MicroRNA-21 via Dysregulation of WW Domain-Containing Protein 1 Regulate Atrial Fibrosis in Atrial Fibrillation

2018 ◽  
Vol 27 (1) ◽  
pp. 104-113 ◽  
Author(s):  
Hui Tao ◽  
Meng Zhang ◽  
Jing-Jing Yang ◽  
Kai-Hu Shi
Keyword(s):  
Atrial Fibrillation ◽  
Atrial Fibrosis ◽  
Ww Domain

The Role of Atrial Fibrosis Detected by Delayed - Enhancement MRI in Atrial Fibrillation Ablation

2020 ◽  
Vol 16 (2) ◽  
pp. 135-144 ◽  
Author(s):  
Zsuzsanna Kis ◽  
Astrid Amanda Hendriks ◽  
Taulant Muka ◽  
Wichor M. Bramer ◽  
Istvan Kovacs ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Imaging Modality ◽  
Final Analysis ◽  
Atrial Fibrosis ◽  
Atrial Wall ◽  
Af Ablation ◽  
Left Atrial Wall ◽  
Cmr Imaging

Introduction: Atrial Fibrillation (AF) is associated with remodeling of the atrial tissue, which leads to fibrosis that can contribute to the initiation and maintenance of AF. Delayed- Enhanced Cardiac Magnetic Resonance (DE-CMR) imaging for atrial wall fibrosis detection was used in several studies to guide AF ablation. The aim of present study was to systematically review the literature on the role of atrial fibrosis detected by DE-CMR imaging on AF ablation outcome. Methods: Eight bibliographic electronic databases were searched to identify all published relevant studies until 21st of March, 2016. Search of the scientific literature was performed for studies describing DE-CMR imaging on atrial fibrosis in AF patients underwent Pulmonary Vein Isolation (PVI). Results: Of the 763 citations reviewed for eligibility, 5 articles (enrolling a total of 1040 patients) were included into the final analysis. The overall recurrence of AF ranged from 24.4 - 40.9% with median follow-up of 324 to 540 days after PVI. With less than 5-10% fibrosis in the atrial wall there was a maximum of 10% recurrence of AF after ablation. With more than 35% fibrosis in the atrial wall there was 86% recurrence of AF after ablation. Conclusion: Our analysis suggests that more extensive left atrial wall fibrosis prior ablation predicts the higher arrhythmia recurrence rate after PVI. The DE-CMR imaging modality seems to be a useful method for identifying the ideal candidate for catheter ablation. Our findings encourage wider usage of DE-CMR in distinct AF patients in a pre-ablation setting.

scholarly journals Triggered Firing and Atrial Fibrillation in Transgenic Mice With Selective Atrial Fibrosis Induced by Overexpression of TGF-β1

2012 ◽  
Vol 76 (6) ◽  
pp. 1354-1362 ◽  
Author(s):  
Eue-Keun Choi ◽  
Po-Cheng Chang ◽  
Young-Soo Lee ◽  
Shien-Fong Lin ◽  
Wuqiang Zhu ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Transgenic Mice ◽  
Tgf Beta ◽  
Atrial Fibrosis

Natriuretic peptides and right atrial fibrosis in patients with paroxysmal versus persistent atrial fibrillation

Peptides ◽  
2010 ◽  
Vol 31 (8) ◽  
pp. 1531-1539 ◽  
Author(s):  
Hailong Cao ◽  
Lei Xue ◽  
Yanhu Wu ◽  
Hongtai Ma ◽  
Liang Chen ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Natriuretic Peptides ◽  
Persistent Atrial Fibrillation ◽  
Right Atrial ◽  
Atrial Fibrosis

scholarly journals Role of imaging in assessment of atrial fibrosis in patients with atrial fibrillation: state-of-the-art review

2013 ◽  
Vol 15 (1) ◽  
pp. 1-5 ◽  
Author(s):  
L. Longobardo ◽  
M. C. Todaro ◽  
C. Zito ◽  
M. C. Piccione ◽  
G. Di Bella ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
State Of The Art ◽  
Atrial Fibrosis

scholarly journals Increased α-Actinin-2 Expression in the Atrial Myocardium of Patients with Atrial Fibrillation Related to Rheumatic Heart Disease

Cardiology ◽  
2016 ◽  
Vol 135 (3) ◽  
pp. 151-159 ◽  
Author(s):  
Lei Zhang ◽  
Nan Zhang ◽  
Xuejiao Tang ◽  
Fajin Liu ◽  
Suxin Luo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Disease ◽  
Sinus Rhythm ◽  
Rheumatic Heart Disease ◽  
Collagen Content ◽  
Atrial Fibrosis ◽  
Smad Pathway ◽  
Smad Signaling Pathway ◽  
Tgf Β1 ◽  
Rheumatic Heart

Objectives: Atrial fibrosis, a marker of atrial structural remodeling, plays a critical role in atrial fibrillation (AF). α- Actinin-2 is associated with structural remodeling related to stretching. The transforming growth factor-β1 (TGF-β1)/Smad pathway plays an important role in atrial fibrosis. We investigated the effects of the TGF-β1/Smad signaling pathway on α-actinin-2 in atrial fibrosis in patients with AF. Methods: Forty-one right atrial specimens obtained from patients with rheumatic heart disease (RHD) were divided into a chronic (c)AF group, i.e. RHD + cAF (n = 29), and a sinus rhythm group, i.e. RHD + sinus rhythm (n = 12). Patients with congenital heart disease (CHD) and sinus rhythm who underwent heart surgery served as controls (n = 10). Fibrosis was assessed by histological examination, and expression of α-actinin-2, TGF-β1 and Smad2/phosphorylated Smad2 (p-Smad2) was evaluated by immunohistochemistry, quantitative real-time PCR and Western blotting. In rat atrial fibroblasts treated with TGF-β1, the collagen content was measured using hydroxyproline detection, and α-actinin-2 and p-Smad2 were evaluated by semiquantitative reverse-transcription PCR and Western blotting. Results: The histology results revealed a significant increase in atrial fibrosis in AF patients. The collagen content, mRNA and protein expression levels of α-actinin-2 and the components of the TGF-β1/Smad signaling pathway were significantly gradually increased in the CHD + sinus rhythm, RHD + sinus rhythm and RHD + cAF groups (p < 0.05). The mRNA and protein levels of α-actinin-2 and TGF-β1 in RHD patients were positively correlated with the collagen volume fraction. A positive correlation between the expression of α-actinin-2 and TGF-β1 was also observed. In rat atrial fibroblasts treated with TGF-β1, the collagen content was greater than that in the control group (p < 0.05), and the expression levels of α- actinin-2 and p-Smad2 were also upregulated (p < 0.05). Conclusions: α-Actinin-2 expression was increased in the atrial tissues of patients with AF secondary to RHD. α-Actinin-2 was upregulated via the TGF-β1/Smad pathway in atrial fibroblasts, which suggests that it may be involved in TGF-β1/Smad pathway-induced atrial fibrosis in patients with AF.

Abstract 607: Antiarrhythmic Effects Of Omega-3 Fatty Acids And Cyp-eicosanoids In A Murine Atrial Fibrillation Model

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Bastian Spallek ◽  
Christina Westphal ◽  
Anne Konkel ◽  
Gerd Wallukat ◽  
Darryl C Zeldin ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Fatty Acids ◽  
Vehicle Group ◽  
Synthetic Analog ◽  
Omega 3 ◽  
Atrial Fibrosis ◽  
Adrenergic Stimulation ◽  
Connexin 40 ◽  
Normal Chow

Atrial fibrillation (AF) is the most common arrhythmia in man. Small animal models of AF are rare, limiting the opportunities of mechanistic studies and of evaluating novel treatment strategies. We found that mice can be rendered susceptible to AF by chronic ß-adrenergic stimulation and used this model to test the hypothesis that dietary n-3 polyunsaturated fatty acids (n-3 PUFAs) and endogenously produced cytochrome P450 (CYP)-dependent epoxyeicosanoids protect against AF. Our study included male wild type C57BL/6 mice given either normal chow (WT-n6-group) or a diet supplemented with n-3 PUFAs (2.5% EPA/DHA added to normal chow; WT-n3-group), as well as transgenic littermates with cardiomyocyte-specific overexpression of the human epoxygenase CYP2J2 (CYP-n6 group). All animal groups received 40mg/kg/d of isoproterenol (ISO) or vehicle over 14 days via osmotic mini-pumps. AF induction was tested in vivo by programmed electrical stimulation (PES) and reached 48% (13 of 27 protocols) in ISO-treated WT-n6, compared to 9% (2 of 22) in the vehicle group. ISO-treated WT-n6 mice also featured increased atrial fibrosis, decreased atrial connexin-40 expression, and significantly reduced atrial refractoriness (AERP: 13.1±0.5 vs. 21.7±0.9 ms in vehicle-infused controls). Ventricular refractoriness remained unchanged and ventricular arrhythmias were not inducible. EPA/DHA-supplementation as well as CYP2J2 overexpression significantly reduced ISO-stimulated AF inducibility to 17% (5 of 30 in WT-n3, and 4 of 24 in CYP-n6), decreased atrial fibrosis, and partially prevented connexin-40 down-regulation and AERP reduction (16,1±0,9 in WT-n3 and 17.5±0.5 ms in CYP-n6). Finally, we tested the antiarrhythmic potential of a synthetic analog of 17,18-epoxyeicosatetraenoic acid (17,18-EEQ), an EPA metabolite predominantly produced by CYP2J2 and other epoxygenases. Acute i.v. injection of the 17,18-EEQ compound decreased AF inducibility in ISO-stimulated WT-n6 mice from 67% (14 of 21 in vehicle control) to 33% (10 of 30) and also the mean duration of AF episodes. These results show that ISO-infusion allows establishing a suitable mouse model of AF and indicate an important role of CYP-dependent n-3 PUFA metabolites in preventing AF.

scholarly journals Cadherin-11 Deficiency Attenuates Ang-II-Induced Atrial Fibrosis and Susceptibility to Atrial Fibrillation

2021 ◽  
Vol Volume 14 ◽  
pp. 2897-2911
Author(s):  
Wei Cao ◽  
Shuai Song ◽  
Guojian Fang ◽  
Yingze Li ◽  
Yuepeng Wang ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Ang Ii ◽  
Atrial Fibrosis
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