MG53 knockout enhances I<sub>to,f</sub> remodeling and action potential duration prolongation and increases susceptibility to ventricular arrhythmia in mouse cardiac hypertrophy.
This study describes outcomes of catheter ablation of LVS VAs using intracardiac echo-facilitated 3D electroanatomical mapping (ICE-3D) to avoid fluoroscopy.
In the present study, we aimed to explore whether targeted regulation of sympathetic activity in PVN could reduce the peripheral sympathoexcitatory and attenuate the ventricular arrhythmias (VAs) in myocardial infarction (MI) rats via PI3K-AKT pathway.
Endpoint was to determine the association between noninvasive RV-PA coupling indices (tricuspid annular plane systolic excursion/right ventricular systolic pressure [TAPSE/RVSP] and fractional area change [FAC]/RVSP ratio) and markers of disease severity, and compared this association to that of CMRI-derived RV volumetric indices and markers of disease severity (peak oxygen consumption [VO<sub>2</sub> ], NT-proBNP and atrial and/or ventricular arrhythmias).
Administration of AAV9-GFP-AIP to neonatal mice with a known CPVT mutation (RYR2<sup>R176Q/+</sup>) effectively suppressed ventricular arrhythmias induced by either β-adrenergic stimulation or programmed ventricular pacing, without significant proarrhythmic effect.
I/R rats had ventricular arrhythmias and myocardial apoptosis with activation of the p38 mitogen-activated protein kinase (p38)/factor-associated suicide (Fas)/Fas-associating protein with a novel death domain (FADD) pathway.
In conclusion, miR-155 inhibition downregulated NGF expression via decreasing M1 macrophage polarization and inflammatory responses dependent on the SOCS1/NF-κB pathway, subsequently diminishing MI-induced sympathetic neural remodeling and ventricular arrhythmias (VAs).
Incidence of VAs, serum levels of malondialdehyde (MDA) and superoxide dismutase (SOD), expression of connexin (Cx43), Bcl-2, Bax, caspase-3, tumor necrosis factor (TNF)-α, interleukin-6 (IL-6), and high mobility group box (HMGB)1 were compared.
We performed a disproportionality analysis using the European database of suspected adverse drug reaction (ADR) reports to evaluate the reporting OR (ROR χ<sup>2</sup>) of LQT, TdP and ventricular arrhythmias associated with selective oestrogen receptor modulators (SERMs: tamoxifen and toremifene) as opposed to aromatase inhibitors (AIs: anastrozole, exemestane and letrozole).
We performed a disproportionality analysis using the European database of suspected adverse drug reaction (ADR) reports to evaluate the reporting OR (ROR χ<sup>2</sup>) of LQT, TdP and ventricular arrhythmias associated with selective oestrogen receptor modulators (SERMs: tamoxifen and toremifene) as opposed to aromatase inhibitors (AIs: anastrozole, exemestane and letrozole).
PDE5 inhibitors have been shown to improve contractile function in systolic HF, regress left ventricular hypertrophy, reduce myocardial infarct size and suppress ischaemia-induced ventricular arrhythmias.
We present strong evidence that Tp-Te intervals were increased in patients with COPD, which suggests that there may be an association between COPD and ventricular arrhythmias and cardiac morbidity.
The present study is the first to examine the association between telomerase, a SNP at a locus including TERC, and VA in ischemic cardiomyopathy patients.
K<sub>2P</sub>17.1 (TASK-4, TALK-2) potassium channels are expressed in the heart and represent potential targets for pharmacological management of atrial and ventricular arrhythmias.
We sought to determine the effects of GLP-1R agonist exendin-4 (Ex4) on ventricular action potential duration (APD) and susceptibility to ventricular arrhythmia in the rat heart in vivo and ex vivo.