Abstract
BackgroundAtrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice. Unfortunately, the precise mechanisms and sensitive serum biomarkers of atrial remodeling in AF remain unclear. The aim of this study was to determine whether the expression of the transcription factors NF-AT3 and NF-AT4 correlate with atrial structural remodeling of atrial fibrillation and serum markers for collagen I and III synthesis.MethodsRight and left atrial specimens were obtained from 90 patients undergoing valve replacement surgery. The patients were divided into sinus rhythm (n = 30), paroxysmal atrial fibrillation (n = 30), and persistent atrial fibrillation (n = 30) groups. NF-AT3, NF-AT4, and collagen I and III mRNA and protein expression in atria were measured. We also tested the levels of the carboxyl-terminal peptide from pro-collagen I, the N-terminal type I procollagen propeptides, the N-terminal type III procollagen propeptides, and TGF-β1 in serum using an enzyme immunosorbent assay.ResultsNF-AT3 and NF-AT4 mRNA and protein expression were increased in the AF groups, especially in the left atrium. NF-AT3 and NF-AT4 expression in the right atrium was increased in the persistent atrial fibrillation group compared the sinus rhythm group with similar valvular disease. In patients with AF, the expression levels of nuclear NF-AT3 and NF-AT4 correlated with those of collagens I and III in the atria and with PICP and TGF-β1 in blood.ConclusionsThese data support the hypothesis that nuclear NF-AT3 and NF-AT4 participates in atrial structural remodeling, and that PICP and TGF-β1 levels may be sensitive serum biomarkers to estimate atrial structural remodeling with atrial fibrillation.
Highlights
Atrial fibrillation (AF) is the most common cardiac arrhythmia in clinical practice
Serum N-terminal type I procollagen propeptides (PINP), N-terminal type III procollagen propeptides (PIIINP), Carboxyl-terminal peptide from pro-collagen I (PICP), and TGF-β1 levels were increased in the AF groups The levels of PICP and TGF-β1 were significantly increased in the persistent AF (PeAF) group compared with the paroxysmal AF (PaAF) and sinus rhythm (SR) groups
We demonstrated that collagen I, collagen III, total Nuclear factor of activated T cells 3 (NF-AT3), and Nuclear factor of activated T cells 4 (NF-AT4) expression were upregulated in the AF groups using Reverse transcription-polymerase chain reaction (RT-PCR) and western blotting (Figure 3A,B; Figure 4A,B)
Summary
The precise mechanisms and sensitive serum biomarkers of atrial remodeling in AF remain unclear. Valvular heart disease (VHD), which comprises pathological changes in the mitral or aortic valves, causes AF. Atrial fibrosis is a hallmark of arrhythmogenic structural remodeling [10,11]. Cardiac fibrosis is defined as a detrimental process causing imbalanced extracellular matrix deposition and heart degradation. Expansion of the extracellular matrix between cardiomyocytes may cause conduction delays and create alternate conduction pathways. These changes result in ectopic foci and anisotropic conduction, creating nonuniform wave fronts that facilitate abnormal reentrant arrhythmias [13]. The precise mechanisms of atrial remodeling in AF remain unclear
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