(470h) Optimal Mechano-Electric Treatment of Ventricular Fibrillation

Ventricular fibrillation (VF) [1] is a life-threatening cardiac arrhythmia (irregular heartbeat) resulting in uncoordinated contraction of the ventricular myocardium and causing a failure of the heart to pump blood to the rest of the body, this leads to sudden cardiac death, which is one of the most common causes of death in the industrialized world. In its turn, contraction of the heart causes cardiac tissue deformation which feeds back on the wave propagation and affects electrophysiological properties via mechano-electric feedback (MEF) [2]. Electrical-excitation and contraction of the heart can be linked by an electromechanical model of cardiac tissue.

Strong electrical shocks that are given to the heart to reset the heartbeat back to its normal beat have remained the most reliable approach to terminate VF, this is known as defibrillation. This electrical therapy can damage tissue and leave scars which are considered as major sources of substrates for cardiac arrhythmias. These electric-based realization algorithms have not considered mechanical properties of cardiac tissue, despite the fact that mechanical deformation is shown to influence electrical activity of the heart tissue. Many studies have shown the importance of the MEF and, for instance, mechanical impact on chest, in the area directly over the heart, can either cause Commotio Cordis when chest receives a blow, or terminate cardiac arrhythmia such as VF using the human fist on the chest during precordial thump. We [5] recently presented a novel mechanical perturbation algorithm to control cardiac alternans [3], which is a perturbation in the heart rhythm, in relevantly sized cardiac tissues using an electromechanical model that couples the mathematical models of cardiac mechanics and electrophysiology.

Controlling the complex spatio-temporal dynamics underlying life-threatening cardiac arrhythmias is extremely difficult [4]. Computational simulation is increasingly recognized as an important tool for the investigation and termination of ventricular arrhythmias, including fibrillation [4]. In this work a strongly realistic electromechanical model where the excitable behavior is modeled using a bidomain description of cardiac tissue. 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 Ten Tusscher [5] model is used to represent the electrophysiological properties, and the mechanical properties of the passive myocardium are described using the exponential Guccione passive elasticity model [6] which is the most cited model in the literature. The active tension that couples the electrophysiological model with the cardiac mechanics model is generated using the Niederer-Hunter-Smith [7] model which is advanced model. In this work, we will explore the possibility of Cardiac Defibrillation by combining the electrical shock and mechanical stimuli delivered to the heart in order to minimize defibrillation energy and avoid adverse side effects associated with high voltage shocks. This is the first attempt to combine electro-physiologically relevant cardiac models of electrical wave propagation and contractility of cardiac tissue in a synergistic effort to terminate VF.

[1]- Zevitz, M.E. Ventricular fibrillation [online]. eMedicine. http://www.emedicine.com/med/topic2363.htm (2004).

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

[3] - Azzam Hazim, Youssef Belhamadia, Stevan Dubljevic, Control of cardiac alternans in an electromechanical model of cardiac tissue, Computers in Biology and Medicine 63 (2015) 108-117.

[4]- Alfio Quarteroni. Modeling the Heart and the Circulatory System. Springer, New York, 2015

[5] Ten Tusscher KH, Panfilov AV. Alternans and spiral breakup in a human ventricular tissue model. Am J Physiol Heart Circ Physiol 291: H1088-H1100, 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.

[7] 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.