Competitive Drivers of Atrial Fibrillation: The Interplay Between Focal Drivers and Multiwavelet Reentry.

Richard T Carrick,Peter S Spector,Oliver R J Bates,Bryce E Benson

doi:10.3389/fphys.2021.633643

Richard T Carrick, Peter S Spector + Show 2 more

Open Access

https://doi.org/10.3389/fphys.2021.633643

Copy DOI

Abstract

BackgroundThere is debate whether human atrial fibrillation is driven by focal drivers or multiwavelet reentry. We propose that the changing activation sequences surrounding a focal driver can at times self-sustain in the absence of that driver. Further, the relationship between focal drivers and surrounding chaotic activation is bidirectional; focal drivers can generate chaotic activation, which may affect the dynamics of focal drivers.Methods and ResultsIn a propagation model, we generated tissues that support structural micro-reentry and moving functional reentrant circuits. We qualitatively assessed (1) the tissue’s ability to support self-sustaining fibrillation after elimination of the focal driver, (2) the impact that structural-reentrant substrate has on the duration of fibrillation, the impact that micro-reentrant (3) frequency, (4) excitable gap, and (5) exposure to surrounding fibrillation have on micro-reentry in the setting of chaotic activation, and finally the likelihood fibrillation will end in structural reentry based on (6) the distance between and (7) the relative lengths of an ablated tissue’s inner and outer boundaries. We found (1) focal drivers produced chaotic activation when waves encountered heterogeneous refractoriness; chaotic activation could then repeatedly initiate and terminate micro-reentry. Perpetuation of fibrillation following elimination of micro-reentry was predicted by tissue properties. (2) Duration of fibrillation was increased by the presence of a structural micro-reentrant substrate only when surrounding tissue had a low propensity to support self-sustaining chaotic activation. Likelihood of micro-reentry around the structural reentrant substrate increased as (3) the frequency of structural reentry increased relative to the frequency of fibrillation in the surrounding tissue, (4) the excitable gap of micro-reentry increased, and (5) the exposure of the structural circuit to the surrounding tissue decreased. Likelihood of organized tachycardia following termination of fibrillation increased with (6) decreasing distance and (7) disparity of size between focal obstacle and external boundary.ConclusionFocal drivers such as structural micro-reentry and the chaotic activation they produce are continuously interacting with one another. In order to accurately describe cardiac tissue’s propensity to support fibrillation, the relative characteristics of both stationary and moving drivers must be taken into account.

Highlights

MATERIALS AND METHODSWhen the cardiac arrhythmia atrial fibrillation was first identified more than 100 years ago (McMichael, 1982; Silverman, 1994; Flegel, 1995), it was defined in descriptive terms as an atrial rhythm with a perpetually changing pattern of activation (Lip and Beevers, 1995; Nattel et al, 2002)
It is generally tacitly assumed that this, “fibrillatory conduction” (FC), is a purely passive phenomenon; i.e., FC would cease in the absence of a focal driver
We examine structural micro-reentry as a focal driver of fibrillation and use a computational model of propagation to qualitatively study the ability of chaotic activation to sustain after driver elimination, the interactions between these chaotically propagating waves and the spatially fixed structural reentrant substrate, and the impact that these interactions have on the overall duration of fibrillation

Summary

Introduction

MATERIALS AND METHODSWhen the cardiac arrhythmia atrial fibrillation was first identified more than 100 years ago (McMichael, 1982; Silverman, 1994; Flegel, 1995), it was defined in descriptive terms as an atrial rhythm with a perpetually changing pattern of activation (Lip and Beevers, 1995; Nattel et al, 2002). In the FD hypothesis, a stationary driver (e.g., focal rotor) generates waves that propagate to the surrounding tissue in a non-uniform fashion (Scherf et al, 1948; Allessie et al, 1977; Fareh et al, 1998; Ogawa et al, 2002; Oliveira et al, 2007; Narayan et al, 2012). This changing activation confers the irregularity that is emblematic of fibrillation. The relationship between focal drivers and surrounding chaotic activation is bidirectional; focal drivers can generate chaotic activation, which may affect the dynamics of focal drivers

Results

Discussion

Conclusion