Atrial stretch causes remodeling that predisposes to atrial fibrillation. We tested the hypothesis that peaks in left atrial (LA) wall stress are associated with focal remodeling.
Nineteen patients underwent LA mapping before catheter ablation for persistent atrial fibrillation. Finite Element Analysis was used to predict wall stress distribution based on LA geometry from CT. The relationship was assessed between wall stress and (1) electrogram voltage and (2) complex fractionated atrial electrograms (CFAE), using CFAE mean (the mean interval between deflections). Wall stress varied widely within atria and between subjects (median, 36 kPa; interquartile range, 26-51 kP). Peaks in wall stress (≥90th percentile) were common at the pulmonary vein (PV) ostia (93%), the appendage ridge (100%), the high posterior wall (84%), and the anterior wall and septal regions (42-84%). Electrogram voltage showed an inverse relationship across quartiles for wall stress (19% difference across quartiles, P=0.016). There was no effect on CFAE mean across quartiles of wall stress. Receiver operating characteristic analysis showed high wall stress was associated with low voltage (ie, <0.5 mV) and electrical scar (ie, <0.05 mV; both P<0.0001) and with absence of CFAE (ie, CFAE mean <120 ms; P<0.0001). However, peaks in wall stress and CFAE were found at 88% of PV ostia.
Peaks in wall stress were associated with areas of low voltage, suggestive of focal remodeling. Although peaks in wall stress were not associated with LA CFAE, the PV ostia may respond differently.
"Atrial dilatation, myocarditis, myocardial fibrosis and increased autonomic nervous tension all serve as triggering factors and/or an electrical substrate to lead to AF. Triggering factors and the electrical substrate may be located in the same place or at different locations. Radiofrequency ablation is used to treat AF through the isolation of triggering factors and interference with the electrical substrate (33,34). "
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to analyze the therapeutic effects of various methods for the treatment of chronic atrial fibrillation (AF). Randomized controlled trials (RCT) concerning drug therapy and catheter ablation for the treatment of chronic AF were retrieved. The RevMan 5.1 software package was used for the meta-analysis. A total of 20 papers were assessed in this study. The results of the analysis indicated that the success rate was lower [odds ratio (OR), 8.94; 95% confidence interval (CI), 4.70-17.02; P<0.0001] and the relapse rate was higher (OR, 0.07, 95% CI, 0.05-0.10; P<0.0001) for drug therapy compared with that for catheter ablation. With regard to different catheter ablation procedures, the success rate for pulmonary vein antrum isolation (PVAI) was lower compared with that for PVAI plus complex fractionated atrial electrogram (CFAE; OR, 0.53; 95% CI, 0.37-0.78; P=0.0001). Pulmonary vein isolation (PVI) plus left atrial ablation (LAA) had a higher success rate compared with PVI alone (OR, 2.79; 95% CI, 1.59-4.88, P=0.0003). There was not identified to be a significant difference in the success rates between PVAI and CFAE (OR, 2.05; 95% CI, 0.06-205.74; P=0.76) or between PVI and circumferential pulmonary vein isolation (CPVI; OR, 0.94; 95% CI, 0.29-3.00; P=0.91). All the funnel plots of publication bias were essentially symmetrical. In conclusion, the success rate was higher and the relapse rate was lower for catheter ablation compared with drug therapy. Among the different procedures of catheter ablation, there were no significant differences in success rate between two single procedures; however, the success rates were higher for the combined methods compared with those for the single methods.
Experimental and therapeutic medicine 08/2013; 6(2):489-496. DOI:10.3892/etm.2013.1158 · 1.27 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in human beating hearts. AF initiates self-perpetuating changes in electrophysiology, structure and functional properties of the atria, a phenomenon known as atrial remodeling. Hypertension, heart failure, valvular heart disease, sleep apnea, congenital heart disease are well known risk factors for AF that contribute to the development of atrial substrate. There is some evidence that reversal of atrial remodeling is possible with correction of antecedent conditions, however the timing of the intervention or upstream therapy may be critical. This review will describe the pathophysiology of atrial remodeling as it pertains to AF. We will describe components of remodeling including changes in atrial refractoriness, conduction and atrial structure, in addition to autonomic changes and anatomic factors that predispose to remodeling. We will discuss our current understanding of the electrophysiological changes that contribute to AF persistence. We will describe nature of atrial and pulmonary vein remodeling in the context of different forms of AF, with and without predisposing risk factors. We will describe the nature of remodeling over time following therapeutic interventions such as AF ablation in order to show that it does not necessarily improve and may worsen.
Progress in Biophysics and Molecular Biology 08/2012; 110(2-3). DOI:10.1016/j.pbiomolbio.2012.07.011 · 2.27 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of this study was to investigate the correlation between the altered expression of genes involved in the regulation of ion channels in atrial myocytes and the risk of atrial fibrillation (AF) in patients with heart failure (HF). Right atrial appendages were obtained from 18 HF patients and 18 patients with normal cardiac functions who had undergone surgery. The mRNA expression levels of Kv4.3α, KvLQT1, Kv1.5, L-Caα1c and NCX were measured by reverse transcription-PCR (RT-PCR). Protein expression levels were also detected by western blotting. In comparison with the control group exhibiting normal cardiac functions, the mRNA and protein expression levels of Kv4.3α, KvLQT1 and L-Caα1c were significantly reduced in HF patients. By contrast, the mRNA and protein expression levels of NCX were significantly increased in HF patients compared with the control group (P<0.01). The mRNA expression levels of Kv1.5 were not evidently altered. We demonstrated that increased levels of Kv4.3α, KvLQT1 and L-Caα1c and decreased levels of NCX are correlated with the risk of AF in HF patients. Changes in the gene expression of ion channel-related proteins may therefore be used as biological markers of AF occurring in HF patients in future studies.
Experimental and therapeutic medicine 04/2013; 5(4):1239-1243. DOI:10.3892/etm.2013.949 · 1.27 Impact Factor
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