Abstract 18492: Phase Analysis Detects Human Atrial Fibrillation Sources While Classical Activation Mapping May Not: Reconciling Classical and Computational Mapping

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Junaid A Zaman ◽  
Gautam G Lalani ◽  
Tina Baykaner ◽  
Shirley Park ◽  
David E Krummen ◽  
...  

Introduction: The mechanisms maintaining human persistent AF are elusive. It is striking how most optical mapping studies in animal and recently human AF show rotors and focal sources, while most classical activation mapping studies of electrograms do not. We tested the hypothesis that sites in human persistent AF showing rotors by phase analysis may, due to precession (‘wobble’) and fibrillatory collision, rarely reveal sources in activation maps. Methods: We studied 25 patients with persistent AF (LA 47 mm, CHADS2=1.9), in whom phase-mapping of electrograms from 64 pole baskets revealed rotors/focal sources where ablation terminated AF. Electrograms (fig A) were annotated (Matlab) using minimum dV/dt (unipoles, fig B) and peak amplitude criteria (bipoles) to create contours (isochrones), that were classified into a) complete, b) partial or c) unresolvable sources. Results: In each case, ablation at phase-identified rotors/sources (4.0±5.7 mins) terminated persistent AF to sinus rhythm (fig C, 64%) or atrial tachycardia. Notably, isochrones detected sources in only 5/25 (20%) of cases (fig D), more easily in unipolar than bipolar signals. Isochrones revealed partial sources in 11 (44%) and were unresolvable in 9 (36%). Source detection in classical maps was obscured by low signal: noise, varying sequence (rotor precession), or electrode noise that phase analysis resolved by analyzing neighboring sites (fig E). The figure summarizes these steps for a case with perfect agreement between activation and phase maps. Conclusions: Rotors and focal sources for human persistent AF detected by phase analysis were mostly undetected in activation maps, due to rotor precession and fibrillatory conduction. These data may inform approaches to revise classical criteria to better map AF.

2003 ◽  
Vol 8 (1_suppl) ◽  
pp. S5-S11 ◽  
Author(s):  
Stanley Nattel

Atrial fibrillation is the most common cardiac arrhythmia in clinical practice, and its management remains challenging. A solid understanding of the scientific basis for atrial fibrillation therapy requires insight into the mechanisms underlying the arrhythmia, about which an enormous amount has been learned over the past 10 years. The basic information presently available about atrial fibrillation mechanisms is reviewed. The particular properties of normal atrial electrophysiology are discussed, including salient ionic determinants of the atrial action potential and key anatomic features. Reviewed are three crucial arrhythmia mechanisms long held to be involved in atrial fibrillation: 1) rapid ectopic activity, 2) single-circuit reentry with fibrillatory conduction, and 3) multiple-circuit reentry. The determinants of each and the evidence for their involvement in clinical and/or experimental atrial fibrillation are noted. The physiological consequences, various contributing mechanisms, and clinical implications of the role of atrial-tachycardia remodeling are analyzed. Atrial-tachycardia remodeling links the potential mechanisms of atrial fibrillation, since atrial fibrillation beginning by any mechanism is likely to cause tachycardia-remodeling and thus promote the maintenance of atrial fibrillation by multiple-circuit reentry. Atrial structural remodeling is discussed as a paradigm of atrial fibrillation in which the classic features required for reentry (reduced refractory period and reentrant wavelength) may be lacking. Finally, the importance of recent insights into potential genetic determinants of atrial fibrillation is reviewed. The classic understanding of atrial fibrillation pathophysiology saw the different possible mechanisms as being alternative and opposing hypotheses. We now consider the multiple potential mechanisms as contributing to the pathophysiology of the arrhythmia to a different extent in different clinical settings and interacting with each other in a dynamic way at various stages of the natural history in many patients. It is hoped that this improved mechanistic understanding will lead to the development of improved therapeutic options.


2016 ◽  
Vol 32 (2) ◽  
pp. 141-144 ◽  
Author(s):  
Naoko Sasaki ◽  
Yasuo Okumura ◽  
Ichiro Watanabe ◽  
Andrew Madry ◽  
Yuki Hamano ◽  
...  

2020 ◽  
Vol 30 (6) ◽  
pp. 899-902
Author(s):  
Mitchell I. Cohen ◽  
Jordan A. Cohen ◽  
Connor Shope ◽  
Lauren Stollar ◽  
Lucas Collazo

AbstractMultifocal atrial tachycardia has certain electrocardiographic similarities to atrial fibrillation. The mechanism of atrial fibrillation is heterogenous but in some cases may arise from a single ectopic driver with fibrillatory conduction to the rest of the atria. This has led to the speculation that multifocal atrial tachycardia may have a similar mechanistic unifocal site that disperses through the atrium in a fibrillatory pattern. Ivabradine has been reported to be efficacious in an adult with paroxysmal atrial fibrillation as well as in children with junctional or ectopic atrial tachycardias. This is the first report of successfully using ivabradine, a novel anti-arrhythmic If blocking agent, to convert multifocal atrial tachycardia in a 5-month-old critically ill infant to a pattern indicating a single ectopic atrial focus. This allowed the patient’s single atrial focus to be ablated with return to sinus rhythm and decannulation from ventriculoarterial extracorporeal membrane oxygenation. This case suggests that multifocal atrial tachycardia may arise from a single automatic focus with downstream fibrillatory conduction to the atria.


2014 ◽  
Vol 25 (12) ◽  
pp. 1284-1292 ◽  
Author(s):  
VIJAY SWARUP ◽  
TINA BAYKANER ◽  
ARMAND ROSTAMIAN ◽  
JAMES P. DAUBERT ◽  
JOHN HUMMEL ◽  
...  

2004 ◽  
Vol 52 (S 1) ◽  
Author(s):  
S Dhein ◽  
A Boldt ◽  
J Garbade ◽  
L Polontchouk ◽  
U Wetzel ◽  
...  

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Rujirachun ◽  
P Wattanachayakul ◽  
N Charoenngam ◽  
A Winijkul ◽  
P Ungprasert

Abstract Background and objectives Little is known about atrial involvement in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC). Recent studies have suggested that atrial arrhythmia (AA), including atrial fibrillation (AF), atrial flutter (AFL), and atrial tachycardia (AT), was common among these patients although the reported prevalence varied considerably across the studies. Methods We searched for published articles indexed in MEDLINE and EMBASE databases from inception through Sep 22, 2019 to identify cohort studies of patients with ARVC that described the prevalence of atrial arrhythmia among the participants. The pooled prevalence across studies was calculated. Results A total of 16 cohort studies with 1,986 patients with ARVC were included into this meta-analysis. The pooled prevalence of overall AA among patients with ARVC was 17.9% (95% CI, 13.0%–24.0%; I2 88%), the pooled prevalence of AF of 12.9% (95% CI, 9.6%–17.0%; I2 78%), the pooled prevalence of AFL of 5.9% (95% CI, 3.7%–9.2%; I2 70%), and the pooled prevalence of AT of 7.1% (95% CI, 3.7%–13.0%; I2 49%). Conclusions AA is common among patient with ARVC with the pooled prevalence of approximately 18%, which is substantially higher than the reported prevalence of AA in general population. Funding Acknowledgement Type of funding source: None


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