scholarly journals 073_16387-H5 Role of Right Atrial for Effective Radiofrequency Ablation for Paroxysmal and Persistent Atrial Fibrillation

2017 ◽  
Vol 3 (10) ◽  
pp. S26
Author(s):  
E.A. Artyukhina ◽  
A.S.h. Revishvili ◽  
V.A. Vaskovsky ◽  
M.V. Yashkov
Keyword(s):  
Atrial Fibrillation ◽  
Radiofrequency Ablation ◽  
Persistent Atrial Fibrillation ◽  
Right Atrial

scholarly journals Persistent Atrial Fibrillation: The Role of Left Atrial Posterior Wall Isolation and Ablation Strategies

2021 ◽  
Vol 10 (14) ◽  
pp. 3129
Author(s):  
Riyaz A. Kaba ◽  
Aziz Momin ◽  
John Camm
Keyword(s):  
Atrial Fibrillation ◽  
Left Atrial ◽  
Pulmonary Veins ◽  
Treatment Strategies ◽  
Persistent Atrial Fibrillation ◽  
Posterior Wall ◽  
Cardiovascular Death ◽  
Good Effect ◽  
Complex Forms

Atrial fibrillation (AF) is a global disease with rapidly rising incidence and prevalence. It is associated with a higher risk of stroke, dementia, cognitive decline, sudden and cardiovascular death, heart failure and impairment in quality of life. The disease is a major burden on the healthcare system. Paroxysmal AF is typically managed with medications or endocardial catheter ablation to good effect. However, a large proportion of patients with AF have persistent or long-standing persistent AF, which are more complex forms of the condition and thus more difficult to treat. This is in part due to the progressive electro-anatomical changes that occur with AF persistence and the spread of arrhythmogenic triggers and substrates outside of the pulmonary veins. The posterior wall of the left atrium is a common site for these changes and has become a target of ablation strategies to treat these more resistant forms of AF. In this review, we discuss the role of the posterior left atrial wall in persistent and long-standing persistent AF, the limitations of current endocardial-focused treatment strategies, and future perspectives on hybrid epicardial–endocardial approaches to posterior wall isolation or ablation.

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

Simultaneous Catheter and Epicardial Ablations Enable a Comprehensive Atrial Fibrillation Procedure

2011 ◽  
Vol 6 (4) ◽  
pp. 243-247 ◽  
Author(s):  
Andy C. Kiser ◽  
Mark D. Landers ◽  
Ker Boyce ◽  
Matjaž šinkovec ◽  
Andrej Pernat ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Radiofrequency Ablation ◽  
Sinus Rhythm ◽  
Pulmonary Veins ◽  
Persistent Atrial Fibrillation ◽  
Chronic Atrial Fibrillation ◽  
Lesion Pattern ◽  
Atrial Size ◽  
Cardiac Surgeon ◽  
Successful Collaboration

Objective Transmural and contiguous ablations and a comprehensive lesion pattern are difficult to create from the surface of a beating heart but are critical to the successful treatment of persistent, isolated atrial fibrillation. A codisciplinary simultaneous epicardial (surgical) and endocardial (catheter) procedure (Convergent procedure) addresses these issues. Methods Patients with symptomatic atrial fibrillation who failed medical treatment were evaluated. Using only pericardioscopy, the surgeon performed near-complete epicardial isolation of the pulmonary veins and a “box” lesion on the posterior left atrium using unipolar radiofrequency ablation. Simultaneous endocardial catheter radiofrequency ablation completed pulmonary vein isolation, performed a mitral annular and cavotricuspid isthmus line of block, and debulked the coronary sinus. Twelve-month results for the Convergent procedure were compared with 12-month results for concomitant and pericardioscopic (stand-alone transdiaphragmatic/thoracoscopic) atrial fibrillation procedures using unipolar radiofrequency ablation. Results Sixty-five patients underwent the Convergent procedure (mean age, 62 y; mean body surface area, 2.17 m2; mean atrial fibrillation duration, 4.8 y; mean left atrial size, 5.2 cm). Ninety-two percent were in persistent or long-standing persistent atrial fibrillation. At 12 months, evaluation with 24-hour Holter monitors found 82% of patients in sinus rhythm, while only 47% of pericardioscopic and 77% of concomitant patients treated with unipolar radiofrequency ablation were in sinus rhythm. Conclusions Simultaneous epicardial and endocardial ablation improves outcomes for patients with persistent or longstanding persistent atrial fibrillation. This successful collaboration between cardiac surgeon and electrophysiologist is an important treatment option for patients with large left atriums and chronic atrial fibrillation.

Role of Scar and Rotors in Persistent Atrial Fibrillation

2021 ◽  
Vol 7 (7) ◽  
pp. 920-922
Author(s):  
Ravi Mandapati ◽  
Tahmeed Contractor ◽  
Rahul Bhardwaj
Keyword(s):  
Atrial Fibrillation ◽  
Persistent Atrial Fibrillation

Abstract P780: Myosin Light Chain Dephosphorylation by Ppp1r12c Promotes Atrial Hypocontractility in Atrial Fibrillation

Stroke ◽  
2021 ◽  
Vol 52 (Suppl_1) ◽  
Author(s):  
Francisco J Gonzalez-Gonzalez ◽  
Perike Srikanth ◽  
Andrielle E Capote ◽  
Alsina Katherina M ◽  
Benjamin Levin ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Molecular Mechanisms ◽  
Contractile Function ◽  
Right Atrial ◽  
Western Blots

Atrial fibrillation (AF) is the most common sustained arrhythmia, with an estimated prevalence in the U.S.of 6.1 million. AF increases the risk of a thromboembolic stroke in five-fold. Although atrial hypocontractility contributes to stroke risk in AF, the molecular mechanisms reducing myofilament contractile function in AF remains unknown. We have recently identified protein phosphatase 1 subunit 12c (PPP1R12C) as a key molecule targeting myosin light-chain phosphorylation in AF. Objective: We hypothesize that the overexpression of PPP1R12C causes hypophosphorylation of atrial myosin light-chain 2 (MLC2a), thereby decreasing atrial contractility in AF. Methods and Results: Left and right atrial appendage tissues were isolated from AF patients versus sinus rhythm (SR). To evaluate the role of the PP1c-PPP1R12C interaction in MLC2a de-phosphorylation, we utilized Western blots, co-immunoprecipitation, and phosphorylation assays. In patients with AF, PPP1R12C expression was increased 3.5-fold versus SR controls with an 88% reduction in MLC2a phosphorylation. PPP1R12C-PP1c binding and PPP1R12C-MLC2a binding were significantly increased in AF. In vitro studies of either pharmacologic (BDP5290) or genetic (T560A), PPP1R12C activation demonstrated increased PPP1R12C binding with both PP1c and MLC2a, and dephosphorylation of MLC2a. Additionally, to evaluate the role of PPP1R12C expression in cardiac function, mice with lentiviral cardiac-specific overexpression of PPP1R12C (Lenti-12C) were evaluated for atrial contractility using echocardiography, versus wild-type and Lenti-controls. Lenti-12C mice demonstrated a 150% increase in left atrium size versus controls, with reduced atrial strain and atrial ejection fraction. Also, programmed electrical stimulation was performed to evaluate AF inducibility in vivo. Pacing-induced AF in Lenti-12C mice was significantly higher than controls. Conclusion: The overexpression of PPP1R12C increases PP1c targeting to MLC2a and provokes dephosphorylation, associated with a reduction in atrial contractility and an increase in AF inducibility. All these discoveries suggest that PP1 regulation of sarcomere function at MLC2a is a main regulator of atrial contractility in AF.

Abstract 15570: Direct Evidence of Endo-Epicardial Dissociation of the Atrial Wall in Patients With Longstanding Persistent Atrial Fibrillation

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Natasja de Groot ◽  
Lisette vd Does ◽  
Ameeta Yaksh ◽  
Paul Knops ◽  
Pieter Woestijne ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Direct Evidence ◽  
Persistent Atrial Fibrillation ◽  
Right Atrial ◽  
Electrode Arrays ◽  
Atrial Wall ◽  
Ablative Therapies ◽  
Epicardial Layer ◽  
Right Atrial Appendage ◽  
The Right

Introduction: Transition of paroxysmal to longstanding persistent atrial fibrillation (LsPAF) is associated with progressive longitudinal dissociation in conduction and a higher incidence of focal fibrillation waves. The aim of this study was to provide direct evidence that the substrate of LsPAF consists of an electrical double-layer of dissociated waves, and that focal fibrillation waves are caused by endo-epicardial breakthrough. Hypothesis: LsPAF in humans is caused by electrical dissociation of the endo- and epicardial layer. Methods: Intra-operative mapping of the endo- and epicardial right atrial wall was performed in 9 patients with induced (N=4), paroxysmal (N=1), persistent (N=2) or longstanding-persistent AF (N=2). A clamp of two rectangular electrode-arrays (128 electrodes; inter-electrode distance 2mm) was introduced through an incision in the right atrial appendage. Series of 10 seconds of AF were analyzed and the incidence of endo-epicardial dissociation (≥15ms) was determined for all 128 endo-epicardial recording sites. Results: In patients with LsPAF the averaged degree of endo-epicardial dissociation was highest (24.9% vs. 5.9%). Using strict criteria for breakthrough (presence of an opposite wave within 4mm and <15ms before the origin of the focal wave), the far majority (77%) of all focal fibrillation waves could be attributed to endo-epicardial excitation. Conclusions: During LsPAF considerable differences in activation of the right endo- and epicardial wall exist. Endo-epicardial fibrillation waves that are out of phase, may conduct transmurally and create breakthrough waves in the opposite layer. This may explain the high persistence of AF and the low succes rate of ablative therapies in patients with LsPAF.

Abstract P458: Myosin Light Chain Dephosphorylation By Ppp1r12c Promotes Atrial Hypocontractility In Atrial Fibrillation

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Francisco J Gonzalez-Gonzalez ◽  
Srikanth Perike ◽  
Frederick Damen ◽  
Andrielle Capote ◽  
Katherina M Alsina ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Light Chain ◽  
Myosin Light Chain ◽  
Molecular Mechanisms ◽  
Contractile Function ◽  
Right Atrial ◽  
Western Blots

Introduction: Atrial fibrillation (AF), is the most common sustained arrhythmia, with an estimated prevalence in the U.S. of 2.7 million to 6.1 million and is predictive to increase to 12.1 million in 2030. AF increases the chances of a thromboembolic stroke in five-fold. Although atrial hypocontractility contributes to stroke risk in AF, the molecular mechanisms reducing myofilament contractile function in AF remains unknown. Objective: The overexpression of PPP1R12C, causes hypophosphorylation of atrial myosin light chain 2 (MLC2a), decreasing atrial contractility. Methods and Results: Left and right atrial appendage tissues were isolated from AF patients versus sinus rhythm (SR). To evaluated the role of PP1c-PPP1R12C interaction in MLC2a de-phosphorylation we used Western blots, coimmunoprecipitation, and phosphorylation assays. In patients with AF, PPP1R12C expression was increased 3.5-fold versus SR controls with an 88% reduction in MLC2a phosphorylation. PPP1R12C-PP1c binding and PPP1R12C-MLC2a binding were significantly increased in AF. In vitro studies of either pharmacologic (BDP5290) or genetic (T560A) PPP1R12C activation demonstrated increased PPP1R12C binding with both PP1c and MLC2a, and dephosphorylation of MLC2a. Additionally, to evaluate the role of PPP1R12C expression in cardiac function, mice with lentiviral cardiac-specific overexpression of PPP1R12C (Lenti-12C) were evaluated for atrial contractility using echocardiography, versus wild-type and Lenti-controls. Lenti-12C mice demonstrated a 150% increase in left atrium size versus controls, with reduced atrial strain and atrial ejection fraction. Also, programmed electrical stimulation was performed to evaluate AF inducibility in vivo. Pacing-induced AF in Lenti-12C mice was significantly higher than controls. Conclusion: The Overexpression of PPP1R12C increases PP1c targeting to MLC2a and provokes dephosphorylation, that cause a reduction in atrial contractility and increases AF inducibility. All these discoveries advocate that PP1 regulation of sarcomere function at MLC2a is a main regulator of atrial contractility in AF.

scholarly journals Atrial Fibrillation Progression Is Associated with Cell Senescence Burden as Determined by p53 and p16 Expression

2019 ◽  
Vol 9 (1) ◽  
pp. 36
Author(s):  
Laurence Jesel ◽  
Malak Abbas ◽  
Sin-Hee Park ◽  
Kensuke Matsushita ◽  
Michel Kindo ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Heart Surgery ◽  
Open Heart Surgery ◽  
Right Atrial ◽  
Atrial Remodeling ◽  
Inflammatory Proteins ◽  
Underlying Mechanisms ◽  
The Right ◽  
New Evidence

Background: Whilst the link between aging and thrombogenicity in atrial fibrillation (AF) is well established, the cellular underlying mechanisms are unknown. In AF, the role of senescence in tissue remodeling and prothrombotic state remains unclear. Aims: We investigated the link between AF and senescence by comparing the expression of senescence markers (p53 and p16), with prothrombotic and inflammatory proteins in right atrial appendages from patients in AF and sinus rhythm (SR). Methods: The right atrial appendages of 147 patients undergoing open-heart surgery were harvested. Twenty-one non-valvular AF patients, including paroxysmal (PAF) or permanent AF (PmAF), were matched with 21 SR patients according to CHA2DS2-VASc score and treatment. Protein expression was assessed by tissue lysates Western blot analysis. Results: The expression of p53, p16, and tissue factor (TF) was significantly increased in AF compared to SR (0.91 ± 0.31 vs. 0.58 ± 0.31, p = 0.001; 0.76 ± 0.32 vs. 0.35 ± 0.18, p = 0.0001; 0.88 ± 0.32 vs. 0.68 ± 0.29, p = 0.045, respectively). Expression of endothelial NO synthase (eNOS) was lower in AF (0.25 ± 0.15 vs. 0.35 ± 0.12, p = 0.023). There was a stepwise increase of p53, p16, TF, matrix metalloproteinase-9, and an eNOS progressive decrease between SR, PAF, and PmAF. AF was the only predictive factor of p53 and p16 elevation in multivariate analysis. Conclusions: The study brought new evidence indicating that AF progression is strongly related to human atrial senescence burden and points at a link between senescence, thrombogenicity, endothelial dysfunction and atrial remodeling.

scholarly journals Epicardial Unipolar Lead Loss of Ventricular Capture during Radiofrequency Ablation of Atrial Fibrillation

2020 ◽  
Vol 2020 ◽  
pp. 1-3
Author(s):  
Daniel J. Chu ◽  
Wilson W. Lam
Keyword(s):  
Atrial Fibrillation ◽  
Radiofrequency Ablation ◽  
Pulmonary Vein ◽  
Case History ◽  
Pulse Generator ◽  
Persistent Atrial Fibrillation ◽  
Dual Chamber ◽  
Dual Chamber Pacemaker ◽  
Cellular Changes ◽  
Unipolar Lead

Introduction. Abnormal pacemaker behavior can occur during radiofrequency ablation. The behaviors are varied and include loss of capture. The mechanisms in this context have not been well described in the literature. We describe a case of epicardial unipolar lead loss of ventricular capture during pulmonary vein isolation. Case History. A 48-year-old man with an epicardial dual chamber pacemaker and persistent atrial fibrillation presented for radiofrequency ablation (RFA) of his abnormal rhythm. During RFA, intermittent loss of ventricular capture was witnessed. Review of the device settings prior to and after the procedure showed an increase in ventricular threshold after the procedure. Loss of capture was shown to be dependent on location and RF energy delivered. It was independent of QTc and independent of local cellular changes that would increase threshold. Conclusion. We hypothesize the mechanism of loss of ventricular capture in this patient with an epicardial pacemaker with unipolar leads is related to intermittent shunt of voltage from the pulse generator to the grounding pad rather than the unipolar lead.

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