Our results reveal a significant putative HCM causative gene, P2X7, for the first time and show that germ-line mutations in P2X7 may cause a defective phenotype, suggesting purinergic receptor involvement in heart failure mediated through arrhythmias which need further investigations to be targeted for therapeutic interventions.
Our results reveal a significant putative HCM causative gene, P2X7, for the first time and show that germ-line mutations in P2X7 may cause a defective phenotype, suggesting purinergic receptor involvement in heart failure mediated through arrhythmias which need further investigations to be targeted for therapeutic interventions.
Here we present our approach to CRT programming that suppressed the clinical arrhythmia without the need of catheter ablation and achieving the high biventricular pacing capture rate along with optimal hemodynamic CRT-D performance.
Mutations of genes specific for the developmental processes and/or functional status of cardiac conduction system including ion channel promoter (minK-lacZ), GATA family of zinc finger proteins (GATA4), the homeodomain transcription factor (Nkx2.5), the homeodomain-only protein (Hop) and the T-box transcription factors (Tbx2, Tbx3 and Tbx5), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) and connexins, may cause fetal arrhythmias.
In conclusion, our results demonstrated that exposure to PM2.5 was capable of increasing propensity to cardiac arrhythmias which could be attenuated with TRPC3 inhibition.
Our findings also suggest that the autosomal recessive PGM1-CDG might be highly associated with life-threatening cardiomyopathy with arrhythmia or sudden cardiac death as the first symptom presenting from childhood and adolescence.
We found that GDF11 reduced arrhythmia severity and successfully attenuated myocardial infarction; GDF11 also increased cardiac function after I-R, enhanced HO-1 expression and decreased oxidative damage.
Consistent with its predominant expression in striated muscle, Popdc1 and Popdc2 null mutants in mouse and zebrafish develop cardiac arrhythmia and muscular dystrophy.
Our results reveal a significant putative HCM causative gene, P2X7, for the first time and show that germ-line mutations in P2X7 may cause a defective phenotype, suggesting purinergic receptor involvement in heart failure mediated through arrhythmias which need further investigations to be targeted for therapeutic interventions.
Our results reveal a significant putative HCM causative gene, P2X7, for the first time and show that germ-line mutations in P2X7 may cause a defective phenotype, suggesting purinergic receptor involvement in heart failure mediated through arrhythmias which need further investigations to be targeted for therapeutic interventions.
Through evaluating serum native thiol, malonaldehyde (MDA) and nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) in these patients and describing the effects on oxidative parameters of CPAP therapy for 3 months, we confirmed the impact of oxidative stress on arrhythmias.
Mutations of genes specific for the developmental processes and/or functional status of cardiac conduction system including ion channel promoter (minK-lacZ), GATA family of zinc finger proteins (GATA4), the homeodomain transcription factor (Nkx2.5), the homeodomain-only protein (Hop) and the T-box transcription factors (Tbx2, Tbx3 and Tbx5), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) and connexins, may cause fetal arrhythmias.
We aimed to explore whether specific high-sucrose intake in older female rats affects myocardial electrical coupling protein, connexin-43 (Cx43), protein kinase C (PKC) signaling, miR-1 and miR-30a expression, and susceptibility of the heart to malignant arrhythmias.
Mutations of genes specific for the developmental processes and/or functional status of cardiac conduction system including ion channel promoter (minK-lacZ), GATA family of zinc finger proteins (GATA4), the homeodomain transcription factor (Nkx2.5), the homeodomain-only protein (Hop) and the T-box transcription factors (Tbx2, Tbx3 and Tbx5), hyperpolarization-activated cyclic nucleotide-gated channel 4 (HCN4) and connexins, may cause fetal arrhythmias.
The ECG in 8 of the 10 control cases was read as AF by at least 80% percent of observers even though the EGMs from the Constellation showed organized activation and consistent DF (STD of DF < 0.001) in all the electrodes confirming the arrhythmia as AFL in 10/10 cases.