In further tertile studies, subjects in the lower tertile of Cav-3 concentrations were more likely to become paroxysmal AF and had much lower LAD (<i>P</i> < 0.05).
In subgroup studies, patients with permanent atrial fibrillation had higher serum chemerin concentrations than those with persistent and paroxysmal atrial fibrillation.
The ADH1B*2 alleles (hazard ratio: ADH1B*1/*2 vs *1/*1: 2.64; ADH1B*2/*2 vs *1/*1: 1.80, P = 0.02) and the levels of alcohol consumption were independently associated with AF recurrence in the patients with paroxysmal AF after catheter ablation.
Patients with paroxysmal AF or persistent AF showed higher IL-37 mRNAs and serum protein levels compared with those with permanent AF as well as healthy controls.
We investigated the clinical characteristics and outcomes of asymptomatic vs symptomatic patients in the paroxysmal AF (PAF; n = 1,837) and persistent/permanent (sustained atrial fibrillation [SAF]; n = 1,912) subgroups.
Integrated analysis of microRNA and mRNA expression profiles in the left atrium of patients with nonvalvular paroxysmal atrial fibrillation: Role of miR-146b-5p in atrial fibrosis.
Using qRT-PCR and 3'UTR luciferase reporter assays, the interaction between upregulation of miR-199a-5p and downregulation of FKBP5 was confirmed in samples from pAF patients.
Quantitative real-time polymerase chain reaction showed that the levels of mature miR-106b, miR-93, and miR-25 were lower in atria of patients with paroxysmal AF when compared with patients in sinus rhythm.
These results suggest that miR-106b-25 cluster-mediated post-transcriptional regulation of RyR2 is a potential molecular mechanism involved in paroxysmal AF pathogenesis.
We found miRNA-150 levels to be reduced by a factor of approximately 17 in PAF relative to controls and a factor of approximately 20 in PersAF relative to controls (P<.0001).
Among the patients with SAP, platelet-bound-SDF-1 is increased in patients with paroxysmal AF compared with SR or to persistent/permanent AF (P < 0.05 for both).
We show in this paper for the first time that Azelaoyl PAF significantly increases the intracellular frataxin levels by twofold in the neuroblastoma cell line SKNBE and fibroblasts from FRDA patients and that Azelaoyl PAF increases frataxin protein through a transcriptional mechanism.
The PPARgamma mRNA was markedly decreased in the hypertensive AF group as compared with the hypertensive non-AF group, and it was significantly lower in persistent AF than paroxysmal AF (0.222 +/- 0.0702 vs 0.564 +/- 0.0436, P<0.01).
Increased atrial VCAM-1 expression was confirmed by Western blotting in patients with persistent and paroxysmal AF (persistent AF 207+/-42% versus sinus rhythm 100+/-16%, P=0.028; paroxysmal AF 193+/-42%, P=0.024 versus sinus rhythm).
We speculate that the gain-of-function mechanism underlies the mild skeletal phenotype and paroxysmal atrial fibrillation and suggest a possible role of TBX5 in the development of (paroxysmal) atrial fibrillation based on a gain-of-function either through a direct stimulation of target genes via TBX5 or indirectly via TBX5 stimulated TBX3.
In addition to cardiac TnI (cTnI), low expression of slow-twitch skeletal TnI (ssTnI) protein was found in 60% of patients in sinus rhythm or paroxysmal AF and in 8% of patients with chronic AF.