Evaluation of Personalised Canine Electromechanical Models

International audienceCardiac modelling aims at understanding cardiac diseases and predicting cardiac responses to therapies. By generating the elec-trical propagation, the contraction and the mechanical response, we are able to simulate cardiac motion from non-invasive imaging techniques. Four healthy canine clinical data (left ventricles) were provided by the STACOM'2014 challenge. Our study is based on Bestel-Clement-Sorine mechanical modelling, while the electrophysiological phenomena is driven by an Eikonal model. Our model has been calibrated by a quantitative sensitivity study as well as a personalized automatic calibration. Results and comparison with clinical measures are shown in terms of left ventricular volume, flow, pressure and ejection fraction

Personal-by-design: a 3D Electromechanical Model of the Heart Tailored for Personalisation

International audienceIn this work we present a coupled electromechanical model of the heart for patient-specific simulations, and in particular cardiac resynchronisation therapy. To this end, we propose a fast fully autonomous and flexible pipeline to generate and optimise the data required to run the mechanical simulation. After the meshing of the biventricular segmentation image and the construction of the associated fibres arrangement, we compute the electrical potential propagation in the myocardial tissue from selected onset points on the endocardium. We generate a 12-lead electrocardiogram corresponding to the latter activation map by extrapolating the electrical potential on a virtual torso. This electrical activation is coupled to a mechanical model, featuring a small set of interpretable parameters. We also propose an efficient algorithm to optimise the model parameters, based on patient data. The whole pipeline including a cardiac cycle is computed in 30 minutes, enabling to use this digital twin for diagnosis and therapy planning

Coupled Personalisation of Electrophysiology Models for Simulation of Induced Ischemic Ventricular Tachycardia

International audienceDespite recent efforts in cardiac electrophysiology modelling, there is still a strong need to make macroscopic models usable in planning and assistance of the clinical procedures. This requires model personalisation i.e. estimation of patient-specific model parameters and computations compatible with clinical constraints. Fast macroscopic models allow a quick estimation of the tissue conductivity, but are often unreliable in prediction of arrhythmias. On the other side, complex biophysical models are quite expensive for the tissue conductivity estimation, but are well suited for arrhythmia predictions. Here we present a coupled personalisation framework, which combines the benefits of the two models. A fast Eikonal (EK) model is used to estimate the conductivity parameters, which are then used to set the parameters of a biophysical model, the Mitchell-Schaeffer (MS) model. Additional parameters related to Action Potential Duration (APD) and APD restitution curves for the tissue are estimated for the MS model. This framework is applied to a clinical dataset provided with an hybrid X-Ray/MR imaging on an ischemic patient. This personalised MS Model is then used for in silico simulation of clinical Ventricular Tachycardia (VT) stimulation protocol to predict the induction of VT. This proof of concept opens up possibilities of using VT induction modelling directly in the intervention room, in order to plan the radio-frequency ablation lines

Longitudinal Parameter Estimation in 3D Electromechanical Models: Application to Cardiovascular Changes in Digestion

International audienceComputer models of the heart are of increasing interest for clinical applications due to their discriminative and predictive abilities. However the number of simulation parameters in these models can be high and expert knowledge is required to properly design studies involving these models, and analyse the results. In particular it is important to know how the parameters vary in various clinical or physiological settings. In this paper we build a data-driven model of cardiovascular parameter evolution during digestion, from a clinical study involving more than 80 patients. We first present a method for longitudinal parameter estimation in 3D cardiac models, which we apply to 21 patient-specific hearts geometries at two instants of the study, for 6 parameters (two fixed and four time-varying parameters). From these personalised hearts, we then extract and validate a law which links the changes of cardiac output and heart rate under constant arterial pressure to the evolution of these parameters, thus enabling the fast simulation of hearts during digestion for future patients

Quantitative comparison of two cardiac electrophysiology models using personalisation to optical and MR data

International audienceIn order to translate the important modelling work into clinical tools, the selection of the best model for a given application is crucial. In this paper, we quantitatively compare personalisation of two different cardiac electrophysiology models on the same dataset, in order to help such a selection. One is a phenomenological model, the AlievPanfilov model (1996), and the other one is a simplified ionic model, the Mitchell-Schaeffer model (2003). In the preliminary steps of model personalisation, we optimise the forward problem with the determination of an optimum time integration scheme for each model, which could result in stable and accurate simulations without the use of unnecessary expensive high temporal and spatial resolutions. Next, we personalise the two models by optimising their respective parameters, to match the depolarisation and repolarisation maps obtained ex-vivo from optical imaging of large porcine healthy heart. Last, we compare the personalisation results of the two different model

Interactive real time simulation of cardiac radio-frequency ablation

Best Paper AwardInternational audienceVirtual reality based therapy simulation meets a growing interest from the medical community due to its potential impact for the training of medical residents and the planning of therapies. In this paper, we describe a prototype for rehearsing radio-frequency ablation of the myocardium in the context of cardiac arrhythmia. Our main focus has been on the real-time modeling of electrophysiology which is suitable for representing simple cases of arrhythmia (ectopic focus, ventricular tachycardia). To this end, we use an anisotropic multi-front fast marching method to simulate transmembrane potential propagation in cardiac tissues. The electric propagation is coupled with a pre-recorded beating heart model. Thanks to a 3D user interface, the user can interactively measure the local extracellular potential, pace locally the myocardium or simulate the burning of cardiac tissue as done in radiofrequency ablation interventions. To illustrate this work, we show the simulation of various arrhythmias cases built from patient specific medical images including the right and left ventricles, the fiber orientation and the location of ischemic regions

Anisotropic Fast-Marching on cartesian grids using Lattice Basis Reduction

We introduce a modification of the Fast Marching Algorithm, which solves the generalized eikonal equation associated to an arbitrary continuous riemannian metric, on a two or three dimensional domain. The algorithm has a logarithmic complexity in the maximum anisotropy ratio of the riemannian metric, which allows to handle extreme anisotropies for a reduced numerical cost. We prove the consistence of the algorithm, and illustrate its efficiency by numerical experiments. The algorithm relies on the computation at each grid point of a special system of coordinates: a reduced basis of the cartesian grid, with respect to the symmetric positive definite matrix encoding the desired anisotropy at this point.Comment: 28 pages, 12 figure

Patient-Specific Identification of Atrial Flutter Vulnerability–A Computational Approach to Reveal Latent Reentry Pathways

Atypical atrial flutter (AFlut) is a reentrant arrhythmia which patients frequently develop after ablation for atrial fibrillation (AF). Indeed, substrate modifications during AF ablation can increase the likelihood to develop AFlut and it is clinically not feasible to reliably and sensitively test if a patient is vulnerable to AFlut. Here, we present a novel method based on personalized computational models to identify pathways along which AFlut can be sustained in an individual patient. We build a personalized model of atrial excitation propagation considering the anatomy as well as the spatial distribution of anisotropic conduction velocity and repolarization characteristics based on a combination of a priori knowledge on the population level and information derived from measurements performed in the individual patient. The fast marching scheme is employed to compute activation times for stimuli from all parts of the atria. Potential flutter pathways are then identified by tracing loops from wave front collision sites and constricting them using a geometric snake approach under consideration of the heterogeneous wavelength condition. In this way, all pathways along which AFlut can be sustained are identified. Flutter pathways can be instantiated by using an eikonal-diffusion phase extrapolation approach and a dynamic multifront fast marching simulation. In these dynamic simulations, the initial pattern eventually turns into the one driven by the dominant pathway, which is the only pathway that can be observed clinically. We assessed the sensitivity of the flutter pathway maps with respect to conduction velocity and its anisotropy. Moreover, we demonstrate the application of tailored models considering disease-specific repolarization properties (healthy, AF-remodeled, potassium channel mutations) as well as applicabiltiy on a clinical dataset. Finally, we tested how AFlut vulnerability of these substrates is modulated by exemplary antiarrhythmic drugs (amiodarone, dronedarone). Our novel method allows to assess the vulnerability of an individual patient to develop AFlut based on the personal anatomical, electrophysiological, and pharmacological characteristics. In contrast to clinical electrophysiological studies, our computational approach provides the means to identify all possible AFlut pathways and not just the currently dominant one. This allows to consider all relevant AFlut pathways when tailoring clinical ablation therapy in order to reduce the development and recurrence of AFlut

Patient-Specific Identification of Atrial Flutter Vulnerability–A Computational Approach to Reveal Latent Reentry Pathways

Atypical atrial flutter (AFlut) is a reentrant arrhythmia which patients frequently develop after ablation for atrial fibrillation (AF). Indeed, substrate modifications during AF ablation can increase the likelihood to develop AFlut and it is clinically not feasible to reliably and sensitively test if a patient is vulnerable to AFlut. Here, we present a novel method based on personalized computational models to identify pathways along which AFlut can be sustained in an individual patient. We build a personalized model of atrial excitation propagation considering the anatomy as well as the spatial distribution of anisotropic conduction velocity and repolarization characteristics based on a combination of a priori knowledge on the population level and information derived from measurements performed in the individual patient. The fast marching scheme is employed to compute activation times for stimuli from all parts of the atria. Potential flutter pathways are then identified by tracing loops from wave front collision sites and constricting them using a geometric snake approach under consideration of the heterogeneous wavelength condition. In this way, all pathways along which AFlut can be sustained are identified. Flutter pathways can be instantiated by using an eikonal-diffusion phase extrapolation approach and a dynamic multifront fast marching simulation. In these dynamic simulations, the initial pattern eventually turns into the one driven by the dominant pathway, which is the only pathway that can be observed clinically. We assessed the sensitivity of the flutter pathway maps with respect to conduction velocity and its anisotropy. Moreover, we demonstrate the application of tailored models considering disease-specific repolarization properties (healthy, AF-remodeled, potassium channel mutations) as well as applicabiltiy on a clinical dataset. Finally, we tested how AFlut vulnerability of these substrates is modulated by exemplary antiarrhythmic drugs (amiodarone, dronedarone). Our novel method allows to assess the vulnerability of an individual patient to develop AFlut based on the personal anatomical, electrophysiological, and pharmacological characteristics. In contrast to clinical electrophysiological studies, our computational approach provides the means to identify all possible AFlut pathways and not just the currently dominant one. This allows to consider all relevant AFlut pathways when tailoring clinical ablation therapy in order to reduce the development and recurrence of AFlut