibrosis by Activating NO/cGMP Signaling Pathway.","authors":"Jie Liu, Defeng Pan, Yuanyuan Luo, Wanling Wu, Tingbo Jiang","doi":"10.14744/AnatolJCardiol.2024.4605","DOIUrl":"10.14744/AnatolJCardiol.2024.4605","url":null,"abstract":"<p><strong>Background: </strong>Cardiac fibrosis, a key contributor to heart failure, is driven by the activation of cardiac fibroblasts (CFs), often induced by angiotensin II (Ang II). Relaxin, a peptide hormone, has been reported to counteract fibrotic processes. This study aims to investigate the antifibrotic effects of relaxin on Ang II-induced CF activation, with a focus on the involvement of the nitric oxide/cyclic guanosine monophosphate (NO/cGMP) signaling pathway.</p><p><strong>Methods: </strong>Primary CFs were isolated and treated with Ang II to induce fibrotic activation. Relaxin was used to assess its antifibrotic effects. Inhibitors of the NO/cGMP pathway, NG-nitro-L-arginine methyl ester (L-NAME) (a nitric oxide synthase inhibitor) and 1H-(1 ,2,4) -Oxadiazolo-(4, 3-a) quinoxalin-1-one (ODQ) (a guanylyl cyclase inhibitor), were co-administered to examine their effects on relaxin-mediated inhibition. Proliferation and migration were assessed using 5-Ethynyl-2'-de oxyur idine incorporation and Transwell assays. Western blot analysis was conducted to measure the expression of alpha-smooth muscle actin (α-SMA), collagen I, and collagen III, key markers of fibroblast activation. Nitric oxide, cGMP, total nitric oxide synthase (TNOS), and inducible nitric oxide synthase (iNOS) levels were measured in the culture media.</p><p><strong>Results: </strong>Ang II significantly increased CF proliferation, migration, and the expression of fibrosis markers α-SMA, collagen I, and collagen III. Relaxin treatment markedly reduced these effects. Inhibition of the NO/cGMP pathway by L-NAME or ODQ partially reversed relaxin's suppressive effects on CF proliferation and migration. Relaxin restored Ang II-induced reductions in NO, cGMP, and TNOS levels, while iNOS levels remained largely unchanged, except for a reduction in the L-NAME group.</p><p><strong>Conclusion: </strong>Relaxin attenuates Ang II-induced cardiac fibroblast activation and fibrosis primarily through the NO/cGMP signaling pathway.</p>","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11793803/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142863119","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":"Acute GLP-1 Agonism Induces Arrhythmogenic Electrical Activity in Aged Mice Heart Through Impaired Cellular Na+ and Ca2+ Handlings: The Role of CK2 Hyperphosphorylation.","authors":"Yusuf Olgar, Ayşegül Durak, Belma Turan","doi":"10.14744/AnatolJCardiol.2024.4719","DOIUrl":"10.14744/AnatolJCardiol.2024.4719","url":null,"abstract":"<p><strong>Background: </strong>Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are known for their benefits in conditions like cardiovascular diseases in type 2 diabetes and obesity. They also show promise for aging-related conditions with minimal side effects. However, their impact on cardiovascular risk is still debated. Notably, some long-acting GLP-1RAs cause a sustained increase in heart rate on the first day of use without a clear mechanism. To understand their short-term effects, we examined acute GLP-1R agonism on the electrical activity of elderly hearts.</p><p><strong>Methods: </strong>In this study, we utilized in vivo electrocardiography, in vitro cellular electrophysiology experiments, and biochemical measurements on heart preparations from 6-month-old (Adult) and 24-month-old (aged) BALB/c mice.</p><p><strong>Results: </strong>A single liraglutide injection (0.3 mg/kg) induced repetitive, self-sustained arrhythmogenic electrocardiograms in aged mice (24 months old) but had no effect on adults (6 months old) within the first 10 minutes. Acute application of liraglutide to isolated ventricular cardiomyocytes from aged mice significantly prolonged the late phase of action potential repolarization (APR90). This was due to suppressed K+ currents and increased persistent Na+currents (Late-INa), primarily through delayed recovery from inactivation of Na+ currents. Additionally, liraglutide increased Ca2+ spark frequency and wave formation by enhancing Ca2+ release from the sarcoplasmic reticulum, affecting both Na+ and Ca2+ regulation in aging cells. Liraglutide also induced casein kinase 2 (CK2) hyperphosphorylation in aged cardiomyocytes, which a CK2 inhibitor could reverse, normalizing APR90 by reducing Late-INa and enhancing K+ currents.</p><p><strong>Conclusion: </strong>These findings reveal that acute GLP-1R agonism can disrupt electrical signaling and induce arrhythmia in aged mice through CK2 hyperphosphorylation, providing new insights into the cardiovascular effects of GLP-1RAs in the elderly.</p>","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11793800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142799127","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":"BMI and TAVR, Ablation for AF and HOCM….","authors":"Çetin Erol","doi":"10.14744/AnatolJCardiol.2024.12","DOIUrl":"10.14744/AnatolJCardiol.2024.12","url":null,"abstract":"","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":"28 12","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11633782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142724698","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":"Bioinformatic Analysis and Molecular Docking Identify Isorhamnetin Is a Candidate Compound in the Treatment of Pulmonary Artery Hypertension.","authors":"Chen Shao, Wei Xia, Yang Liu","doi":"10.14744/AnatolJCardiol.2024.4723","DOIUrl":"10.14744/AnatolJCardiol.2024.4723","url":null,"abstract":"<p><strong>Background: </strong>The current study aims to identify the key pathways and potential therapeutic targets for pulmonary arterial hypertension (PAH) and to further evaluate the anti-PAH effects of isorhamnetin.</p><p><strong>Methods: </strong>The dataset of gene expression profiling for PAH (GSE113439) was downloaded from the gene expression omnibus (GEO) database. Isorhamnetin target genes were extracted from the comparative toxicogenomics database (CTD). Various bioinformatics methods were employed to identify the core pathways associated with PAH and potential intervention targets. Molecular docking was conducted between the interacting target and the candidate compound, isorhamnetin.</p><p><strong>Results: </strong>One thousand nine hundred sixty-two upregulated genes and 642 downregulated genes were identified. Molecular complex detection analyses revealed that the significant biological processes associated with upregulated genes included DNA damage response, mitotic cell cycle, and chromosome organization. In contrast, the signifi ant biological processes related to downregulated genes encompassed cellular response to growth factor stimulus, response to growth factor, and blood vessel development. Immune infilt ation analysis indicated that PAH is associated with signifi ant changes in the distribution of immune cells and differential expression of immune checkpoints. Furthermore, 58 isorhamnetin targets were extracted from the CTD, and we identified 1 interacting gene, NFE2L2, among the differentially expressed genes (DEGs), DEGs related to ferroptosis, and isorhamnetin targets. Isorhamnetin demonstrated strong affinities with vascular endothelial growth factor (VEGF) receptors and transcription factors (ATM and ZNF24) associated with VEGFs, as well as the ferroptosis protein NFE2L2.</p><p><strong>Conclusions: </strong>Pulmonary arterial hypertension is characterized by a series of abnormalities in downstream molecular signaling pathways, including DNA damage, immune dysregulation, VEGF signaling deficienc , and the ferroptosis process. These may represent the core pathophysiological mechanisms of PAH. Ferroptosis-related genes, such as NFE2L2 and TF (ATM, ZNF24) associated with VEGFs, are potential therapeutic targets that contribute to the mechanisms mentioned above. Isorhamnetin is a promising candidate compound for the treatment of PAH.</p>","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11793806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142738137","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":"Recognizing Intramural Hematoma of the Pulmonary Artery: A Warning Sign That May Precede Aortic Dissection.","authors":"Merve Solak, Nur Hürsoy, Doğuş Hemşinli","doi":"10.14744/AnatolJCardiol.2024.4664","DOIUrl":"10.14744/AnatolJCardiol.2024.4664","url":null,"abstract":"","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-11-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11793799/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142715278","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":"Evaluating the Prognostic Nutritional Index for Predicting the Clinical Relevance of Angiographically Intermediate Coronary Lesions.","authors":"Can Özkan, Abdullah Kadir Dolu, Muhammet Cihat Çelik, Bekir Demirtaş, Orhan Karayiğit","doi":"10.14744/AnatolJCardiol.2024.4407","DOIUrl":"10.14744/AnatolJCardiol.2024.4407","url":null,"abstract":"<p><strong>Background: </strong>Coronary artery disease (CAD) is a widespread health issue globally, linked to significant morbidity and mortality. While oxidative stress, dysregulated lipid metabolism, and unhealthy lifestyle choices contribute to CAD, recent research highlights the role of immune responses and inflammation. Malnutrition, a modifiable risk factor, notably impacts CAD prognosis. The prognostic nutritional index (PNI), derived from serum albumin and lymphocyte count, predicts outcomes in various diseases. This study aims to elucidate the relationship between malnutrition, as assessed by the PNI score, and the functional significance of coronary artery stenosis, evaluated by fractional flow reserve (FFR) measurements.</p><p><strong>Methods: </strong>A retrospective analysis involved 232 patients with single intermediate-grade coronary stenosis who underwent FFR measurement between January 2022 and January 2024. Prognostic nutritional index values were calculated from serum albumin and lymphocyte counts. Patients were divided into 2 groups based on FFR values.</p><p><strong>Results: </strong>Patients with hemodynamically significant coronary stenosis (FFR ≤ 0.80) exhibited higher inflammatory markers and triglycerides, while those with FFR > 0.80 showed elevated albumin and PNI levels. Triglycerides and PNI emerged as independent predictors of significant coronary stenosis.</p><p><strong>Conclusions: </strong>This study demonstrates that PNI is independently associated with the functional significance of coronary artery stenosis as determined by FFR. Since lymphocytes, total protein and albumin values, which are readily available from routine blood tests, form the basis for PNI, this index can be easily used in clinical settings to predict hemodynamically significant coronary artery stenosis. However, the results of this study should be further expanded and validated through studies involving larger samples and prospective designs.</p>","PeriodicalId":7835,"journal":{"name":"Anatolian Journal of Cardiology","volume":" ","pages":""},"PeriodicalIF":1.4,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11694685/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142709043","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}