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This article develops a robust adaptive boundary output regulation approach for a class of complex anticollocated hyperbolic partial differential equations subjected to multiplicative unknown faults in both the boundary sensor and actuator. The regulator design is based on the internal model principle, which amounts to stabilize a coupled cascade system, which consists of a finite-dimensional internal model driven by a hyperbolic distributed parameter system (DPS). To this end, a systematic sliding mode equipped with a backstepping approach is developed such that the robust state feedback control can be realized. Moreover, since the available information is a faulty boundary measurement at the right side point, state estimation is required. However, due to the presence of boundary unknown faults, we need to solve an issue of joint fault-state estimation. Restrictive persistent excitation conditions are usually required to guarantee the exact estimation of faults but are unrealistic in practice. To this end, a novel concurrent learning (CL) adaptive observer is proposed so that exponential convergence is obtained. It is the first time that the spirit of CL is introduced to the field of DPSs. Consequently, the observer-based adaptive boundary fault tolerant control scheme is developed, and rigorous theoretical analysis is given such that the exponential output regulation can be achieved. Finally, the effectiveness of the proposed methodology is demonstrated via comparative simulations.

This article investigates the adaptive neural tracking control problem for a class of hyperbolic PDE with boundary actuator dynamics described by a set of nonlinear ordinary differential equations (ODEs). Particularly, the control input appears in the ODE subsystem with unknown nonlinearities requiring to be estimated and compensated, which makes the control task rather difficult. It is the first time to consider tracking control of such a class of systems, rendering our contributions essentially different from the existing literature that merely focus on the stabilization problem. By formulating a virtual exosystem to generate a reference trajectory, we propose a novel design of the adaptive geometric controller for the considered system where neural networks (NNs) are employed to approximately estimate nonlinearities, and finite and infinite-dimensional backstepping techniques are leveraged. Moreover, rigorously theoretical proofs based on the Lyapunov theory are provided to analyze the stability of the closed-loop system. Finally, we illustrate the results through two numerical simulations.

The deformation of the heart tissue due to the contraction can modulate the excitation, a phenomenon referred to as mechanoelectrical feedback (MEF), via stretch-activated channels. The effects of MEF on the electrophysiology at high pacing rates are shown to be proarrhythmic in general. However, more studies need to be done to elucidate the underlying mechanism. In this work, we investigate the effects of MEF on cardiac alternans, which is an alternation in the width of the action potential that typically occurs when the heart is paced at high rates, using a biophysically detailed electromechanical model of cardiac tissue. We observe that the transition from spatially concordant alternans to spatially discordant alternans, which is more arrhythmogenic than concordant alternans, may occur in the presence of MEF and when its strength is sufficiently large. We show that this transition is due to the increase of the dispersion of conduction velocity. In addition, our results also show that the MEF effects, depending on the stretch-activated channels' conductances and reversal potentials, can result in blocking action potential propagation., (Copyright © 2020 Biophysical Society. Published by Elsevier Inc. All rights reserved.)

Cardiac alternans is a heart rhythm instability that is associated with cardiac arrhythmias and may lead to sudden cardiac death. The onset of this instability, which is linked to period-doubling bifurcation and may be a route to chaos, is of particular interest. Mechano-electric feedback depicts the effects of tissue deformation on cardiac excitation. The main effect of mechano-electric feedback is delivered via the so-called stretch-activated ion channels and is caused by stretch-activated currents. Mechano-electric feedback, which is believed to have proarrhythmic and antiarrhythmic effects on cardiac electrophysiology, affects the action potential duration in a manner dependent on cycle length, but the mechanisms by which this occurs remain to be elucidated. In this study, a biophysically detailed electromechanical model of cardiac tissue is employed to show how a stretch-activated current can affect the action potential duration at cellular and tissue levels, illustrating its effects on the onset of alternans. Also, using a two-dimensional iterated map that incorporates stretch-activated current effects, we apply linear stability analysis to study the stability of the bifurcation. We show that alternans bifurcation can be prevented depending on the strength of the stretch-activated current.

Cardiac alternans is a disturbance in heart rhythm that is linked to the onset of lethal cardiac arrhythmias. Mechanical perturbation control has been recently used to suppress alternans in cardiac tissue of relevant size. In this control strategy, cardiac tissue mechanics are perturbed via active tension generated by the heart's electrical activity, which alters the tissue's electric wave profile through mechanoelectric coupling. We analyze the effects of mechanical perturbation on the dynamics of a map model that couples the membrane voltage and active tension systems at the cellular level. Therefore, a two-dimensional iterative map of the heart beat-to-beat dynamics is introduced, and a stability analysis of the system of coupled maps is performed in the presence of a mechanical perturbation algorithm. To this end, a bidirectional coupling between the membrane voltage and active tension systems in a single cardiac cell is provided, and a discrete form of the proposed control algorithm, that can be incorporated in the coupled maps, is derived. In addition, a realistic electromechanical model of cardiac tissue is employed to explore the feasibility of suppressing alternans at cellular and tissue levels. Electrical activity is represented in two detailed ionic models, the Luo-Rudy 1 and the Fox models, while two active contractile tension models, namely a smooth variant of the Nash-Panfilov model and the Niederer-Hunter-Smith model, are used to represent mechanical activity in the heart. The Mooney-Rivlin passive elasticity model is employed to describe passive mechanical behavior of the myocardium.

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., (Copyright © 2015 Elsevier Ltd. All rights reserved.)

A persistent alternation in the cardiac action potential duration has been linked to the onset of ventricular arrhythmia, which may lead to sudden cardiac death. A coupling between these cardiac alternans and the intracellular calcium dynamics has also been identified in previous studies. In this paper, the system of PDEs describing the small amplitude of alternans and the alternation of peak intracellular Ca(2+) are stabilized by optimal boundary and spatially distributed actuation. A simulation study demonstrating the successful annihilation of both alternans on a one-dimensional cable of cardiac cells by utilizing the full-state feedback controller is presented. Complimentary to these studies, a three variable Nash-Panfilov model is used to investigate alternans annihilation via mechanical (or stretch) perturbations. The coupled model includes the active stress which defines the mechanical properties of the tissue and is utilized in the feedback algorithm as an independent input from the pacing based controller realization in alternans annihilation. Simulation studies of both control methods demonstrate that the proposed methods can successfully annihilate alternans in cables that are significantly longer than 1 cm, thus overcoming the limitations of earlier control efforts.

The presence of the electrical alternans induces, through the mechanism of the excitation-contraction coupling, an alternation in the heart muscle contractile activity. In this work, we demonstrate the cardiac alternans annihilation by applied mechanical perturbation. In particular, we address annihilation of alternans in realistic heart size tissue by considering ionic currents suggested by Luo-Rudy-1 (LR1) model, in which the control algorithm involves a combined electrical boundary pacing control and a spatially distributed calcium based control which perturbs the calcium in the cells. Complimentary to this, we also address a novel mechanism of alternans annihilation which uses a Nash Panfilov model coupled with the stress equilibrium equations. The coupled model includes an additional variable to represent the active stress which defines the mechanical properties of the tissue.

A beat-to-beat variation in the electric wave propagation morphology in myocardium is referred to as cardiac alternans and it has been linked to the onset of life threatening arrhythmias and sudden cardiac death. Experimental studies have demonstrated that alternans can be annihilated by the feedback modulation of the basic pacing interval in a small piece of cardiac tissue. In this work, we study the capability of feedback control to suppress alternans both spatially and temporally in an extracted rabbit heart and in a cable of cardiac cells. This work demonstrates real-time control of cardiac alternans in an extracted rabbit heart and provides an analysis of the control methodology applied in the case of a one-dimensional (1D) cable of cardiac cells. The real-time system control is realized through feedback by proportional perturbation of the basic pacing cycle length (PCL). The measurements of the electric wave propagation are obtained by optical mapping of fluorescent dye from the surface of the heart and are fed into a custom-designed software that provides the control action signal that perturbs the basic pacing cycle length. In addition, a novel pacing protocol that avoids conduction block is applied. A numerical analysis, complementary to the experimental study is also carried out, by the ionic model of a 1D cable of cardiac cells under a self-referencing feedback protocol, which is identical to the one applied in the experimental study. Further, the amplitude of alternans linear parabolic PDE that is associated with the 1D ionic cardiac cell cable model under full state feedback control is analyzed. We provide an analysis of the amplitude of alternans parabolic PDE which admits a standard evolutionary form in a well defined functional space. Standard modal decomposition techniques are used in the analysis and the controller synthesis is carried out through pole-placement. State and output feedback controller realizations are developed and the important issue of measurement noise in the controller implementation is addressed. The analysis of stabilization of the amplitude of alternans PDE is in agreement with the experimental results and numerical results produced by the ionic 1D cable of cardiac cells model. Finally, a discussion is provided in light of these results in order to use control to suppress alternans in the human myocardium.