Structural contributions to fibrillatory rotors in a patient-derived computational model of the atria

Abstract

These model findings highlight the importance of structural features in rotor dynamics and suggest that regions of fibrosis may anchor fibrillatory rotors. Increasing extent of fibrosis and scar may eventually convert fibrillation to excitable gap reentry. Such macro-reentry can then be eliminated by extending the obstacle or by external stimuli that penetrate the excitable gap.

Three‐dimensional Integrated Functional, Structural, and Computational Mapping to Define the Structural “Fingerprints” of Heart‐Specific Atrial Fibrillation Drivers in Human Heart Ex Vivo

“…The computed atrial wall thickness in the left atrial appendage was found to be affected by the extremely complex and trabecular atrial anatomy,30 and thus wall thickness of the left atrial appendage was not reported. The atrial cellular activation model is based on a simplified Fenton‐Karma model, not biophysics‐based cellular models10, 12 for the sake of computational efficiency, although it was validated by optical mapping data in this study and widely used by us15, 27 and others 28. Additionally, because of a single uniform cellular model used across the atria in the computer model, APDs in some regions (eg, distal side of PV sleeves) may not match well between modeling and optical mapping.…”

“…In this study, we have adapted the simplified 3‐current Fenton‐Karma cellular activation models to recreate the optically recorded regional conduction velocities and action potential durations (APDs) in the PLA region from the same heart, which was then applied across both atria of the model (Figure 8). 15, 28 Atrial 3D geometry with a resolution of 180 μm 3 including accurate wall thickness, myofiber orientations, and transmural fibrosis, was integrated with the adapted cellular model into a 3D computer model. Electrical conductivities were set at an anisotropic ratio of 9:1, which led to ≈3:1 regional anisotropic ratio for conduction velocities along the long axis of the cell and allowed the proper reproduction of the experimentally mapped conduction velocities as utilized by previous atrial modeling studies 4, 15.…”

Myofiber Architecture of the Human Atria as Revealed by Submillimeter Diffusion Tensor Imaging

“…37,38 Accurate human atrial fiber orientation data are essential for the construction of computational models of the whole human atria, 14,39,40 and the need for it has been acknowledged in numerous studies. [41][42][43][44][45] The DTMRI results presented here provide unprecedented detail about fiber architecture that can easily be incorporated in atrial models by coregistration and morphing methodologies. 25,46 The presented set of the major bundles ( Figure 5) in combination with information about wall thickness and transmural distribution of fiber orientation could form the basis for an accurate mathematical reconstruction of atrial fiber architecture (ie, a rule-based approach, comprising of fiber orientation rules based on the present data), thus enabling atrial model construction from purely geometric data (eg, CT or MRI scans) of individual patient atria.…”

Influence of left atrial geometry on rotor core trajectories in a model of atrial fibrillation

“…Clinical studies [6] and human myocardium-based computational studies [7] suggest that rotors may be constrained temporarily or persistently in limited areas of the LA, because of discontinuities in the fibre architecture. In addition, human atria exhibit fibrosis and scar outside the pulmonary veins (PV) to a considerable degree, which may contribute to the initiation mechanisms for AF in many patients [8].…”

“…Until recently, the presence of rotors was only observed in animal experimental studies [3], but localized and stable rotors in human AF have now been identified [4,5]. This progress may increase the efficacy of targeted left atrial ablation therapy.Clinical studies [6] and human myocardium-based computational studies [7] suggest that rotors may be constrained temporarily or persistently in limited areas of the LA, because of discontinuities in the fibre architecture. In addition, human atria exhibit fibrosis and scar outside the pulmonary veins (PV) to a considerable degree, which may contribute to the initiation mechanisms for AF in many patients [8].…”