Stability of Rotors and Focal Sources for Human Atrial Fibrillation: Focal Impulse and Rotor Mapping (FIRM) of AF Sources and Fibrillatory Conduction

Swarup, Vijay; Baykaner, Tina; Rostamian, Armand; Daubert, James P.; Hummel, John D.; Krummen, David E.; Trikha, B S Rishi; Miller, John M.; Tomassoni, Gery; Narayan, Sanjiv M.

doi:10.1111/jce.12559

Cited by 58 publications

(45 citation statements)

References 47 publications

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“…Multicentre experiences in more than 300 41 patients at over 10 independent laboratories support these results from FIRM-guided ablation. 44,48 Notably as demonstrated by Miller et al, 44 Recently, results from a high-frequency source ablation (HFSA) approach showed non-inferiority at 12 months versus PV isolation (PVI), with improved safety outcomes.…”

Section: Focal Impulse and Rotor Modulation Outcomes In Multicentre Tsupporting

confidence: 60%

“…40 Finally, studying only short ECG segments between QRS complexes from the inverse solution 37 may diminish stability evident when AF is mapped for longer periods. 41 Re-mapping after rotor elimination may help to validate rotors that are physiological and eliminated by ablation, a central element of FIRM-guided ablation. Figure 3).…”

Section: Conventional Ablation For Atrial Fibrillation With or Withoumentioning

confidence: 99%

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Role of Rotors in the Ablative Therapy of Persistent Atrial Fibrillation

Schricker¹,

Zaman²,

Narayan³

2015

Arrhythmia &Amp; Electrophysiology Review

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Catheter ablation is more effective than pharmacological therapy for the secondary prevention of patients with paroxysmal 1,2 and persistent 3,4 atrial fibrillation (AF) and has an emerging role in the primary prevention of paroxysmal AF. 5,6 Nevertheless, in randomised clinical trials (RCTs) its success in treating patients with paroxysmal AF is 40-60 % for a single procedure and 70 % for multiple procedures at one year, 1,2 and results for persistent AF are lower. 7,8 Thus, there is an urgent unmet need to improve our understanding of mechanistic targets for AF in each patient, to match recent advances in ablation energy delivery and catheter positioning.This report reviews mechanistic data on human AF, mapping technologies that provide the opportunity to reconcile fundamental mechanisms in individual patients and their therapeutic application. Atrial Fibrillation MechanismsAF is initiated by triggers predominantly near the pulmonary veins (PV), 9 with increasingly recognised sites outside the PVs. [10][11][12] To improve success, ablation to eliminate AF triggers should thus also target non-PV triggers, although they are transient and difficult to locate. Another potential ablative target is the mechanistic cascade by which triggers initiate AF, yet this is relatively unstudied. We recently showed -using wide-area mapping during spont aneous and induced AF -that the first cycles of AF after a trigger exhibit a single organised re-entrant spiral wave or focal driver (see Figure 1) that subsequently disorganises. 13 Remarkably, these AF-initiating mechanisms may be relatively spatially fixed for each patient -even for different triggers from both atria -separated by 2.1 ± 1.7 cm from trigger sites (see Figure 1). 13 Thus, AF initiation is likely to be a two-step mechanistic process, in which 1) a trigger initiates an organised spiral wave or focal source at patient-specific anatomical sites that 2) lead rapidly to disorganisation to produce the classical AF phenotype. This begs the question of whether AF maintenance is driven by self-sustaining disorganisation, or whether disorganisation is actually sustained by localised AF drivers (rotors or focal drivers).Self-sustaining disorganisation was traditionally considered the mechanism of AF maintenance. This mechanism is supported by computational models in which multiple wavelets sustain AF if there is enough room in the atrium ('critical mass'), 14 proposals that dissociation between the epicardium and endocardium may be contributory 15 and plaque recordings from the atria of patients in the operating room showing re-entry without apparent organisation. Limitations to these studies are that fibrillatory maps are based upon recordings that poorly represent local activation;16 only small areas of the atria were mapped (<10-20 %) and while these studies show that disorganisation exists they did not test if it self-sustains. The success of widespread ablation or Maze surgery supports the concept of self-sustaining disorganisation, but are also consistent with coinci...

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Section: Focal Impulse and Rotor Modulation Outcomes In Multicentre Tsupporting

confidence: 60%

Section: Conventional Ablation For Atrial Fibrillation With or Withoumentioning

confidence: 99%

Role of Rotors in the Ablative Therapy of Persistent Atrial Fibrillation

Schricker¹,

Zaman²,

Narayan³

2015

Arrhythmia &Amp; Electrophysiology Review

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“…AF sources identified using contact mapping precess (‘wobble’) in reproducible and limited areas 14 for long periods of time 30 , while drivers mapped by the inverse solution also occur in reproducible and limited regions for days 3 .…”

Section: Methodsmentioning

confidence: 99%

Mechanisms for the Termination of Atrial Fibrillation by Localized Ablation

Rappel

Zaman

Narayan

2015

Circ: Arrhythmia and Electrophysiology

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Background Human atrial fibrillation (AF) can terminate after ablating localized regions, that supports the existence of localized rotors (spiral waves) or focal drivers. However, it is unclear why ablation near a spiral wave tip would terminate AF and not anchor reentry. We addressed this question by analyzing competing mechanisms for AF termination in numerical simulations, referenced to clinical observations. Methods and Results Spiral wave reentry was simulated in monodomain 2D myocyte sheets using clinically realistic rate-dependent values for repolarization and conduction. Heterogeneous models were created by introduction of parameterized variations in tissue excitability. Ablation lesions were applied as non-conducting circular regions. Computational models confirmed localized ablation may anchor spiral wave reentry, producing organized tachycardias. Several mechanisms also explained termination of AF to sinus rhythm. First, lesions may create an excitable gap vulnerable to invasion by fibrillatory waves. Second, ablation of rotors in regions of low-excitability (from remodeling) produced reentry in more excitable tissue allowing collision of wave-front and back. Conversely, ablation of rotors in high-excitability regions migrated spiral waves to less excitable tissue, where they detached to collide with non-conducting boundaries. Third, ablation may connect rotors to non-conducting anatomic orifices. Fourth, reentry through slow conducting channels may terminate if ablation closes these channels. Conclusions Limited ablation can terminate AF by several mechanisms. These data shed light on how clinical AF may be sustained in patients’ atria, emphasizing heterogeneities in tissue excitability, slow-conducting channels and obstacles that are increasingly detectable in patients and should be the focus of future translational studies.

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“…Atrial fibrillation maps were used to diagnose sustained rotors or focal sources if observed on multiple epochs (1 min recording segments). The core regions of AF sources are spatially reproducible within precession areas of 2 cm 2 for tens of seconds 14 (i.e. bounded by two electrodes in each axis) with spiral arms that disorganize via fibrillatory conduction.…”

Section: Firm Atrial Fibrillation Mapping Detailsmentioning

confidence: 99%