1,721,010 research outputs found
Exploring anodal and cathodal make and break cardiac excitation mechanisms in a 3D anisotropic bidomain model
No full textPublished studies have investigated the relevance of cardiac virtual electrode responses to unipolar cathodal and anodal stimulations for explaining the make and break excitation mechanisms. Most of these studies have considered 2D bidomain models or cylindrical domains that by symmetry reduce to the 2D case, so the triggering mechanisms and onset of excitation have not yet been fully elucidated in 3D anisotropic models. The goal of this work is to revisit these excitation mechanisms with 3D bidomain simulations considering two tissue types with unequal anisotropy ratio, including transmural fiber rotation and augmenting the Luo–Rudy I membrane model with the so-called funny and the electroporation currents. In addition to usual snapshots of transmembrane potential patterns, we compute from the action potential waveforms the activation time and associated isochrone sequences, yielding a detailed 3D description of the instant and location of excitation origin, shape and propagation of activation wavefronts. A specific aim of this work is to detect the location of the excitation onset and whether its trigger mechanism is (a) electrotonic, i.e. originating from discharge diffusion of currents flowing between virtual cathodes and anods and/or (b) membrane-based, i.e. arising only from intrinsic depolarizing membrane currents. Our results show that the electrotonic mechanism is observed independently of the degree of unequal anisotropy in diastolic anode make and systolic cathode break. The membrane-based mechanism is observed in diastolic cathode make, diastolic anode break, only for a relative weak anisotropy, and systolic anode break. The excitation trigger mechanism, the location of the excitation origin and the pattern of the isochrone sequence are independent of the degree of anisotropy for diastolic cathode make, systolic cathode and anode break, while they might depend on the degree of anisotropy for diastolic anode make and break. Moreover, the tissue anisotropy has a strong influence on the threshold amplitude of the stimulation pulse triggering these mechanisms
A reliability analysis of cardiac repolarization time markers
No full textOnly a limited number of studies have addressed the reliability of extracellular markers of cardiac repolarization time, such as the classical marker RTeg defined as the time of maximum upslope of the electrogram T wave. This work presents an extensive three-dimensional simulation study of cardiac repolarization time, extending the previous one-dimensional simulation study of a myocardial strand by Steinhaus [B.M. Steinhaus, Estimating cardiac transmembrane activation and recovery times from unipolar and bipolar extracellular electrograms: a simulation study, Circ. Res. 64 (3) (1989) 449]. The simulations are based on the bidomain - Luo-Rudy phase I system with rotational fiber anisotropy and homogeneous or heterogeneous transmural intrinsic membrane properties. The classical extracellular marker RTeg is compared with the gold standard of fastest repolarization time RTtap, defined as the time of minimum derivative during the downstroke of the transmembrane action potential (TAP). Additionally, a new extracellular marker RT 90eg is compared with the gold standard of late repolarization time RT 90tap, defined as the time when the TAP reaches 90% of its resting value. The results show a good global match between the extracellular and transmembrane repolarization markers, with small relative mean discrepancy (≤ 1.6 %) and high correlation coefficients (≥ 0.92), ensuring a reasonably good global match between the associated repolarization sequences. However, large local discrepancies of the extracellular versus transmembrane markers may ensue in regions where the curvature of the repolarization front changes abruptly (e.g. near front collisions) or is negligible (e.g. where repolarization proceeds almost uniformly across fiber). As a consequence, the spatial distribution of activation-recovery intervals (ARI) may provide an inaccurate estimate of (and weakly correlated with) the spatial distribution of action potential durations (APD)
Dynamical effects of myocardial ischemia in anisotropic cardiac models in three dimensions
No full textThe interaction between the presence of moderate or severe subendocardial ischemic regions and the anisotropic structure of the cardiac muscle is investigated here by means of numerical simulations based on anisotropic Bidomain and Monodomain models. The ischemic effects on cardiac excitation, recovery and distribution of action potential duration are discussed, showing the presence of ischemic epicardial markers. Extracellular potential distributions during the ST and TQ intervals are computed separately using non-stationary models. During the ST interval, the extracellular potential patterns differ from those simulated with stationary models used in the literature. These differences are explained by decomposing the cardiac current sources into conormal, axial and orthogonal components and by determining which component is dominant during the ST and TQ intervals
Computing cardiac recovery maps from electrograms and monophasic action potentials under heterogeneous and ischemic conditions
No full textThe currently available techniques to investigate the 3D sequence of activation and recovery in the cardiac atria and ventricles, with high spatial resolution, are based on extracellular electrical recordings. The goal of the present work is to provide an extensive quantitative analysis of the accuracy level of commonly used recovery time (RT) markers, under heterogeneous and pathological conditions of the myocardial tissue, such as myocardial ischemia. A widely used technique is based on unipolar electrograms (EGs); an alternative technique is based on hybrid monophasic action potentials (HMAPs), obtained as the potential difference between a permanently depolarized site and an exploring site. The RT markers derived from EGs and HMAPs are compared with two transmembrane action potential (TAP) markers considered here as gold standards for the fastest and final recovery phase, respectively. The analysis is based on 3D numerical simulations of the action potential propagation in anisotropic and insulated cardiac blocks, modeled by the Bidomain system coupled with the Luo–Rudy I membrane model. These demanding simulations have been made possible by recent advances in computing power and multilevel Bidomain solvers. The results show that the extracellular RT markers considered are reliable estimates of the gold standard TAP markers, with low relative mean discrepancies and high correlation coefficients. We also investigate the capability of the markers to discriminate different transmural dispersions of recovery times and action potential durations. In some specific pathological cases when the EG markers fail, the HMAP markers may offer reliable alternatives
Modeling ventricular repolarization: effects of transmural and apex-to-base heterogeneities in action potential durations
No full textHeterogeneities in the densities of membrane ionic currents of myocytes cause regional variations in action potential duration (APD) at various intramural depths and along the apico-basal and circumferential directions in the left ventricle. This work extends our previous study of cartesian slabs to ventricular walls shaped as an ellipsoidal volume and including both transmural and apex-to-base APD heterogeneities. Our 3D simulation study investigates the combined effect on repolarization sequences and APD distributions of: (a) the intrinsic APD heterogeneity across the wall and along the apex-to-base direction, and (b) the electrotonic currents that modulate the APDs when myocytes are embedded in a ventricular wall with fiber rotation and orthotropic anisotropy. Our findings show that: (i) the transmural and apex-to-base heterogeneities have only a weak influence on the repolarization patterns on myocardial layers parallel to the epicardium; (ii) the patterns of APD distribution on the epicardial surface are mostly affected by the apex-to-base heterogeneities and do not reveal the APD transmural heterogeneity; (iii) the transmural heterogeneity is clearly discernible in both repolarization and APD patterns only on transmural sections; (iv) the apex-to-base heterogeneity is clearly discernible only in APD patterns on layers parallel to the epicardium. Thus, in our orthotropic ellipsoidal wall, the complex 3D electrotonic modulation of APDs does not fully mix the effects of the transmural and apex-to-base heterogeneity. The intrinsic spatial heterogeneity of the APDs is unmasked in the modulated APD patterns only in the appropriate transmural or intramural sections. These findings are independent of the stimulus location (epicardial, endocardial) and of Purkinje involvement
Monophasic action potentials generated by bidomain modeling as a tool for detecting cardiac repolarization times
No full textUnipolar electrograms (EGs) and hybrid (or unorthodox or unipolar) monophasic action potentials (HMAPs) are currently the only proposed extracellular electrical recording techniques for obtaining cardiac recovery maps with high spatial resolution in exposed and isolated hearts. Estimates of the repolarization times from the HMAP downstroke phase have been the subject of recent controversies. The goal of this paper is to computationally address the controversies concerning the HMAP information content, in particular the reliability of estimating the repolarization time from the HMAP downstroke phase. Three-dimensional numerical simulations were performed by using the anisotropic bidomain model with a region of short action potential durations. EGs, transmembrane action potentials (TAPs), and HMAPs elicited by an epicardial stimulation close or away from a permanently depolarized site were computed. The repolarization time was computed as the moment of EG fastest upstroke (RTeg) during the T wave, of HMAP fastest downstroke (RT HMAP), and of TAP fastest downstroke (RTtap). The latter was taken as the gold standard for repolarization time. We also compared the times (RT90HMAP, RT90tap) when the HMAP and TAP first reach 90% of their resting value during the downstroke. For all explored sites, the HMAP downstroke closely followed the TAP downstroke, which is the expression of local repolarization activity. Results show that HMAP and TAP markers are highly correlated, and both markers RTHMAP and RTeg (RT90HMAP) are reliable estimates of the TAP reference marker RT tap (RT90tap). Therefore, the downstroke phase of the HMAP contains valuable information for assessing repolarization times
Simulating patterns of excitation, repolarization and action potential duration with cardiac Bidomain and Monodomain models,
No full textParallel numerical simulations of excitation and recovery in three
dimensional myocardial domains are presented. The simulations are based on the
anisotropic Bidomain and Monodomain models, inluding intramural fiber rotation
and orthotropic or axisymmetric anisotropy of the intra- and extra-cellular
conductivity tensors. The Bidomain model consist of a system of two
reaction-diffusion equations, while the Monodomain model consists of one
reaction-diffusion equation. Both models are coupled with the phase I Luo-Rudy
membrane model describing the ionic currents. Simulations of excitation and
repolarization sequences on myocardial slabs of different sizes show how the
distribution of the action potential durations (APD) is influenced by both the
anisotropic electrical conduction and the fiber rotation. This influence occurs
in spite of the homogeneous intrinsic properties of the cell membrane. The APD
dispersion patterns are closely correlated to the anisotropic curvature of the
excitation wavefront
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