<b>Objective:</b> The present study investigated whether the NRG1/ErbB4 signaling system affects the activity of major atrial ganglionated plexi (GP) in a paroxysmal atrial fibrillation (AF) model by 6-h rapid atrial pacing (RAP).
PAF participants were found to have normal abundance of the NE transporter (NET) protein, together with very low levels of tyrosine hydroxylase (TH) (<i>P</i><0.0001) and reduced vesicular monoamine transporter 2 (VMAT2) (<i>P</i><0.05) protein expression compared with control and MSA participants.
PAF participants were found to have normal abundance of the NE transporter (NET) protein, together with very low levels of tyrosine hydroxylase (TH) (<i>P</i><0.0001) and reduced vesicular monoamine transporter 2 (VMAT2) (<i>P</i><0.05) protein expression compared with control and MSA participants.
PAF participants were found to have normal abundance of the NE transporter (NET) protein, together with very low levels of tyrosine hydroxylase (TH) (<i>P</i><0.0001) and reduced vesicular monoamine transporter 2 (VMAT2) (<i>P</i><0.05) protein expression compared with control and MSA participants.
Paroxysmal atrial fibrillation (AF) can be caused by gain-of-function mutations in genes, encoding the cardiac potassium channel subunits KCNJ2, KCNE1, and KCNH2 that mediate the repolarizing potassium currents I<sub>k1</sub>, I<sub>ks</sub>, and I<sub>kr</sub>, respectively.
DRAGON (UMIN-CTR, UMIN000015332) aimed to elucidate the efficacy of pace-capture-guided ablation following contact-force-guided PV isolation ablation in paroxysmal atrial fibrillation (AF) patients.
IL-6 levels and MMP-9/TIMP-1 ratio were significantly higher in AF patients than in non-AF controls (P < .001), and in persistent than in paroxysmal AF (P < .001), in line with NT-proBNP and LA diameter.
TGF-β1 was negatively correlated with NT-proBNP (r = -0.53, P = .001 in paroxysmal AF and r = -0.71, P < .001 in persistent AF) and LA diameter (r = -0.44, P = .006 in paroxysmal AF and r = -0.51, P = .003 in persistent AF).
A novel mutation in the RYR2 gene leading to catecholaminergic polymorphic ventricular tachycardia and paroxysmal atrial fibrillation: dose-dependent arrhythmia-event suppression by β-blocker therapy.