Spectral Characteristics of Human Atrial Fibrillation Waves of the Right Atrial Free Wall With Respect to the Duration of Atrial Fibrillation and Effect of Class I Antiarrhythmic Drugs

The mechanism of atrial flutter and fibrillation induced by rapid pacing in 22 dogs with 3-day-old sterile pericarditis was investigated by computerized epicardial mapping of atrial activation before and after administration of agents known to modify atrial electrophysiologic properties: procainamide, isoproterenol, and electrical stimulation of the vagosympathetic trunks. Before the administration of any of these agents, a total of 30 episodes of sustained atrial flutter (> 1 min duration, monomorphic; regular cycle length, 127 ± 12 ms, mean ± SD) was induced in 15 out of 22 dogs and 9 episodes of unstable atrial flutter (duration, <1 min; cycle length, 129 ± 34 ms; monomorphic, alternating with fibrillation) were induced in the remaining 7 preparations. In the latter, administration of procainamide transformed unstable atrial flutter and atrial fibrillation to sustained atrial flutter (cycle length, 142 ± 33 ms; n = 9 episodes). During control atrial flutter, atrial maps displayed circus movement of excitation in the right atrial free wall with faster conduction parallel to the orientation of intra-atrial myocardial bundles. Vagal stimulation changed atrial flutter to atrial fibrillation in 32 of 73 trials; this was associated with acceleration of conduction in the lower right atrium, leading to fragmentation of the major wave front. Isoproterenol produced a 6–25% increase of the atrial rate in 6 out of 14 trials of atrial flutter and induced atrial fibrillation in 4. After procainamide, the reentrant pathway was lengthened and conduction was slowed further in the right atrium. Maps obtained during unstable atrial flutter showed incomplete circuits involving the right atrium. Following procainamide infusion, the area of functional dissociation or block was enlarged and a stable circus movement pattern, which was similar to the pattern seen in control atrial flutter, was established in the right atrium. We conclude that (1) the transitions among atrial fibrillation, atrial flutter, and sinus rhythm occur between different functional states of the same circus movement substratum primarily located in the lower right atrial free wall, and (2) the anisotropic conduction properties of the right atrium may contribute to these reentrant arrhythmias and may be potentiated by acute pericarditis.Key words: atrial flutter, atrial fibrillation, atrial mapping, antiarrhythmic drugs, vagal stimulation.

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Intraoperative mapping of the right atrial free wall during sinus rhythm: variety of activation patterns and incidence of postoperative atrial fibrillation

European Journal of Cardio-Thoracic Surgery ◽

10.1016/j.ejcts.2006.03.060 ◽

2006 ◽

Vol 30 (1) ◽

pp. 132-139 ◽

Cited By ~ 5

Author(s):

S SAKAMOTO ◽

S YAMAUCHI ◽

H YAMASHITA ◽

H IMURA ◽

Y MARUYAMA ◽

...

Keyword(s):

Atrial Fibrillation ◽

Sinus Rhythm ◽

Postoperative Atrial Fibrillation ◽

Right Atrial ◽

Free Wall ◽

Activation Patterns ◽

Intraoperative Mapping ◽

The Right

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Extensive right atrial free wall low-voltage zone as the substrate for atrial fibrillation: successful ablation by scar homogenization

EP Europace ◽

10.1093/europace/euaa233 ◽

2020 ◽

Author(s):

Ahmed M Al-Kaisey ◽

Ramanathan Parameswaran ◽

Stephen A Joseph ◽

Peter M Kistler ◽

Joseph B Morton ◽

...

Keyword(s):

Atrial Fibrillation ◽

Radiofrequency Ablation ◽

Low Voltage ◽

Clinical Syndrome ◽

Right Atrial ◽

Free Wall ◽

Complex Signals ◽

The Right ◽

Low Amplitude

Abstract Aims Prior studies have described a variety of mechanisms for atrial fibrillation (AF) originating in the right atrium (RA). In this study, we report a series of patients in whom an extensive right atrial free wall low-voltage zone (LVZ) served as the AF substrate. Methods and results Five patients with a clinical syndrome of paroxysmal AF and atrial tachycardia (AT) underwent electrophysiologic evaluation. Five patients (3 M; age 52 ± 7 years) had symptomatic paroxysmal AF for (28 ± 17 months) not responsive to medical therapy. At the initial EP study, AT was inducible in four patients and was spontaneous in one patient. In all patients, tachycardia instability precluded detailed AT mapping. Sinus or pace maps indicated an extensive LVZ in the lateral RA trabeculated free wall which consisted of regions of low amplitude complex signals interspersed between electrically silent areas. Radiofrequency ablation aimed at rendering the LVZ electrical inert was successful in eliminating AF in four of five patients. At a follow-up of 28 ± 15 months, one patient had an isolated recurrence of AF. However, two patients required repeat ablation for recurrent AT. Conclusion An extensive LVZ in the trabeculated RA free wall constitutes an unusual substrate for AF. These patients also demonstrate unstable ATs originating from the same zone. Radiofrequency ablation to render the low-voltage zone electrically inert is an effective strategy to manage AF and AT.

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Atrial dilation as a substrate for atrial fibrillation in the canine complete chronic atrioventricular block model

European Heart Journal ◽

10.1093/ehjci/ehaa946.0471 ◽

2020 ◽

Vol 41 (Supplement_2) ◽

Author(s):

A Smoczynska ◽

H.D.M Beekman ◽

R.W Chui ◽

S Rajamani ◽

M.A Vos

Keyword(s):

Atrial Fibrillation ◽

Atrioventricular Block ◽

Volume Overload ◽

Right Atrial ◽

Funding Source ◽

Private Company ◽

Structural Remodeling ◽

2D Echocardiography ◽

Atrial Enlargement ◽

The Right

Abstract Background Atrial fibrillation (AF) is the most common cardiac arrhythmia treated in clinical practice. Structural remodeling is characterized by atrial enlargement and contributes to the therapeutic resistance in patients with long-standing AF. Purpose To study the atrial arrhythmogenic and echocardiographic consequences induced by volume overload in the complete chronic atrioventricular block (CAVB) dog. Methods Echocardiographic and electrophysiological data was obtained in 14 anaesthetized Mongrel dogs, in acute AV-block (AAVB), after 6 weeks of CAVB (CAVB6) and CAVB10. Left atrial (LA) volume was determined with 2D echocardiography by using the biplane method. An electrocardiogram and monophasic action potentials (MAP) at the right atrial (RA) free wall were recorded. Atrial effective refractory period (AERP) was determined by continuous programmed electrical stimulation (PES) of 20 beats with a cycle length of 400 ms and an extrastimulus with decremental design until refractoriness was reached. A continuous PES protocol of 20 beats with an extrastimulus 5 ms longer than the AERP was applied for 150 seconds to trigger AF. After 5 min without arrhythmias, autonomic neuromodulation was performed by intravenous infusion (IV) of acetylcholine (1,5μg/kg/min to 6,0μg/kg/min) for 20 min followed by prompt IV infusion of isoprenaline (3μg/min) until the atrial heart rate increased by 20 bpm. PES with an extrastimulus was repeated for 150 seconds to induce AF. Results LA volume increased from 13.7±3.2 ml at AAVB to 20.5±5.9 ml* at CAVB6, and 22.7±6.0 ml* at CAVB10 (Fig. 1A). AERP was similar at AAVB, CAVB6, and CAVB10 (115.8±11.9, 117.3±11.7, and 106.8±12.1 ms respectively). Repetitive AF paroxysms of >10 seconds were induced in 1/14 (7%) dogs at AAVB, 1/11 (9%) at CAVB6, and 5/10 (50%)* at CAVB10 (*p<0.05) upon PES (Fig. 1B). Combined neuromodulation and PES did not increase the AF inducibility rate, but prolonged the longest episode of AF in the inducible dogs from 55±49 seconds to 236±202 seconds* at CAVB10 (Fig. 1C). LA volume was higher in inducible dogs 25.0±4.9 ml compared to 18.4±4.2 ml in non-inducible dogs at CAVB10. Conclusion Sustained atrial dilation forms a substrate for repetitive paroxysms of AF. Neuro-modulation prolongs AF episode duration in susceptible dogs. This animal model can be used to study structural remodeling of the atria and possible therapeutic advances in the management of AF. Figure 1 Funding Acknowledgement Type of funding source: Private company. Main funding source(s): Amgen Research

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Right Atrial Thrombosis and Pulmonary Embolism: A Narrative Review

Seminars in Thrombosis and Hemostasis ◽

10.1055/s-0040-1718399 ◽

2020 ◽

Vol 46 (08) ◽

pp. 895-907

Author(s):

Nina D. Anfinogenova ◽

Oksana Y. Vasiltseva ◽

Alexander V. Vrublevsky ◽

Irina N. Vorozhtsova ◽

Sergey V. Popov ◽

...

Keyword(s):

Atrial Fibrillation ◽

Pulmonary Embolism ◽

High Risk ◽

Transesophageal Echocardiography ◽

Three Dimensional ◽

Right Atrial ◽

Treatment Protocols ◽

High Risk Patients ◽

Risk Patients ◽

The Right

AbstractPrompt diagnosis of pulmonary embolism (PE) remains challenging, which often results in a delayed or inappropriate treatment of this life-threatening condition. Mobile thrombus in the right cardiac chambers is a neglected cause of PE. It poses an immediate risk to life and is associated with an unfavorable outcome and high mortality. Thrombus residing in the right atrial appendage (RAA) is an underestimated cause of PE, especially in patients with atrial fibrillation. This article reviews achievements and challenges of detection and management of the right atrial thrombus with emphasis on RAA thrombus. The capabilities of transthoracic and transesophageal echocardiography and advantages of three-dimensional and two-dimensional echocardiography are reviewed. Strengths of cardiac magnetic resonance imaging (CMR), computed tomography, and cardiac ventriculography are summarized. We suggest that a targeted search for RAA thrombus is necessary in high-risk patients with PE and atrial fibrillation using transesophageal echocardiography and/or CMR when available independently on the duration of the disease. High-risk patients may also benefit from transthoracic echocardiography with right parasternal approach. The examination of high-risk patients should involve compression ultrasonography of lower extremity veins along with the above-mentioned technologies. Algorithms for RAA thrombus risk assessment and protocols aimed at identification of patients with RAA thrombosis, who will potentially benefit from treatment, are warranted. The development of treatment protocols specific for the diverse populations of patients with right cardiac thrombosis is important.

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

Circulation ◽

10.1161/circ.132.suppl_3.15570 ◽

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.

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Prolonged Sinus Pauses upon Termination of Paroxysmal Atrial Fibrillation: Abnormal Right Atrial Electrophysiologic and Electroanatomic Findings

Texas Heart Institute Journal ◽

10.14503/thij-15-5493 ◽

2017 ◽

Vol 44 (2) ◽

pp. 107-114 ◽

Cited By ~ 1

Author(s):

Zhengyu Bao ◽

Hongwu Chen ◽

Bing Yang ◽

Michael Shehata ◽

Weizhu Ju ◽

...

Keyword(s):

Atrial Fibrillation ◽

Sinus Node ◽

P Wave ◽

Right Atrial ◽

Control Group ◽

Paroxysmal Supraventricular Tachycardia ◽

Group A ◽

Group B ◽

Activation Times ◽

The Right

The efficacy of pulmonary vein antral isolation for patients with prolonged sinus pauses (PSP) on termination of atrial fibrillation has been reported. We studied the right atrial (RA) electrophysiologic and electroanatomic characteristics in such patients. Forty patients underwent electroanatomic mapping of the RA: 13 had PSP (group A), 13 had no PSP (group B), and 14 had paroxysmal supraventricular tachycardia (control group C). Group A had longer P-wave durations in lead II than did groups B and C (115.5 ± 15.4 vs 99.5 ± 10.9 vs 96.5 ± 10.4 ms; P=0.001), and RA activation times (106.8 ± 13.8 vs 99 ± 8.7 vs 94.5 ± 9.1 s; P=0.02). Group A's PP intervals were longer during adenosine triphosphate testing before ablation (4.6 ± 2.3 vs 1.7 ± 0.6 vs 1.5 ± 1 s; P <0.001) and after ablation (4.7 ± 2.5 vs 2.2 ± 1.4 vs 1.6 ± 0.8 s; P <0.001), and group A had more complex electrograms (11.4% ± 5.4% vs 9.3% ± 1.6% vs 5.8% ± 1.6%; P <0.001). Compared with group C, group A had significantly longer corrected sinus node recovery times at a 400-ms pacing cycle length after ablation, larger RA volumes (100.1 ± 23.1 vs 83 ± 22.1 mL; P=0.04), and lower conduction velocities in the high posterior (0.87 ± 0.13 vs 1.02 ± 0.21 mm/ms; P=0.02) and high lateral RA (0.89 ± 0.2 vs 1.1 ± 0.35 mm/ms; P=0.04). We found that patients with PSP upon termination of atrial fibrillation have RA electrophysiologic and electroanatomic abnormalities that warrant post-ablation monitoring.

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Hydrodynamic compression of the right atrial free wall, a new highly-sensitive echocardiographic sign of cardiac tamponade

The American Journal of Cardiology ◽

10.1016/0002-9149(82)92447-x ◽

1982 ◽

Vol 49 (4) ◽

pp. 1010 ◽

Cited By ~ 5

Author(s):

Linda D. Gillam ◽

David Guyer ◽

Mary Etta King ◽

Jane Marshall ◽

Arthur E. Weyman

Keyword(s):

Cardiac Tamponade ◽

Right Atrial ◽

Free Wall ◽

Highly Sensitive ◽

The Right

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

Journal of Clinical Medicine ◽

10.3390/jcm9010036 ◽

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.

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