1,720,964 research outputs found
Diffuse fibrosis and repolarization disorders explain ventricular arrhythmias in Brugada syndrome: a computational study
Full text linkIn this work, we reported a computational study to quantitatively determine the individual contributions of three candidate arrhythmic factors associated with Brugada Syndrome. In particular, we focused our analysis on the role of structural abnormalities, dispersion of repolarization, and size of the diseased region. We developed a human phenomenological model capable of replicating the action potential characteristics both in Brugada Syndrome and in healthy conditions. Inspired by physiological observations, we employed the phenomenological model in a 2D geometry resembling the pathological RVOT coupled with healthy epicardial tissue. We assessed the insurgence of sustained reentry as a function of electrophysiological and structural abnormalities. Our computational study indicates that both structural and repolarization abnormalities are essential to induce sustained reentry. Furthermore, our results suggest that neither dispersion of repolarization nor structural abnormalities are sufficient on their own to induce sustained reentry. It should be noted how our study seems to explain an arrhythmic mechanism that unifies the classic repolarization and depolarization hypotheses of the pathophysiology of the Brugada Syndrome. Finally, we believe that this work may offer a new perspective on the computational and clinical investigation of Brugada Syndrome and its arrhythmic behaviour
A transmurally heterogeneous model of the ventricular tissue and its application for simulation of Brugada Syndrome
No full textWe present a transmurally heterogeneous phenomenological model of ventricular tissue that is designed to reproduce the most important features of action potential propagation of endocardial, midmyocardial, and epicardial tissue. Our model consists of only 3 variables and 20 parameters. Therefore, it is highly computational efficient and easy to fit to experimental data. We exploited our myocyte model to simulate action potential propagation in a 3D slab of cardiac tissue both in healthy conditions and in presence of Brugada syndrome. The results show that our model can accurately reproduce the transmural heterogeneity of the ventricular wall and the main characteristics of electrocardiographic pattern both in healthy and pathological conditions
A reaction-diffusion heart model for the closed-loop evaluation of heart-pacemaker interaction
Full text linkThe purpose of this manuscript is to develop a reaction-diffusion heart model for closed-loop evaluation of heart-pacemaker interaction, and to provide a hardware setup for the implementation of the closed-loop system. The heart model, implemented on a workstation, is based on the cardiac monodomain formulation and a phenomenological model of cardiac cells, which we fitted to the electrophysiological properties of the different cardiac tissues. We modelled the pacemaker as a timed automaton, deployed on an Arduino 2 board. The Arduino and the workstation communicate through a PCI acquisition board. Additionally, we developed a graphical user interface for easy handling of the framework. The myocyte model resembles the electrophysiological properties of atrial and ventricular tissue. The heart model reproduces healthy activation sequence and proved to be computationally efficient (i.e., 1 s simulation requires about 5 s). Furthermore, we successfully simulated the interaction between heart and pacemaker models in three well-known pathological contexts. Our results showed that the PDE formulation is appropriate for the simulation in closed-loop. While computationally more expensive, a PDE model is more flexible and allows to represent more complex scenarios than timed or hybrid automata. Furthermore, users can interact more easily with the framework thanks to the graphical representation of the spatiotemporal evolution of the membrane potentials. By representing the heart as a reaction-diffusion model, the proposed closed-loop system provides a novel and promising framework for the assessment of cardiac pacemakers
A smoothed boundary bidomain model for cardiac simulations in anatomically detailed geometries
Full text link: This manuscript presents a novel finite difference method to solve cardiac bidomain equations in anatomical models of the heart. The proposed method employs a smoothed boundary approach that represents the boundaries between the heart and the surrounding medium as a spatially diffuse interface of finite thickness. The bidomain boundary conditions are implicitly implemented in the smoothed boundary bidomain equations presented in the manuscript without the need of a structured mesh that explicitly tracks the heart-torso boundaries. We reported some significant examples assessing the method's accuracy using nontrivial test geometries and demonstrating the applicability of the method to complex anatomically detailed human cardiac geometries. In particular, we showed that our approach could be employed to simulate cardiac defibrillation in a human left ventricle comprising fiber architecture. The main advantage of the proposed method is the possibility of implementing bidomain boundary conditions directly on voxel structures, which makes it attractive for three dimensional, patient specific simulations based on medical images. Moreover, given the ease of implementation, we believe that the proposed method could provide an interesting and feasible alternative to finite element methods, and could find application in future cardiac research guiding electrotherapy with computational models
Low cardiac frequency associated with higher number of extrasistoles in a computational model of Brugada Syndrome
No full textBrugada Syndrome is a form of idiopathic ventricular fibrillation, to date there is no definitive theory about how ventricular fibrillation is initiated or its substrate. Starting from the clinical observation that cardiac episodes are more frequent at rest, we developed a model in order to study the effect of cardiac frequency on reentrant activity. Our results suggest that the combination of arrhythmic substrate and cardiac frequency has a role in the insurgence of cardiac arrhythmia
Incremental Pacing Induces Sustained Reentry in a Computational Model of Brugada Syndrome
No full textBrugada Syndrome is a form of idiopathic ventricular fibrillation. To date, there is no definitive theory about how ventricular fibrillation is initiated, or a consensus on its substrate. In this work, we report a computational study aimed at determining the role of the pacing protocol on the induction of sustained arrhythmias in Brugada Syndrome. We developed a computational model of Brugada Syndrome, including both structural and electrophysiological abnormalities in a slab of transmurally heterogeneous cardiac tissue. Starting from the clinical observation that cardiac episodes are more frequent at rest, we studied the effect of incremental pacing (i.e., with increasing pacing cycle length) on the generation of reentrant activity. Our results suggest that incremental pacing can unmask the arrhythmogenic substrate of Brugada Syndrome
A 3D Transmurally Heterogeneous Computational Model of the Brugada Syndrome Phenotype
No full textIn this work, we present a computational study of the Brugada Syndrome (BrS) phenotype aimed at investigating the main factors contributing to the development of arrhythmias. We developed a model that incorporated a BrS substrate within a region resembling the right ventricular outflow tract (RVOT) in a three-dimensional anisotropic ventricular cardiac tissue with transmural heterogeneity. Consistent with our previous two-dimensional study, our results confirmed the requirement of both electrophysiological alterations and structural abnormalities to trigger arrhythmic events. In particular, we found that the combination of electrophysiological alterations and structural abnormalities caused percolation in the tissue, eventually leading to sustained reentry. Moreover, our model is able to replicate the majority of epicardial electrogram features observed in the arrhythmic substrate of Brugada patients, furthermore, the behavior of our model agrees with clinical findings on BrS patients. We identified the density and size of structural abnormalities, the degree of myocyte electrophysiological alteration, and the size of the arrhythmic substrate as risk factors for the genesis of arrhythmias. These findings could be used in a model-based approach to develop processing techniques that highlight arrhythmogenic features in BrS patients’ recorded electrograms, improving risk stratification in patients
Electrophysiological patterns and structural substrates of Brugada syndrome: Critical appraisal and computational analyses
No full text: Brugada syndrome (BrS) is a cardiac electrophysiological disease with unknown etiology, associated with sudden cardiac death. Symptomatic patients are treated with implanted cardiac defibrillator, but no risk stratification strategy is effective in patients that are at low to medium arrhythmic risk. Cardiac computational modeling is an emerging tool that can be used to verify the hypotheses of pathogenesis and inspire new risk stratification strategies. However, to obtain reliable results computational models must be validated with consistent experimental data. We reviewed the main electrophysiological and structural variables from BrS clinical studies to assess which data could be used to validate a computational approach. Activation delay in the epicardial right ventricular outflow tract is a consistent finding, as well as increased fibrosis and subclinical alterations of right ventricular functional and morphological parameters. The comparison between other electrophysiological variables is hindered by methodological differences between studies, which we commented. We conclude by presenting a recent theory unifying electrophysiological and structural substrate in BrS and illustrate how computational modeling could help translation to risk stratification
Going Beyond Counting First Authors in Author Co-citation Analysis
Full text linkThe present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation
counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings
are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that
only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into
account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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