three-dimensional-modeling-left-atrium-pulmonary-veins-with-precise

Three-Dimensional Modeling of the Left Atrium and Pulmonary Veins with a Precise Intracardiac Echocardiography Approach

Intracardiac echocardiography (ICE) is a novel tool for estimating cardiac anatomy during pulmonary vein isolation procedures, particularly the left ...

China-Japan Union Hospital of Jilin University

Left ventricular non-compaction cardiomyopathy (LVNC) is a rare heart disorder related to thrombosis. Anticoagulant therapy is suggested for the treatment of this disease. The success of the novel oral anticoagulant rivaroxaban as a treatment option for this disorder is unclear.

Daily 10 mg rivaroxaban as a therapy for ventricular thrombus related to left ventricular non-compaction cardiomyopathy: A case report.

Atrial premature contractions (APCs) are commonly encountered in clinical practice. The APCs may influence heart conduction system and induce other arrhythmia. The disorder of atrioventricular conduction is related to electrophysiological phenomena, difficult to understand and diagnose.

A confused ECG with multiple rhythms caused by atrial premature contractions: A case report.

Anti-thrombosis therapy for atrial fibrillation (AF) management and stroke prevention is an important aspect of disease management. Novel oral anticoagulants (NOACs) are recommended by guidelines for AF management. However, if one can switch one NOAC to another when the former showed a poor effect has not been fully determined.

Dabigatran as an alternative for atrial thrombosis resistant to rivaroxaban: A case report.

Inhibition of hypoxia/reoxygenation (H/R)-induced insult in cardiac microvascular endothelial cells (CMECs) has been considered as a promising therapeutic strategy for the treatment of ischemic cardiovascular disease. In the present study, we found that H/R significantly increased the expression of dipeptidyl peptidase (DPP)-4 in CMECs. Treatment with the DPP-4 inhibitor sitagliptin, a licensed drug used for the treatment of type 2 diabetes mellitus (T2DM), ameliorated H/R-induced oxidative stress by decreasing the expression of NOX-4 and restoring the intracellular level of GSH in CMECs. Sitagliptin could also improve H/R-induced mitochondrial dysfunction by increasing intracellular MMP and ATP. Additionally, we found that the presence of sitagliptin prevented H/R-induced reduced cell viability and LDH release. Notably, our findings indicate that sitagliptin possesses an anti-inflammatory effect against H/R-induced expression of IL-6, IL-8, and TNF-α as well as secretion of HMGB1. Mechanistically, we found that sitagliptin suppresses activation of p38/NF-κB signaling. These findings suggest that sitagliptin may have potential as a therapeutic agent for the treatment of cardiovascular diseases.

Sitagliptin protects against hypoxia/reoxygenation (H/R)-induced cardiac microvascular endothelial cell injury.

Increased free fatty acids (FFA) are one of the risk factors for type 2 diabetes. FFA also contribute to endothelial dysfunction in both the prediabetes and diabetes conditions. Therefore, FFA are an important link between diabetes and endothelial dysfunction. In therapeutic application, GLP-1 receptor agonists have been implemented to lower blood glucose in diabetes. Here, we investigate the role of the common clinically used GLP-1 receptor agonist lixisenatide in endothelial cells. We demonstrate that lixisenatide could protect endothelial cells from high FFA-induced toxicity and cell death. Lixisenatide also suppresses FFA-caused cellular ROS generation and production of the lipid oxidation byproduct 4-HNE. Lixisenatide inhibits FFA-triggered production of TNF-α, IL-6, VCAM-1 and ICAM-1. The presence of lixisenatide in co-culture experiments suppresses adhesion of monocytes to endothelial cells. Moreover, lixisenatide ameliorates FFA-induced decreased eNOS phosphorylation and NO reduction. We also demonstrate that lixisenatide inhibits FFA-induced IκBα activation, nuclear p65 translocation and NF-κB activation. This evidence indicates that lixisenatide suppresses activation of the NF-κB pathway in endothelial cells. Collectively, our findings suggest that lixisenatide might have therapeutic potential to modulate diabetes-associated vascular complications.

GLP-1 receptor agonist lixisenatide protects against high free fatty acids-induced oxidative stress and inflammatory response.

(. (SSLK) helps reduce the risk of coronary heart disease (CHD) but its effects on rheumatic heart disease (RHD) patients remain unclear. 80 RHD patients were recruited and randomly assigned into SG (to receive SSLK treatment) and CG (to receive placebo) groups, and the intervention lasted for 3 months. The following cardiac indexes were measured, including mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), blood lactate, fatigue, shortness of breath, palpitation, and chest pain. ELISA kits were used to analyze creatine kinase isoenzyme (CK-MB), serum troponin T (cTnT), CRP, IL-1, IL-6, and TNF-, malondialdehyde (MDA), and superoxide dismutase (SOD). Relative percentages of CD4CD25FoxP3 regulatory (Treg) and CD4IL-17 T cells were measured using flow cytometry. After 3-month therapy, SSLK intervention improved MAP, HR, CVP, fatigue, palpitation, and shortness breath of CHD patients, reduced the levels of blood lactate, CK-MB, cTnT, CRP, IL-1, IL-6, TNF-, MDA, and increased SOD level ( < 0.05). Meanwhile, SSLK treatment increased the percentages of CD4CD25FoxP3 Treg cells and reduced relative percentages of CD4IL-17 T cells in a dose-dependent way ( < 0.05). Relative percentage of CD4CD25FoxP3 Treg cells had negative relationship while CD4IL17 T cells had positive relationship with CK-MB, cTnT, CRP, and TNF-a ( < 0.01). SSLK ameliorated RHD by affecting the balance of CD4CD25FoxP3 Treg and CD4IL17 T cells.

 Ameliorates Rheumatic Heart Disease by Affecting Relative Percentages of CD4CD25FoxP3 Treg and CD4IL17 T Cells.

The present study aimed to integrate the mRNA and microRNA (miRNA) expression profiles of spontaneously hypertensive rats (SHR rats) and stroke‑prone spontaneously hypertensive rats (SHRSP rats) to screen for potential therapeutic targets for hypertension and stroke. The datasets GSE41452, GSE31457, GSE41453 and GSE53363 were collected from the Gene Expression Omnibus (GEO) database to screen differentially expressed genes (DEGs). The GSE53361 dataset was obtained to analyze differentially expressed miRNAs (DEMs). The DEGs and DEMs were identified between SHR (or SHRSP) rats and normotensive Wistar‑Kyoto (WKY) rats using the Linear Models for Microarray (limma) data method. Venn diagrams were used to show the SHR‑specific, SHRSP‑specific and SHR‑SHRSP shared DEGs and DEMs, and these were utilized to construct the protein‑protein interaction (PPI) and miRNA‑mRNA regulatory networks. The Database for Annotation, Visualization and Integrated Discovery (DAVID) was used to explore the function of the genes. Subsequently, the connectivity Map (CMAP) database was searched to identify small‑molecule drugs. Comparisons between the GSE41452‑GSE31457‑GSE41453 merged and GSE53363 datasets identified 2 SHR‑specific, 8 SHRSP‑specific and 15 SHR‑SHRSP shared DEGs. Function enrichment analysis showed that SHRSP‑specific D‑box binding PAR bZIP transcription factor (Dbp) was associated with circadian rhythm, and SHR‑SHRSP shared carnitine O‑octanoyltransferase (Crot) was involved in fatty acid metabolic processes or the inflammatory response via interacting with epoxide hydrolase 2 (EPHX2). SHR‑SHRSP shared mitochondrial ribosomal protein L4 (Mrpl4) may exert roles by interacting with the threonine‑tRNA ligase, TARS2. The miRNA regulatory network predicted that upregulated Dbp could be regulated by rno‑miR‑126a‑5p, whereas downregulated Crot and Mrpl4 could be modulated by rno‑miR‑31a. The CMAP database predicted that small‑molecule drugs, including botulin, Gly‑His‑Lys, and podophyllotoxin, may possess therapeutic potential. In conclusion, the present study has identified Dbp, Crot and Mrpl4 as potential targets for the treatment of hypertension and stroke. Furthermore, the expression of these genes may be reversed by the above miRNAs or drugs.

miR‑126a‑5p‑Dbp and miR‑31a‑Crot/Mrpl4 interaction pairs crucial for the development of hypertension and stroke.

Although long noncoding RNAs (lncRNAs) and circular RNAs (circRNAs) have been suggested to play important roles in the pathogenesis of diseases, atherosclerosis-related lncRNAs and circRNAs remain rarely reported. This study aimed to explore the underlying molecular mechanisms of atherosclerosis based on the competing endogenous RNA (ceRNA) regulatory hypothesis of lncRNAs and circRNAs. The expression profiles of circRNAs, lncRNAs, and mRNAs in human THP-1 macrophages treated with oxidized low-density lipoprotein (an  atherosclerosis model), or not, were obtained from the Gene Expression Omnibus database under accession numbers GSE107522, GSE54666, and GSE54039, respectively. The present study identified 29 differentially expressed circRNAs in GSE107522, 544 differentially expressed genes (DEGs) in GSE54666, and 502 DEGs and 231 differentially expressed lncRNAs in GSE54039 datasets by using the Linear Models for Microarray Data method. Eight DEGs were found to be shared and expressed with the consistent trend in GSE54666 and GSE54039 datasets. Two of them (, aspartate beta-hydroxylase; and , phosphodiesterase 3B) were suggested to be crucial based on functional enrichment, protein-protein interaction, and ceRNA network analyses. , through interaction with  (calcium voltage-gated channel auxiliary subunit alpha2delta 4), may be associated with atherosclerosis by regulating the cellular response to calcium ion; and  may exert roles in negative regulation of angiogenesis through cross talk with  (engulfment and cell motility 1). Furthermore, the expression of  and  may be regulated by hsa_circ_0028198/hsa_circ_0092317/XIST-miR-543;  expression may be also modulated by hsa_circ_0092317/hsa_circ_0003546/H19/XIST-miR-326. In conclusion, our identified ceRNA interaction axes may possibly be important targets for treatment of atherosclerosis.

circRNA/lncRNA-miRNA-mRNA Network in Oxidized, Low-Density, Lipoprotein-Induced Foam Cells.

Oxidized low-density lipoprotein (ox-LDL)-induced endothelial inflammation plays an important role in the development of cardiovascular diseases. G protein-coupled receptors (GPCR) are gaining traction as potential treatment targets due to their roles in mediating a wide range of physiological processes. GPR120 is a recently identified omega-3 fatty acid receptor. We hypothesized that agonism of GPR120 might attenuate ox-LDL-induced endothelial dysfunction. In the present study, we tested the effects of two GPR120 agonists-GW9508 and TUG-891-in mitigating endothelial insult induced by ox-LDL in human aortic endothelial cells (HAECs). Real-time PCR, western blot, and ELISA analyses were used in our experiments. Our findings demonstrate that GPR120 is downregulated by exposure to ox-LDL, suggesting a role for GPR120 in mediating ox-LDL insult. Furthermore, we found that agonism of GPR120 could suppress oxidative stress and inflammation by inhibiting the production of reactive oxygen species and the expression of proinflammatory cytokines. Importantly, we show that agonism of GPR120 prevents the attachment of monocytes to endothelial cells by suppressing the expression of VCAM-1 and E-selectin. Finally, we show that agonism of GPR120 exerts a remarkable atheroprotective effect by elevating the expression level of Krüppel-like factor 2 (KLF2). Together, our results demonstrate a potential role for specific agonism of GPR120 in the prevention of endothelial damages induced by ox-LDL.

Qini Zhao

Cardiology Department

China-Japan Union Hospital of Jilin University

Three-Dimensional Modeling of the Left Atrium and Pulmonary Veins with a Precise Intracardiac Echocardiography Approach

Qini Zhao

.css-o250i3{font-size:18px;font-family:Open Sans,sans-serif;line-height:21.6px;}Cardiology Department

China-Japan Union Hospital of Jilin University

Three-Dimensional Modeling of the Left Atrium and Pulmonary Veins with a Precise Intracardiac Echocardiography Approach

Cardiology Department