Search

AimsAtrial fibrillation (AF) wavefront dynamics are complex and difficult to interpret, contributing to uncertainty about the mechanisms that maintain AF. We aimed to investigate the interplay between rotors, wavelets, and focal sources during fibrillation.Methods and resultsArrhythmia wavefront dynamics were analysed for four optically mapped canine cholinergic AF preparations. A bilayer computer model was tuned to experimental preparations, and varied to have (i) fibrosis in both layers or the epicardium only, (ii) different spatial acetylcholine distributions, (iii) different intrinsic action potential duration between layers, and (iv) varied interlayer connectivity. Phase singularities (PSs) were identified and tracked over time to identify rotational drivers. New focal wavefronts were identified using phase contours. Phase singularity density and new wavefront locations were calculated during AF. There was a single dominant mechanism for sustaining AF in each of the preparations, either a rotational driver or repetitive new focal wavefronts. High-density PS sites existed preferentially around the pulmonary vein junctions. Three of the four preparations exhibited stable preferential sites of new wavefronts. Computational simulations predict that only a small number of connections are functionally important in sustaining AF, with new wavefront locations determined by the interplay between fibrosis distribution, acetylcholine concentration, and heterogeneity in repolarization within layers.Conclusion We were able to identify preferential sites of new wavefront initiation and rotational activity, in order to determine the mechanisms sustaining AF. Electrical measurements should be interpreted differently according to whether they are endocardial or epicardial recordings.

Atrial and ventricular fibrillation are complex arrhythmias, and their underlying mechanisms remain widely debated and incompletely understood. This is partly because the electrical signals recorded during myocardial fibrillation are themselves complex and difficult to interpret with simple analytical tools. There are currently a number of analytical approaches to handle fibrillation data. Some of these techniques focus on mapping putative drivers of myocardial fibrillation, such as dominant frequency, organizational index, Shannon entropy and phase mapping. Other techniques focus on mapping the underlying myocardial substrate sustaining fibrillation, such as voltage mapping and complex fractionated electrogram mapping. In this review, we discuss these techniques, their application and their limitations, with reference to our experimental and clinical data. We also describe novel tools including a new algorithm to map microreentrant circuits sustaining fibrillation., Highlights • Mechanism of atrial and ventricular fibrillation remains poorly understood. • Rotational drivers of fibrillation can be mapped using phase analysis. • Voltage mapping can identify fibrotic substrate of fibrillation. • Conduction delay algorithm identifies lines of conduction block at reentry core. • Substrate and driver mapping is limited by resolution of clinical data sets.

The understanding of the underlying mechanisms of the persistence of atrial fibrillation remains poor. Key to this is the relationship between structure - myocardial architecture, and function - electrical activity, and how these can be measured, interpreted and correlated clinically. We sought to address the hypothesis that the local electrogram morphology is determined by local atrial myocardial activation patterns, which are in turn determined by local atrial myocardial architecture. In addressing this hypothesis, we utilised improved techniques of atrial segmentation and detection of wall enhancements to more accurately delineate underlying de novo atrial myocardial fibrosis, with late-gadolinium enhanced cardiac magnetic resonance imaging (LGE- CMRI). Here, we demonstrated a predilection of native structural remodelling on the posterior left atrial wall. The electrophysiological changes underlying late-gadolinium enhancements were interrogated with high-density electroanatomic 3D mapping using a Kernel as a unit of measure, in the varying rhythms of AF, sinus and pacing, with drop in tissue voltages and conduction velocities in regions of fibrosis, but counter-intuitively, a higher extent of electrogram fractionation in healthy myocardium. We observed the rate and wavefront-activation dependency of voltage, emphasizing the importance of voltage maps being interpreted in the context of its rhythm. We have also described a novel technique of AF voltage mapping, with the metric of mean AF voltage sampled over 8 secs correlating well with LGE-CMRI defined fibrosis, and surprisingly better than that of sinus rhythm voltage suggesting that this metric may be more representative of the underlying atrial substrate. Lastly, reverse translational cell monolayer experiments in novel co-cultured neonatal ventricular rat myocytes and fibroblasts were carried out to corroborate clinical in vivo observations under the control of the basic science laboratory. These emphasized the contributions of the structural and functional changes to electrogram morphology (voltage and fractionation). The contact electrogram is the result of a complex dynamic functional electrophysiology, and its interactions with the underlying atrial myocardium. This increased understanding of structure and function (electroarchitecture) provides mechanistic insights essential if we are to progress beyond the current empiricism of catheter ablation strategies of persistent AF. Open Access