Effect of C reactive protein on the sodium-calcium exchanger 1 in cardiomyocytes.

Numerous previous studies have found that C-reactive protein (CRP) is associated with cardiac arrhythmia and cardiac remodeling. However, the underlying mechanisms of this association remain unclear. Sodium-calcium exchanger 1 (NCX1) serves an important role in the regulation of intracellular calcium concentration, which is closely related with cardiac arrhythmia and cardiac remodeling.

Interleukin-33 alleviates diabetic cardiomyopathy through regulation of endoplasmic reticulum stress and autophagy via insulin-like growth factor-binding protein 3.

Prolonged endoplasmic reticulum (ER) stress is the key driving force behind diabetic cardiomyopathy (DCM). Autophagy is extensively implicated in adaptive mechanisms for cell survival. Interleukin-33 (IL-33) is known to be a potent cardiac protector, but its roles in DCM, ER stress, and autophagy are currently unknown.

A Low-Normal Free Triiodothyronine Level Is Associated with Adverse Prognosis in Euthyroid Patients with Heart Failure Receiving Cardiac Resynchronization Therapy.

Thyroid dysfunction is prevalent in patients with heart failure (HF) and hypothyroidism is related to the adverse prognosis of HF subjects receiving cardiac resynchronization therapy (CRT). We aim to investigate whether low-normal free triiodothyronine (fT3) level is related to CRT response and the prognosis of euthyroid patients with HF after CRT implantation.One hundred and thirteen euthyroid patients who received CRT therapy without previous thyroid disease and any treatment affecting thyroid hormones were enrolled.

Clinical effectiveness of telemedicine for chronic heart failure: a systematic review and meta-analysis.

Telemedicine interventions may be associated with reductions in hospital admission rate and mortality in patients with heart failure (HF). The present study is an updated analysis (as of June 30, 2016) of randomized controlled trials, where patients with HF underwent telemedicine care or the usual standard care. Data were extracted from 39 eligible studies for all-cause and HF-related hospital admission rate, length of stay, and mortality.

Disruption of calcium homeostasis by cardiac-specific over-expression of PPAR-γ in mice: A role in ventricular arrhythmia.

Aims: Adverse cardiovascular effects induced by peroxisome proliferator activator receptor-γ (PPAR-γ) activation were observed in clinical setting. But the underlying mechanism is unclear. Now, transgenic mice with cardiac specific peroxisome proliferator activator receptor-γ overexpression (TG-PPAR-γ) were used to explore the possible mechanisms.

Effects of C-reactive protein on K(+) channel interaction protein 2 in cardiomyocytes.

Several studies have found that C-reactive protein (CRP) was associated with QTc interval prolongation and ventricular arrhythmia. However, little is known about the mechanisms involved. K(+) channel interaction protein 2 (KChIP2) is a necessary subunit for the formation of transient outward potassium current (Ito.

Tachycardia pacing induces myocardial neovascularization and mobilizes circulating endothelial progenitor cells partly via SDF-1 pathway in canines.

Neovascularization plays pivotal role in ischemic heart failure; however, it is unclear in non-ischemic heart failure. Non-ischemic heart failure was induced by chronic rapid right ventricular pacing at 200 beats/min, respectively, for 3 and 6 weeks in 12 dogs. Sham-operation was performed in another 6 dogs as control.

Effects of cardiac resynchronization therapy on left ventricular remodeling and dyssynchrony in patients with left ventricular noncompaction and heart failure.

Left ventricular noncompaction (LVNC) is a rare cardiomyopathy with high incidence of heart failure (HF). It is unclear whether LVNC patients with desynchronized HF would benefit from cardiac resynchronization therapy (CRT). In order to evaluate the effect of CRT on LVNC, this study explored left ventricular (LV) remodeling and mechanical synchronicity before and after CRT in LVNC patients, and compare with that in idiopathic dilated cardiomyopathy (DCM) patients.

Dyssynchronous pacing triggers endothelial-mesenchymal transition through heterogeneity of mechanical stretch in a canine model.

Background: Endothelial-mesenchymal transition (EndMT) plays a pivotal role in cardiac fibrosis. However, it is unclear whether EndMT is involved in dyssynchronous heart failure (DHF).

Methods And Results: Twelve dogs received 3-week rapid right ventricular pacing (RVP) to develop DHF and then were randomly divided into a RVP group (n=6; RVP for another 3 weeks) and a biventricular pacing (BiVP) group (n=6; BiVP for 3 weeks), and another 6 dogs were in the control group.

Potential proarrhythmic effect of cardiac resynchronization therapy during perioperative period: data from a single cardiac center.

Background: Cardiac resynchronization therapy (CRT) could improve heart function, symptom status, quality of life and reduce hospitalization and mortality in patients with severe heart failure (HF) with optimal medical management. However, the possible adverse effects of CRT are often ignored by clinicians.

Method: A retrospective analysis of CRT over a 6-year period was made in a single cardiac center.

R25G mutation in exon 1 of LMNA gene is associated with dilated cardiomyopathy and limb-girdle muscular dystrophy 1B.

Background: Mutations of the LMNA gene encoding lamin A and C are associated with dilated cardiomyopathy (DCM), conduction system defects and skeletal muscle dystrophy. Here we report a family with a mutation of the LMNA gene to identify the relationship between genotype and phenotype.

Methods: All 30 members of the family underwent clinical and genetic evaluation.

CRP regulates the expression and activity of tissue factor as well as tissue factor pathway inhibitor via NF-kappaB and ERK 1/2 MAPK pathway.

It was found that C-reactive protein (CRP) could significantly increase the expression and activity of tissue factor (TF), but decrease that of tissue factor pathway inhibitor (TFPI) in human umbilical vein endothelial cells (HUVECs) in dose- and time-dependent manners, which could be antagonized by PDTC and U0126. CRP could also increase protein expression of phosphorylated nuclear factor-kappaB (NF-kappaB), IkappaB-alpha and ERK1/2 in dose- and time-dependent manner. In addition, neutralizing antibody to CD32 (FcgammaR II) could significantly attenuate the expression and activity of TF and TFPI induced by CRP.

[The expression and significance of activator protein-1 and matrix metalloproteinases in the human heart post acute myocardial infarction].

Objective: To investigate the expression and significance of activator protein-1 (AP-1) and matrix metalloproteinases (MMPs) in acute myocardial infarction (AMI) subjects.

Methods: Immunohistochemical techniques were used to detect the subunit of AP-1 (c-Jun), MMP-2 and MMP-9 in human AMI and normal heart tissue and the expressions of c-Jun and MMPs were measured with computer image analysis system.

Results: (1) There were expressions of c-Jun, MMP-2 and MMP-9 in normal heart tissue, mainly in myocardial cells and cardiac fibroblasts, and their expressions in AMI myocardial tissues were all significantly higher than those in normal myocardial tissues (P < 0.

[Clinical analysis of inappropriate shock of implantable cardioverter defibrillators].

Objective: Implantable cardioverter defibrillator (ICD) can effectively treat life-threatening ventricular arrhythmias. The most common side effect is inappropriate discharge. This study analyzes the incidence and causes of inappropriate discharges of ICD in our hospital.

[Effect of AP-1 decoy oligodeoxynucleotides on neonatal rat cardiac fibroblast proliferation and collagen synthesis].

Objective: To investigate the inhibitory effects of AP-1 decoy oligodeoxynucleotides (ODNs) on angiotensin II (AngII)-induced proliferation and collagen synthesis in neonatal rat cardiac fibroblasts (CFs).

Methods: The CFs of neonatal SD rats were cultured in serum-free medium for 24 h and stimulated with 10(-7) mol/L AngII in the presence of AP-1 decoy ODNs or mutational AP-1 decoy ODNs at varied concentrations. MTT assay was employed for quantitative evaluation of the CF proliferation.