Anatolian Journal of Cardiology最新文献

Background: We aimed to find a gene for coronary artery disease (CAD) early diagnosis by detecting co-pathogenic target gene involved in CAD and pulmonary arterial hypertension (PAH). Methods: Datasets were obtained from the Gene Expression Omnibus (GEO) database, including GSE113079, GSE113439, and GSE12288, to investigate gene expression patterns in cardiovascular diseases. Weighted Gene Co-expression Network Analysis (WGCNA) was performed to identify gene modules associated with clinical traits. Differential gene expression analysis and functional enrichment analysis were carried out. Protein-protein interaction (PPI) networks were constructed. JASPAR database and FIMO tool were utilized to predict transcription factor (TF) binding sites. Results: Fifteen key genes were identified in CAD and PAH, with CNTN1 being prioritized for further investigation due to its high connectivity degree. Upstream regulation analysis identified potential TFs (DRGX, HOXD3, and RAX) and 7 miRNAs targeting CNTN1. The expression profile of CNTN1 was significantly upregulated in CAD samples, and ROC analysis indicated potential diagnostic value for CAD. CMap database analysis predicted potential targeted drugs for CAD. Conclusion: CNTN1 was detected as a co-pathogenetic gene for CAD and PAH. It is highly expressed in CAD patients and has potential value for CAD diagnosis. CNTN1 is potentially regulated by 3 TFs and 7 miRNAs.

Background: To compare distal (dTRA) and classical (cTRA) transradial approaches for coronary catheterization with respect to puncture attempts, puncture time, operator and patient comfort, and safety outcomes.

Methods: In this prospective observational study, patients undergoing coronary catheterization for standard indications via dTRA or cTRA approaches from July 2019 to May 2020 were included. Clinicodemographic and laboratory characteristics were recorded. Puncture time, number of puncture attempts, operator and patient comfort on the visual analogue scale (VAS), and access site complications like hematoma and radial artery occlusion were recorded. Patients were analyzed in the same group as the initial puncture, even if there was a cross-over.

Results: Of the 130 patients (40.8% women), 50.8% and 49.2% belonged to dTRA and cTRA groups, respectively. dTRA group required more than one puncture attempt more frequently than cTRA group (30.3% vs. 15.6%; P =.047); consequently, puncture time was longer (60s vs. 50s; P =.031, respectively). However, puncture time was comparable if the puncture was successful in the first attempt (47.5s vs. 45s; P =.492). Patient comfort was comparable (7.2 ± 0.9 vs. 7.2 ± 1.2; P =.852), but operator comfort was more with cTRA approach (8.3 ± 1.6 vs. 8.8 ± 1.2; P =.048). Post-procedure, cTRA had more minor bleeding than dTRA approach. There was no major bleeding in either group. The occurrence of radial artery occlusion was comparable in both groups.

Conclusion: Although dTRA needed more attempts for successful puncture, puncture time was comparable with cTRA when puncture was successful on the first attempt. Therefore, one attempt at dTRA puncture could be a reasonable approach in patients undergoing coronary catheterization.

Background: Gap junction remodeling is an important cause of ventricular arrhythmia in heart failure. However, it remains unclear whether renal denervation (RDN) regulates gap junction remodeling in heart failure. To explore the effect of RDN on gap junction remodeling in dogs with high-pacing-induced heart failure.

Methods: Fifteen dogs were randomly divided into control (n = 5), heart failure (HF) (n = 5), and RDN+HF (n = 5) group. A high-pacing-induced-heart failure model was established using rapid right ventricular pacing for 4 weeks. The RDN+HF group underwent surgical and chemical ablation of both renal arteries before 4 weeks rapid right ventricular pacing. After 4 weeks, echocardiography, High-Performance Liquid Chromatography-Mass Spectrometry test for norepinephrine and epinephrine, and pathological analysis were performed in the above 3 groups. Further, immunohistochemical staining was used to detect tyrosine hydroxylase, ChaT, connexin 43 (Cx43), and connexin 40 (Cx40). Connexin 43 and Cx40 expression was detected by western blotting. Transmission electron microscopy was used to observe the gap junction.

Results: Compared to the control group, myocardial fibrosis and sympathetic hyperactivity were observed in the HF group. Immunohistochemical staining and western blotting showed that Cx40 expression and Cx43 expression was significantly reduced in the HF group. Compared with the HF group, the RDN+HF group showed reduced sympathetic hyperactivity, Cx40 expression, Cx40/Cx43 ratio, and increased Cx43 expression.

Conclusion: Renal denervation alleviates gap junction remodeling in high-pacing-induced heart failure dogs.

The aim of the current work is to present a thorough recapitulation of the emerging understanding of atherosclerotic cardiovascular disease and recommending avenues for future studies. Cardiovascular diseases (CVDs) remain a leading cause of global morbidity and mortality, influenced by a complex interplay of genetic, environmental, and atherothrombotic factors. Atherosclerosis, a multifaceted and dynamic process, is at the core of many CVDs. Recent studies have shed light on the multilayered nature of atherosclerosis and cardiovascular risk, emphasizing the need for a nuanced understanding of these diseases across different populations and disease mechanisms. This review synthesizes findings from 6 pivotal studies, shedding light on the intricate mechanisms underlying atherosclerotic cardiovascular events, the evolving understanding of atherosclerosis, and the potential pathways to attempt implementation in clinical practice. Insights into atherothrombotic factors, the role of macrophages, and the implications of aortic enlargement and coronary artery calcification underscore the complexity of CVD pathogenesis and highlight the need for comprehensive strategies in diagnosis, treatment, and prevention.

Background: It is suggested that myocardial dysfunction in heart failure patients may result from increased oxidative stress-related membrane changes. Thiol/disulfide homeostasis is a new oxidative stress indicator. The aim of this study was to evaluate serum thiol levels and thiol/disulfide homeostasis in patients with heart failure with preserved ejection fraction (HFpEF).

Methods: Eighty-four overweight patients who applied to our clinic between November 2016 and February 2018 and diagnosed with hypertension and left ventricule concentric hypertrophy with normal systolic function are included in the study. Forty-two patients who were asymptomatic and had normal N terminal pro-B type natriuretic peptide (NT-proBNP) levels (≤125) were in the control group. Forty-two patients who have cardiac failure symptoms and have high NT-roBNP levels (>125) were in the patient group.

Results: Native thiol, total thiol, and disulfide values of the patient group are found to be significantly lower than the control group (P =.001; P <.001; P =.041 respectively). There is a statictically significant negative correlation between native thiol, total thiol values, and NT-proBNP. There is a statictically significant negative correlation between native thiol, total thiol values, and carbohydrate antigen 125 (CA-125) values.

Conclusion: As far as we know from literature, this is the first study on HFpEF and thiol/disulfide homeostasis. It is found that native, total thiol, and disulfide values are low in HFpEF patients and that there is a negative correlation between native, total thiol values and NT-proBNP, CA-125 values. It can be said that oxidant/antioxidant balance is impaired in patients with HFpEF and that larger, randomized studies are needed in order to use oxidant/antioxidant balance in diagnosis and treatment of HFpEF.