Evaluation of Linear Lesions in the Left and Right Atrium in Ablation of Longstanding Atrial Fibrillation

2013 ◽  
pp. n/a-n/a
Author(s):  
YUAN-LONG WANG ◽  
XU LIU ◽  
HONG-WEI TAN ◽  
LI ZHOU ◽  
WEI-FENG JIANG ◽  
...  
2012 ◽  
Vol 122 (5) ◽  
pp. 189-194
Author(s):  
Krzysztof Bartuś ◽  
Andy C. Kiser ◽  
Jacek Majewski ◽  
Bogusław Kapelak ◽  
Janusz Konstanty-Kalandyk ◽  
...  

2021 ◽  
Author(s):  
Alexandra S Mighiu ◽  
Alice Recalde ◽  
Klemen Ziberna ◽  
Ricardo Carnicer ◽  
Jakub Tomek ◽  
...  

Abstract Aims Gp91-containing NADPH oxidases (NOX2) are a significant source of myocardial superoxide production. An increase in NOX2 activity accompanies atrial fibrillation (AF) induction and electrical remodelling in animal models and predicts incident AF in humans; however, a direct causal role for NOX2 in AF has not been demonstrated. Accordingly, we investigated whether myocardial NOX2 overexpression in mice (NOX2-Tg) is sufficient to generate a favourable substrate for AF and further assessed the effects of atorvastatin, an inhibitor of NOX2, on atrial superoxide production and AF susceptibility. Methods and results NOX2-Tg mice showed a 2- to 2.5-fold higher atrial protein content of NOX2 compared with wild-type (WT) controls, which was associated with a significant (twofold) increase in NADPH-stimulated superoxide production (2-hydroxyethidium by HPLC) in left and right atrial tissue homogenates (P = 0.004 and P = 0.019, respectively). AF susceptibility assessed in vivo by transoesophageal atrial burst stimulation was modestly increased in NOX2-Tg compared with WT (probability of AF induction: 88% vs. 69%, respectively; P = 0.037), in the absence of significant alterations in AF duration, surface ECG parameters, and LV mass or function. Mechanistic studies did not support a role for NOX2 in promoting electrical or structural remodelling, as high-resolution optical mapping of atrial tissues showed no differences in action potential duration and conduction velocity between genotypes. In addition, we did not observe any genotype difference in markers of fibrosis and inflammation, including atrial collagen content and Col1a1, Il-1β, Il-6, and Mcp-1 mRNA. Similarly, NOX2 overexpression did not have consistent effects on RyR2 Ca2+ leak nor did it affect PKA or CaMKII-mediated RyR2 phosphorylation. Finally, treatment with atorvastatin significantly inhibited atrial superoxide production in NOX2-Tg but had no effect on AF induction in either genotype. Conclusion Together, these data indicate that while atrial NOX2 overexpression may contribute to atrial arrhythmogenesis, NOX2-derived superoxide production does not affect the electrical and structural properties of the atrial myocardium.


2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
K Sakata ◽  
T Tanaka ◽  
S Yamashita ◽  
K Yamashiro

Abstract Background Although catheter ablation targeting ganglionated plexi (GP) playing an important role in formation of triggers and substrates of atrial fibrillation (AF) has been reported as one of the effective ablation strategies in non-paroxysmal AF (non-PAF) patients, its effectiveness varies among the study groups. More recently, ablation targeting spatiotemporal electrogram dispersion (STED) areas, assumed to contain AF drivers in forms of rotational activation is proposed. However, the optimal ablation strategy for non-PAF is still controversial since the exact mechanisms of non-PAF are not well understood. Purpose To investigate the effectiveness of GP ablation for autonomic modification and STED ablation for modulation of AF drivers. Methods Consecutive 149 non-PAF patients who underwent STED ablation in our center were enrolled. We detected STED areas within the whole left and right atrium during AF using PentaRay®, and ablated them. If AF was terminated during STED ablation, we finished the procedure without burning the remaining STED areas. If not, electrical cardioversion was applied. The outcome was compared with that in consecutive 156 non-PAF patients undergoing GP ablation previously in our center. Results (1) The clinical characteristics were comparable between two groups (see Table). (2) A Kaplan-Meier curve showed that there was no significant difference between the freedom rates from non-PAF/non-paroxysmal atrial tachycardia (non-PAT) after single procedure in STED group and GP group (Figure, left). (3) However, the freedom rates from non-PAT in STED group was significantly lower than that GP group (Figure, right). Conclusions The recurrence type of atrial arrhythmia after ablation was remarkably different between ablation of STED and GP. STED ablation might eliminate fibrillatory conduction and control AF driver in patients with non-PAF. Freedom from atrial arrhythmia Funding Acknowledgement Type of funding source: None


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