Characterization of Fractionated Atrial Electrograms Critical for Maintenance of Atrial Fibrillation

Hunter, Ross J.; Diab, Ihab; Tayebjee, Muzahir H.; Richmond, Laura; Sporton, Simon; Earley, Mark J.; Schilling, Richard J.

doi:10.1161/circep.111.962928

Cited by 66 publications

(46 citation statements)

References 35 publications

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“…51,52 Fractionated electrograms can be fixed and caused by anatomic barriers such as scar or inhomogeneous tissue, or they may be functional, dynamic and related to changes in wavefront propagation throughout the myocardium. It has been further proposed that these fractionated sites are important in sustaining AF, 53 and that targeting fractionated electrograms with ablation can terminate AF and prevent its re-induction or recurrence. 52,[54][55][56][57][58][59][60] The data supporting these conclusions are rather weak overall, with only a few small, randomised clinical trials providing guidance, and different studies have arrived at disparate conclusions regarding the importance, or lack thereof, of fractionated electrograms in the pathogenesis of AF.…”

Section: Limitations Of Targeting Rotors With Ablation For the Treatmmentioning

confidence: 99%

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Waks

Josephson²

2014

Arrhythmia &Amp; Electrophysiology Review

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Atrial fibrillation (AF), the most common sustained arrhythmia, is a leading cause of stroke, and is associated with significant morbidity and mortality worldwide. Despite its frequency, clinical importance, and advances in technology and our knowledge of the molecular, ionic and physiological fundamentals of cardiac electrophysiology, our limited understanding of the mechanisms that initiate and sustain AF has prevented us from being able to truly cure this arrhythmia with antiarrhythmic drugs and/or ablation. This contrasts with other arrhythmias, such as AV nodal tachycardia or circus movement tachycardia using an accessory pathway, which have well-defined mechanisms and circuits that can be safely targeted with high rates of cure. The observations that AF may have different mechanisms in different patients, and that paroxysmal, persistent and permanent forms of AF may differ in how they are initiated and sustained, only serves to reinforce our lack of understanding of this ubiquitous arrhythmia. Historical Mechanisms of Atrial Fibrillation and the Multiple Wavelet HypothesisInterest and understanding of the mechanism of AF began to take form in the early 1900s. Given the chaotic and irregular nature of AF on the surface electrocardiogram, rapid firing of automatic atrial foci was considered a potential mechanism. However, after the seminal work of Mayer 1 , Mines 2 and Garrey 3 in laying the foundation for describing and understanding reentrant arrhythmias, atrial reentrant circuits emerged as the likely drivers of AF.4-7 Although these theories were conceptually sound, it was impossible to prove a specific mechanism with the technology of the time. Moe et al. demonstrated that it was probabilistically unlikely that a large number of simultaneous wavefronts would all die out simultaneously, and AF would therefore perpetuate. However, if the number of simultaneous wavelets were small and/or below a critical value (between 15 and 30 in Moe's computer model), 9 at some point all reentrant wavefronts would be simultaneously extinguished, and AF would therefore terminate. 8,9 Allessie et al. provided experimental evidence supporting this mechanism in a canine heart model of AF where four to six simultaneous reentrant wavelets were needed to sustain arrhythmia. 10 Further evidence supporting multiple wavelets in AF was demonstrated in a separate model, which evaluated the effect of various antiarrhythmic drugs on canine myocardium. This model demonstrated that termination of AF was associated with a reduction AbstractAtrial fibrillation (AF) is the most common sustained arrhythmia encountered in clinical practice, yet our understanding of the mechanisms that initiate and sustain this arrhythmia remains quite poor. Over the last 50 years, various mechanisms of AF have been proposed, yet none has been consistently observed in both experimental studies and in humans. Recently, there has been increasing interest in understanding how spiral waves or rotors -which are specific, organised forms of functional reentry -su...

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Section: Limitations Of Targeting Rotors With Ablation For the Treatmmentioning

confidence: 99%

Mechanisms of Atrial Fibrillation – Reentry, Rotors and Reality

Waks

Josephson²

2014

Arrhythmia &Amp; Electrophysiology Review

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“…20 AFCL has been used by others to monitor response to ablation, with an increase Ն5-6 ms considered significant. [21][22][23] Mean AFCL was determined manually over 30 cycles from bipolar electrograms recorded at the apex of the left and right atrial appendages, where electrograms are high-voltage and hence AFCL is unambiguous, before and after ablation of each CFAE lesion. Baseline AFCL variability was measured over 10 successive segments of 30 cycles in all patients before any ablation.…”

Section: Assessment Of Afclmentioning

confidence: 99%

Left Atrial Wall Stress Distribution and Its Relationship to Electrophysiologic Remodeling in Persistent Atrial Fibrillation

Hunter

Liu²,

Lu³

et al. 2012

Circ: Arrhythmia and Electrophysiology

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102

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Background-Atrial stretch causes remodeling that predisposes to atrial fibrillation. We tested the hypothesis that peaks in left atrial (LA) wall stress are associated with focal remodeling. Methods and Results-Nineteen patients underwent LA mapping before catheter ablation for persistent atrial fibrillation.Finite Element Analysis was used to predict wall stress distribution based on LA geometry from CT. The relationship was assessed between wall stress and (1) electrogram voltage and (2) complex fractionated atrial electrograms (CFAE), using CFAE mean (the mean interval between deflections). Wall stress varied widely within atria and between subjects (median, 36 kPa; interquartile range, 26 -51 kP). Peaks in wall stress (Ն90th percentile) were common at the pulmonary vein (PV) ostia (93%), the appendage ridge (100%), the high posterior wall (84%), and the anterior wall and septal regions (42-84%). Electrogram voltage showed an inverse relationship across quartiles for wall stress (19% difference across quartiles, Pϭ0.016). There was no effect on CFAE mean across quartiles of wall stress. Receiver operating characteristic analysis showed high wall stress was associated with low voltage (ie, Ͻ0.5 mV) and electrical scar (ie, Ͻ0.05 mV; both PϽ0.0001) and with absence of CFAE (ie, CFAE mean Ͻ120 ms; PϽ0.0001). However, peaks in wall stress and CFAE were found at 88% of PV ostia. Conclusions-Peaks in wall stress were associated with areas of low voltage, suggestive of focal remodeling. Although peaks in wall stress were not associated with LA CFAE, the PV ostia may respond differently. (Circ Arrhythm Electrophysiol. 2012;5:351-360.)

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“…In the CFAE AF Trial they identified that alone CFAE areas were not define the substrate of arrhythmia by themselves, but were only the expression of speed and homogeneity of AF waves, and them had changed to upwards after catheter ablation. [10] Nevertheless it will be the great mistake to underestimate the role of secondary interventional procedures in maintenance of sinus rhythm in late follow-up. In our study we leaned on significance of primary catheter ablation guided by electroanatomical patterns.…”

Section: Resultsmentioning

confidence: 99%