Cardiac Electrical Propagation Research Articles

Vector Field Heterogeneity (VFH) as a novel quantitative marker of electrical disarray in Arrhythmogenic CardioMyopathy (ACM) with ventricular tachycardia

Abstract Background ACM is a hereditary condition characterized by fibrofatty infiltration and replacement of cardiac myocytes predominantly presenting with ventricular arrhythmias (VA). Cardiac imaging allows for detailed structural phenotyping of scar patterns in ACM. Yet, there is a lack of tools to objectively quantify the electrical substrate alterations that may enable a more precise identification of critical sites that predispose to VA. Purpose To quantify locally disorganized cardiac electrical propagation wavefronts using the Vector Field Heterogeneity (VFH) metric from high-density multi-electrodes in patients with ACM with VT and compare to healthy controls. Methods High density epicardial substrate maps acquired with a 16-pole grid catheter during SR or RV pacing in patients with ACM with VA, who underwent clinically indicated catheter ablation, were retrospectively reviewed. Patients with structurally normal heart and idiopathic VA with epicardial ablation were analysed as a control group. Unipolar contact mapping data was exported & processed offline. From the 4×4 electrode array EGMs, vector maps of the directions of electrical propagation for recorded sites were computed. The VFH was then computed as a quantitative measure of local heterogeneity of propagation, with higher VFH expected to correlate with sites of (micro)structural tissue alterations. VFH was compared between ACM and control patients as well as at sites of normal, border zone & scar based on omnipolar voltage in ACM patients (>1.5mV, 0.5mV–1.5mV, <0.5mV, respectively). Results 10 patients with ACM (70% male, aged 52 ±18 years, ARVC 70%, biventricular 30%, RVEF 40.7±4.7%, LVEF 66±12%) and 2 patients with structurally normal heart (female, 38 & 61 years) were included. Epicardial maps had an average of 9258 ±5412 EGM points. Median VFH was statistically significantly higher in the ACM cohort compared to control for global maps (0.33±0.33 vs 0.13±0.22, p<0.001) and at sites with voltage >1.5mV (i.e. greater disorganization in ACM, p<0.001). In ACM, assessment of VFH according to omnipolar voltage sites (as a surrogate of scar) showed a quantifiable statistically significant increase in electrical disorganized propagation at sites of lower voltage (<0.5mV, median VFH 0.53±0.36) compared to borderzone (0.5-1.5mV, VFH 0.29±0.41) and normal voltage (>1.5mV, VFH 0.15±0.26), p <0.001 respectively. Conclusion Heterogenous electrical propagation as quantified by VFH is significantly increased in patients with ACM at sites of scar, but importantly also in areas of normal voltages when compared to non-ACM controls, possibly indicating microstructural alterations that are missed in traditional assessments of the arrhythmogenic substrate. Identifying and quantifying disorganized conduction patterns by VFH is a promising new mapping approach that could allow improved substrate characterization. Its diagnostic value to guide ablation therapy is currently being validated.VFH Metric ACM and ControlVFH Map Examples

Vector Field Heterogeneity for the Assessment of Locally Disorganised Cardiac Electrical Propagation Wavefronts From High-Density Multielectrodes.

High-density multielectrode catheters are becoming increasingly popular in cardiac electrophysiology for advanced characterisation of the cardiac tissue, due to their potential to identify impaired sites. These are often characterised by abnormal electrical conduction, which may cause locally disorganised propagation wavefronts. To quantify it, a novel heterogeneity parameter based on vector field analysis is proposed, utilising finite differences to measure direction changes between adjacent cliques. The proposed Vector Field Heterogeneity metric has been evaluated on a set of simulations with controlled levels of organisation in vector maps, and a variety of grid sizes. Furthermore, it has been tested on animal experimental models of isolated Langendorff-perfused rabbit hearts. The proposed parameter exhibited superior capturing ability of heterogeneous propagation wavefronts compared to the classical Spatial Inhomogeneity Index, and simulations proved that the metric effectively captures gradual increments in disorganisation in propagation patterns. Notably, it yielded robust and consistent outcomes for [Formula: see text] grid sizes, underscoring its suitability for the latest generation of orientation-independent cardiac catheters.

Relative acceleration of orthonormal basis vectors for the geometric conduction blocks of the cardiac electric signal propagation on anisotropic curved surfaces

Geometric conduction blocks stop cardiac electric propagation due to the shape or conductivity properties of the domain. The blocks are considered to cause many abnormal cardiac electric propagations, leading to cardiac electrophysiological pathologies, such as cardiac fibrillation and arrhythmia. Locating such multidimensional conduction blocks is challenging, particularly in a complex domain with a complex shape and strong anisotropy, such as the heart. To address this problem, we propose a novel mathematical model of the geometric conduction block using the relative acceleration adopted from space-time physics. An efficient numerical scheme for the mathematical model is also proposed to predict the unidirectional conduction block effectively, even in a complex domain. The relative acceleration in the cardiac electric propagation corresponds to the sink-source relationship between the excited (after repolarization) and excitable (before depolarization) cardiac cells, representing the geometric growth rate of the volume of metric balls. The trajectory is constructed from the wavefront of diffusion-reaction equations by aligning orthonormal basis vectors along the gradient of the action potential. Relative acceleration is computed along the propagational direction from the connection 1-form of the basis vectors. The proposed mathematical model and numerical scheme are applied to demonstrate geometric conduction blocks in two-dimensional (2D) simple curved domains with strong anisotropy.

Subcellular diversity of Nav1.5 in cardiomyocytes: distinct functions, mechanisms and targets.

In cardiomyocytes, the rapid depolarisation of the membrane potential is mediated by the α-subunit of the cardiac voltage-gated Na+ channel (NaV 1.5), encoded by the gene SCN5A. This ion channel allows positively charged Na+ ions to enter the cardiomyocyte, resulting in the fast upstroke of the action potential and is therefore crucial for cardiac excitability and electrical propagation. This essential role is underscored by the fact that dysfunctional NaV 1.5 is associated with high risk for arrhythmias and sudden cardiac death. However, development of therapeutic interventions regulating NaV 1.5has been limited due to the complexity of NaV 1.5structure and function and its diverse roles within the cardiomyocyte. In particular, research from the last decade has provided us with increased knowledge on the subcellular distribution of NaV 1.5 as well as the proteins which it interacts with in distinct cardiomyocyte microdomains. We here review these insights, detailing the potential role of NaV 1.5 within subcellular domains as well as its dysfunction in the setting of arrhythmia disorders. We furthermore provide an overview of current knowledge on the pathways involved in (microdomain-specific) trafficking of NaV 1.5, and their potential as novel targets. Unravelling the complexity of NaV 1.5 (dys)function may ultimately facilitate the development of therapeutic strategies aimed at preventing lethal arrhythmias. This is not only of importance for pathophysiological conditions where sodium current is specifically decreased within certain subcellular regions, such as in arrhythmogenic cardiomyopathy and Duchenne muscular dystrophy, but also for other acquired and inherited disorders associated with NaV 1.5.

Physics-constrained deep active learning for spatiotemporal modeling of cardiac electrodynamics

The development of computational modeling and simulation have immensely benefited the study of cardiac disease mechanisms and facilitated the optimal disease diagnosis and treatment design. The dynamic propagation of cardiac electrical signals are often described by electrophysiological models in the form of partial differential equations (PDEs), which are commonly solved by the finite element method (FEM). However, FEM-based simulation only provides the numerical solution of the PDEs and is incapable of incorporating real clinical measurements into the modeling for optimal decision making. Additionally, electrical signals from the heart are commonly collected through cardiac catheterization, which acquires cardiac signals from limited spatial locations. Such sparse sensor measurements significantly challenge traditional machine learning methods for reliable predictive modeling. This paper presents a physics-constrained deep active learning (P-DAL) framework to model spatiotemporal cardiac electrodynamics. Specifically, we adapt the physics-constrained deep learning (P-DL) framework developed in our prior work to integrate the physical laws of the cardiac electrical wave propagation with deep learning for robust predictive modeling of the heart electrical behavior from sparse sensor measurements. Furthermore, we develop a novel active learning strategy to seek the informative spatial locations on the heart surface for data collection to further increase the predictive power of the P-DL method. This active learning criterion combines both the prediction uncertainty of the P-DL and the space-filling design over the heart geometry. We evaluate the performance of the proposed framework to model cardiac electrodynamics in both healthy and diseased heart systems. Numerical results show that the proposed P-DL approach significantly outperforms traditional modeling methods. Specifically, P-DL achieves up to 48.3% and 28.0% reduction in the estimated Relative Error (RE) compared with that from the traditional spatiotemporal Gaussian process (STGP) models in the healthy and diseased systems, respectively. We also demonstrate the efficacy of the proposed active learning procedure by comparing it with traditional learning strategies. Specifically, RE generated from the proposed P-DAL achieves 16.3% and 28.0% (11.1% and 21.2%) reduction compared with RE generated from the P-DL method based on pure space-filling design (i.e., P-DSL) and random data sampling strategy (P-DRL) in the healthy (diseased) heart system, respectively.

Coupling between cardiac cells-An important determinant of electrical impulse propagation and arrhythmogenesis.

Cardiac arrhythmias are an important cause of sudden cardiac death-a devastating manifestation of many underlying causes, such as heart failure and ischemic heart disease leading to ventricular tachyarrhythmias and ventricular fibrillation, and atrial fibrillation causing cerebral embolism. Cardiac electrical propagation is a main factor in the initiation and maintenance of cardiac arrhythmias. In the heart, gap junctions are the basic unit at the cellular level that host intercellular low-resistance channels for the diffusion of ions and small regulatory molecules. The dual voltage clamp technique enabled the direct measurement of electrical conductance between cells and recording of single gap junction channel openings. The rapid turnover of gap junction channels at the intercalated disk implicates a highly dynamic process of trafficking and internalization of gap junction connexons. Recently, non-canonical roles of gap junction proteins have been discovered in mitochondria function, cytoskeletal organization, trafficking, and cardiac rescue. At the tissue level, we explain the concepts of linear propagation and safety factor based on the model of linear cellular structure. Working myocardium is adequately represented as a discontinuous cellular network characterized by cellular anisotropy and connective tissue heterogeneity. Electrical propagation in discontinuous cellular networks reflects an interplay of three main factors: cell-to-cell electrical coupling, flow of electrical charge through the ion channels, and the microscopic tissue structure. This review provides a state-of-the-art update of the cardiac gap junction channels and their role in cardiac electrical impulse propagation and highlights a combined approach of genetics, cell biology, and physics in modern cardiac electrophysiology.

High-Capacity Cardiac Signal Acquisition System for Flexible, Simultaneous, Multidomain Acquisition.

Capturing cardiac electrical propagation or electrocardiographic images demands simultaneous, multidomain recordings of electrocardiographic signals with adequate spatial and temporal resolution. Available systems can be cost-prohibitive or lack the necessary flexibility to capture signals from the heart and torso. We have designed and constructed a system that leverages affordable commercial products (Intantech, CA, USA) to create a complete, cardiac signal acquisition system that includes a flexible front end, analog signal conditioning, and defibrillation protection. The design specifications for this project were to (1) record up to 1024 channels simultaneously at a minimum of 1 kHz, (2) capture signals within the range of ± 30 mV with a resolution of 1 μV, and (3) provide a flexible interface for custom electrode inputs.We integrated the Intantech A/D conversion circuits to create a novel system, which meets all the required specifications. The system connects to a standard laptop computer under control of open-source software (Intantech). To test the system, we recorded electrograms from within the myocardium, on the heart surface, and on the body surface simultaneously from a porcine experimental preparation. Noise levels were comparable to both our existing, custom acquisition system and a commercial competitor. The cost per channel was $32 USD, totaling $33,800 USD for a complete system.

Spontaneous activation under atrial fibrosis: A model using complex order derivatives

The computational modeling of the cardiac electrophysiology allows assertive and quantitative study of the atrial fibrosis under fibrillation conditions. The cardiac electrical propagation is described by the so-called monodomain model, that consists of a nonlinear parabolic reaction-diffusion equation. Fibroblast proliferation, which is an essential component of the fibrotic process, can be modeled by considering the membrane ionic kinetics as a reactive component. However, such a mathematical description does not account the structural feature of fibroblasts. In this work, the electrophysiological properties of fibroblast proliferation and coupling with cardiomyocytes are investigated, using mathematical and computational modelling. The study is focused on the conditions under which spontaneous activations occur in a fibrotic domain. The proposed fibrosis model takes account the electrical and structural interactions of fibroblasts within the myocardium. The electrical component is described through an ionic kinetics formalism, while the structural component is obtained by means of a triplet of complex order derivatives that constructs the diffusion operator. A theoretical analysis determines the model parameters that generate unstable solutions, and numerical simulations illustrate and validate the analytical outcomes. The results evince a strong modulation of the stability conditions of the fibrotic model by the real and imaginary part of the fractional derivative order. The fibrosis structural complexity, controlled by the fractional order, determines the extent of the parameter space that generates spontaneous activation. Moreover, not all the unstable parameter configurations generate electrical propagation. In the cases of electrical conduction after spontaneous activation, the conduction velocity in the fibrotic domain is significantly slower than the one observed in healthy atrial tissue. The results give a new perspective for the development of atrial fibrosis models including the ectopic activity as an initiation factor for fibrillation activity. Indeed, the proposed design exploits the complex order fractional derivatives, to generate a wide set of electrophysiological scenarios.

The radial point interpolation mixed collocation method for the solution of transient diffusion problems

The Radial Point Interpolation Mixed Collocation (RPIMC) method is proposed in this paper for transient analysis of diffusion problems. RPIMC is an efficient purely meshfree method where the solution of the field variable is obtained through collocation. The field function and its gradient are both interpolated (mixed collocation approach) leading to reduced C-continuity requirement compared to strong-form collocation schemes. The accuracy of RPIMC was evaluated in heat conduction benchmark problems and compared against the Meshless Local Petrov–Galerkin Mixed Collocation (MLPG-MC) method and the Finite Element Method (FEM). These three methods were subsequently applied to solve electrical propagation in a cardiac tissue slab and a biventricular geometry. In benchmark problems, RPIMC achieved high accuracy, of the same order as FEM, and always higher than MLPG-MC due to the delta Kronecker property of RPIMC. In solving cardiac electrical propagation, RPIMC rendered activation time maps similar to those of FEM, with an improved performance compared to MLPG-MC. As a conclusion, RPIMC is shown to be a promising meshfree alternative to FEM for transient diffusion problems.

A COMPLEX ORDER MODEL OF ATRIAL ELECTRICAL PROPAGATION FROM FRACTAL POROUS CELL MEMBRANE

Cardiac tissue is characterized by structural and cellular heterogeneities that play an important role in the cardiac conduction system. Under persistent atrial fibrillation (persAF), electrical and structural remodeling occur simultaneously. The classical mathematical models of cardiac electrophysiological showed remarkable progress during recent years. Among those models, it is of relevance the standard diffusion mathematical equation, that considers the myocardium as a continuum. However, the modeling of structural properties and their influence on electrical propagation still reveal several limitations. In this paper, a model of cardiac electrical propagation is proposed based on complex order derivatives. By assuming that the myocardium has an underlying fractal process, the complex order dynamics emerges as an important modeling option. In this perspective, the real part of the order corresponds to the fractal dimension, while the imaginary part represents the log-periodic corrections of the fractal dimension. Indeed, the imaginary part in the derivative implies characteristic scales within the cardiac tissue. The analytical and numerical procedures for solving the related equation are presented. The sinus rhythm and persAF conditions are implemented using the Courtemanche formalism. The electrophysiological properties are measured and analyzed on different scales of observation. The results indicate that the complex order modulates the electrophysiology of the atrial system, through the variation of its real and imaginary parts. The combined effect of the two components yields a broad range of electrophysiological conditions. Therefore, the proposed model can be a useful tool for modeling electrical and structural properties during cardiac conduction.

Simplified Modeling and Mathematical Analysis in Cardiac Electric Field Propagation for Human and Animals

The different characteristics of cardiac electric field (CEF) radiation in humans and other animals are presented in this paper. Physical modeling and mathematical analysis are developed to comprehensively unveil the properties of CEF, based on typical heartbeat waveforms. Our numerical simulation results demonstrate that the frequency bandwidths and the cycle durations of CEF are different for healthy humans versus humans on the verge of death and for humans versus other animals. The results indicate that the present study may extensively contribute towards recognizing human beings or other animal targets quickly and accurately with CEF in dangerous situations or in other applications.

One-dimensional reaction-diffusion dynamics in spatially bounded domains

Abstract We consider the complex dynamics arising in a one-dimensional advection-reaction-diffusion system along with its bistable cubic variant. In both cases, we analyze the dynamics in a bounded domain, assuming, first, Robin, and then periodic boundaries. We study the stability of the solutions obtained and suggest eventual implications in the experimental study of chemical waves as well as in a simplified description of cardiac electric signal propagation.

AMPK-mediated degradation of Nav1.5 through autophagy.

The voltage-gated cardiac sodium channel, Nav1.5, is the key component that controls cardiac excitative electrical impulse and propagation. However, the dynamic alterations of Nav1.5 during cardiac ischemia and reperfusion (I/R) are seldom reported. We found that the protein levels of rat cardiac Nav1.5 were significantly decreased in response to cardiac I/R injury. By simulating I/R injury in cells through activating AMPK by glucose deprivation, AMPK activator treatment, or hypoxia and reoxygenation (H/R), we found that Nav1.5 was down-regulated by AMPK-mediated autophagic degradation. Furthermore, AMPK was found to phosphorylate Nav1.5 at threonine (T) 101, which then regulates the interaction between Nav1.5 and the autophagic adaptor protein, microtubule-associated protein 1 light chain 3 (LC3), by exposing the LC3-interacting region adjacent to T101 in Nav1.5. This study highlights an instrumental role of AMPK in mediating the autophagic degradation of Nav1.5 during cardiac I/R injury.-Liu, X., Chen, Z., Han, Z., Liu, Y., Wu, X., Peng, Y., Di, W., Lan, R., Sun, B., Xu, B., Xu, W. AMPK-mediated degradation of Nav1.5 through autophagy.

Short-term effects of fine particulate matter and ozone on the cardiac conduction system in patients undergoing cardiac catheterization

BackgroundAir pollution-induced changes in cardiac electrophysiological properties could be a pathway linking air pollution and cardiovascular events. The evidence of air pollution effects on the cardiac conduction system is incomplete yet. We investigated short-term effects of particulate matter ≤ 2.5 μm in aerodynamic diameter (PM2.5) and ozone (O3) on cardiac electrical impulse propagation and repolarization as recorded in surface electrocardiograms (ECG).MethodsWe analyzed repeated 12-lead ECG measurements performed on 5,332 patients between 2001 and 2012. The participants came from the Duke CATHGEN Study who underwent cardiac catheterization and resided in North Carolina, United States (NC, U.S.). Daily concentrations of PM2.5 and O3 at each participant’s home address were predicted with a hybrid air quality exposure model. We used generalized additive mixed models to investigate the associations of PM2.5 and O3 with the PR interval, QRS interval, heart rate-corrected QT interval (QTc), and heart rate (HR). The temporal lag structures of the associations were examined using distributed-lag models.ResultsElevated PM2.5 and O3 were associated with four-day lagged lengthening of the PR and QRS intervals, and with one-day lagged increases in HR. We observed immediate effects on the lengthening of the QTc interval for both PM2.5 and O3, as well as delayed effects for PM2.5 (lagged by 3 – 4 days). The associations of PM2.5 and O3 with the PR interval and the association of O3 with the QRS interval persisted until up to seven days after exposure.ConclusionsIn patients undergoing cardiac catheterization, short-term exposure to air pollution was associated with increased HR and delays in atrioventricular conduction, ventricular depolarization and repolarization.

Injectable OPF/graphene oxide hydrogels provide mechanical support and enhance cell electrical signaling after implantation into myocardial infarct.

After myocardial infarction (MI), the scar tissue contributes to ventricular dysfunction by electrically uncoupling viable cardiomyocytes in the infarct region. Injection of a conductive hydrogel could not only provide mechanical support to the infarcted region, but also synchronize contraction and restore ventricular function by electrically connecting isolated cardiomyocytes to intact tissue.Methods: We created a conductive hydrogel by introducing graphene oxide (GO) nanoparticles into oligo(poly(ethylene glycol) fumarate) (OPF) hydrogels. The hydrogels were characterized by AFM and electrochemistry workstation. A rat model of myocardial infarction was used to investigate the ability of OPF/GO to improve cardiac electrical propagation in the injured heart in vivo. Echocardiography (ECHO) was used to evaluate heart function 4 weeks after MI. Ca2+ imaging was used to visualize beating cardiomyocytes (CMs). Immunofluorescence staining was used to visualize the expression of cardiac-specific markers.Results: OPF/GO hydrogels had semiconductive properties that were lacking in pure OPF. In addition, the incorporation of GO into OPF hydrogels could improve cell attachment in vitro. Injection of OPF/GO 4 weeks after myocardial infarction in rats enhanced the Ca2+ signal conduction of cardiomyocytes in the infarcted region in comparison with PBS or OPF alone. Moreover, the injection of OPF/GO hydrogel into the infarct region enhanced the generation of cytoskeletal structure and intercalated disc assembly. Echocardiography analysis showed improvement in load-dependent ejection fraction/fractional shortening of heart function 4 weeks after injection.Conclusions: We prepared a conductive hydrogel (OPF/GO) that provide mechanical support and biological conduction in vitro and in vivo. We found that injected OPF/GO hydrogels can provide mechanical support and electric connection between healthy myocardium and the cardiomyocytes in the scar via activating the canonical Wnt signal pathway, thus upregulating the generation of Cx43 and gap junction associated proteins. Injection of OPF/GO hydrogel maintained better heart function after myocardial infarction than the injection of a nonconductive polymer.

Polypyrrole-chitosan conductive biomaterial synchronizes cardiomyocyte contraction and improves myocardial electrical impulse propagation.

Background: The post-myocardial infarction (MI) scar interrupts electrical impulse propagation and delays regional contraction, which contributes to ventricular dysfunction. We investigated the potential of an injectable conductive biomaterial to restore scar tissue conductivity and re-establish synchronous ventricular contraction.Methods: A conductive biomaterial was generated by conjugating conductive polypyrrole (PPY) onto chitosan (CHI) backbones. Trypan blue staining of neonatal rat cardiomyocytes (CMs) cultured on biomaterials was used to evaluate the biocompatibility of the conductive biomaterials. Ca2+ imaging was used to visualize beating CMs. A cryoablation injury rat model was used to investigate the ability of PPY:CHI to improve cardiac electrical propagation in the injured heart in vivo. Electromyography was used to evaluate conductivity of scar tissue ex vivo.Results: Cell survival and morphology were similar between cells cultured on biomaterials-coated and uncoated-control dishes. PPY:CHI established synchronous contraction of two distinct clusters of spontaneously-beating CMs. Intramyocardial PPY:CHI injection into the cryoablation-induced injured region improved electrical impulse propagation across the scarred tissue and decreased the QRS interval, whereas saline- or CHI-injected hearts continued to have delayed propagation patterns and significantly reduced conduction velocity compared to healthy controls. Ex vivo evaluation found that scar tissue from PPY:CHI-treated rat hearts had higher signal amplitude compared to those from saline- or CHI-treated rat heart tissue.Conclusions: The PPY:CHI biomaterial is electrically conductive, biocompatible and injectable. It improved synchronous contraction between physically separated beating CM clusters in vitro. Intra-myocardial injection of PPY:CHI following cardiac injury improved electrical impulse propagation of scar tissue in vivo.

A composite visualization method for electrophysiology-morphous merging of human heart

BackgroundElectrophysiological behavior is of great importance for analyzing the cardiac functional mechanism under cardiac physiological and pathological condition. Due to the complexity of cardiac structure and biophysiological function, visualization of a cardiac electrophysiological model compositively is still a challenge. The lack of either modality of the whole organ structure or cardiac electrophysiological behaviors makes analysis of the intricate mechanisms of cardiac dynamic function a difficult task. This study aims at exploring 3D conduction of stimulus and electrical excitation reactivity on the level of organ with the authentic fine cardiac anatomy structure.MethodsIn this paper, a cardiac electrical excitation propagation model is established based on the human cardiac cross-sectional data to explore detailed cardiac electrical activities. A novel biophysical merging visualization method is then presented for biophysical integration of cardiac anatomy and electrophysiological properties in the form of the merging optical model, which provides the corresponding position, spatial relationship and the whole process in 3D space with the context of anatomical structure for representing the biophysical detailed electrophysiological activity.ResultsThe visualization result present the action potential propagation of the left ventricle within the excitation cycle with the authentic fine cardiac organ anatomy. In the visualized images, all vital organs are identified and distinguished without ambiguity. The three dimensional spatial position, relation and the process of cardiac excitation conduction and re-entry propagation in the anatomical structure during the phase of depolarization and repolarization is also shown in the result images, which exhibits the performance of a more detailed biophysical understanding of the electrophysiological kinetics of human heart in vivo.ConclusionsResults suggest that the proposed merging optical model can merge cardiac electrophysiological activity with the anatomy structure. By specifying the respective opacity for the cardiac anatomy structure and the electrophysiological model in the merging attenuation function, the visualized images can provide an in-depth insight into the biophysical detailed cardiac functioning phenomena and the corresponding electrophysiological behavior mechanism, which is helpful for further speculating cardiac physiological and pathological responses and is fundamental to the cardiac research and clinical diagnoses.

Spiral wave classification using normalized compression distance: Towards atrial tissue spatiotemporal electrophysiological behavior characterization.

Analysis of electrical activation patterns such as re-entries during atrial fibrillation (Afib) is crucial in understanding arrhythmic mechanisms and assessment of diagnostic measures. Spiral waves are a phenomena that provide intuitive basis for re-entries occurring in cardiac tissue. Distinct spiral wave behaviors such as stable spiral waves, meandering spiral waves, and spiral wave break-up may have distinct electrogram manifestations on a mapping catheter. Hence, it is desirable to have an automated classification of spiral wave behavior based on catheter recordings for a qualitative characterization of spatiotemporal electrophysiological activity on atrial tissue. In this study, we propose a method for classification of spatiotemporal characteristics of simulated atrial activation patterns in terms of distinct spiral wave behaviors during Afib using two different techniques: normalized compressed distance (NCD) and normalized FFT (NFFTD). We use a phenomenological model for cardiac electrical propagation to produce various simulated spiral wave behaviors on a 2D grid and labeled them as stable, meandering, or breakup. By mimicking commonly used catheter types, a star shaped and a circular shaped both of which do the local readings from atrial wall, monopolar and bipolar intracardiac electrograms are simulated. Virtual catheters are positioned at different locations on the grid. The classification performance for different catheter locations, types and for monopolar or bipolar readings were also compared. We observed that the performance for each case differed slightly. However, we found that NCD performance is superior to NFFTD. Through the simulation study, we showed the theoretical validation of the proposed method. Our findings suggest that a qualitative wavefront activation pattern can be assessed during Afib without the need for highly invasive mapping techniques such as multisite simultaneous electrogram recordings.

Control of cardiac alternans in an electromechanical model of cardiac tissue

Electrical alternations in cardiac action potential duration have been shown to be a precursor to arrhythmias and sudden cardiac death. Through the mechanism of excitation–contraction coupling, the presence of electrical alternans induces alternations in the heart muscle contractile activity. Also, contraction of cardiac tissue affects the process of cardiac electric wave propagation through the mechanism of the so-called mechanoelectrical feedback. Electrical excitation and contraction of cardiac tissue can be linked by an electromechanical model such as the Nash–Panfilov model. In this work, we explore the feasibility of suppressing cardiac alternans in the Nash-Panfilov model which is employed for small and large deformations. Several electrical pacing and mechanical perturbation feedback strategies are considered to demonstrate successful suppression of alternans on a one-dimensional cable. This is the first attempt to combine electrophysiologically relevant cardiac models of electrical wave propagation and contractility of cardiac tissue in a synergistic effort to suppress cardiac alternans. Numerical examples are provided to illustrate the feasibility and the effects of the proposed algorithms to suppress cardiac alternans.

Fractional diffusion models of cardiac electrical propagation: role of structural heterogeneity in dispersion of repolarization.

Impulse propagation in biological tissues is known to be modulated by structural heterogeneity. In cardiac muscle, improved understanding on how this heterogeneity influences electrical spread is key to advancing our interpretation of dispersion of repolarization. We propose fractional diffusion models as a novel mathematical description of structurally heterogeneous excitable media, as a means of representing the modulation of the total electric field by the secondary electrical sources associated with tissue inhomogeneities. Our results, analysed against in vivo human recordings and experimental data of different animal species, indicate that structural heterogeneity underlies relevant characteristics of cardiac electrical propagation at tissue level. These include conduction effects on action potential (AP) morphology, the shortening of AP duration along the activation pathway and the progressive modulation by premature beats of spatial patterns of dispersion of repolarization. The proposed approach may also have important implications in other research fields involving excitable complex media.