(182j) Mechanical Perturbation Approach for Treating Cardiac Arrhythmias

Cardiac arrhythmias such as atrial fibrillation (AF) and ventricular fibrillation (VF) are characterized by irregular electrical activity, which lead to asynchronous contraction and may lead to sudden cardiac death. AF and VF can be treated by the application of an electrical shock, which is referred to as electrical defibrillation therapy . This electrical stimulus depolarizes a large amount of the heart muscle cells and has the effect of stopping any propagation of the impulse and terminating reentrant activations. If successful, normal heart beat, which is referred to as sinus rhythm, is restored. This procedure, called defibrillation, has been successfully applied to a human for the first time in 1947. The electrical treatments, which have remained the most reliable approach to terminate AF and VF, may cause a damage to the heart due to delivery of high electrical current.

The electrical waves propagate through the cardiac tissue and initiate contraction in human heart. In its turn, contraction causes cardiac tissue deformation which feeds back on the wave propagation and affects electrophysiological properties via mechano-electric feedback (MEF) [1]. Cardiac excitation and contraction of the heart can be linked by an electromechanical model of cardiac tissue. MEF is used in the literature to describe the influence of mechanical deformation of cardiac tissue on the electrophysiology. Mechanisms of MEF which include immediate influence on the action potential through stretch-activated channels, has been studied in the clinical community for well over a century and has been found to have to have anti- and pro-arrhythmic effects.

Recently, a novel mechanical perturbation algorithm to suppress cardiac alternans [2,3], which is an alternation in the action potential duration, was presented. This mechanical perturbation is reflected in cardiac excitation through the mechanisms of MEF. In this study, we explore this approach in the treatment of VF where MEF plays also a role in restoring normal electrical activity. Our control algorithm considers a modified version of error based feedback control that is implemented using mechanical perturbation control strategy and applied sequentially in subregions of cardiac tissue. To this end, a realistic electromechanical model of cardiac tissue is employed to explore the feasibility of terminating VF at cellular and tissue levels.
The cardiac bidomain model of action potential propagation in tissue is presented. The bidomain model consists of a system of coupled parabolic and elliptic PDEs for two potentials in the cardiac muscle, coupled with a nonlinear system of ODEs describing the ionic currents flowing across the cardiac membrane. The Luo-Rudy 1 [4] model is used to represent the electrophysiological properties of the heart, while for the active contractile tension model, the Niederer-Hunter-Smith [5] model is used to represent mechanical activity. The exponential passive elasticity [6] model is employed to describe passive mechanical behaviour of the myocardium.

1 - M.J. Lab, Mechanoelectric feedback (transduction) in heart: concepts and implications, Cardiovasc.Res, vol.32, p. 3-14, 1996.

2 - A. Hazim, Y. Belhamadia, S. Dubljevic, Control of cardiac alternans in an electromechanical model of cardiac tissue, Computers in Biology and Medicine 63 (2015) 108-117.

3 - A. Hazim, Y. Belhamadia, S. Dubljevic, Mechanical perturbation control of cardiac alternates, Physical Review E, accepted

4 - C. Luo and Y. Rudy, A model of the ventricular cardiac action potential. Depolarization, repolarization, and their interaction, Circ. Res. 68, 1501 (1991).

5 - S. A. Niederer, P. J. Hunter, and N. P. Smith, A quantitative analysis of cardiac myocyte relaxation: a simulation study, J Biophysics, vol. 90, p. 1697-722, 2006.

6 - J. M. Guccione, A. D. McCulloch, L. K. Waldman, Passive material properties of intact ventricular myocardium determined from a cylindrical model, J. Biomech. Eng. 113 (1) (1991) 42-55.