Computationally efficient model of myocardial electromechanics for multiscale simulations

Abstract

A model of myocardial electromechanics is suggested. It combines modified and simplified versions of previously published models of cardiac electrophysiology, excitation-contraction coupling, and mechanics. The mechano-calcium and mechano-electrical feedbacks, including the strain-dependence of the propagation velocity of the action potential, are also accounted for. The model reproduces changes in the twitch amplitude and Ca2+-transients upon changes in muscle strain including the slow response. The model also reproduces the Bowditch effect and changes in the twitch amplitude and duration upon changes in the interstimulus interval, including accelerated relaxation at high stimulation frequency. Special efforts were taken to reduce the stiffness of the differential equations of the model. As a result, the equations can be integrated numerically with a relatively high time step making the model suitable for multiscale simulation of the human heart and allowing one to study the impact of myocardial mechanics on arrhythmias.

Effect of strain‐dependent conduction slowing on the re‐entry formation and maintenance in cardiac muscle: 2D computer simulation

“…Our recent model 25 was used for the simulations performed in this study. The model combines a simple model of cardiomyocyte electrophysiology by Aliev and Panfilov 26 and our model of cardiac mechanics, 27 while a description of electromechanical coupling was based on the model by ten Tusscher and Panfilov 28 .…”

“…The mechano‐calcium feedback was provided by the dependencies of the kinetics of the Ca 2+ binding to regulatory proteins on the sarcomere length and the number of strongly bound actin‐myosin complexes (see details in File S1). Here, we made minor additions and modifications to the model 25 to reproduce more precisely the strain‐dependent variation of the CV observed experimentally.…”

“…The electromechanical model 25 was used with a small modification. The equation for normalized (dimensionless) membrane potential from the Aliev‐Panfilov 26 model was rewritten as where s is a time constant and k = 8, and are dimensionless model parameters; is the kinetic variable of the Aliev‐Panfilov model that obeys an ordinary differential equation 26 ; is a factor that describes the change of the membrane capacitance upon caveolae recruitment and formation, and dimensionless variable characterizes the involvement of caveolae in the cell membrane in a strain‐dependent manner.…”

“…Also, a delay between strain changes and CV slowdown that can affect the reentry was not accounted for in the model 19 . Here we use our recent mathematical model 25 to study the effect of stretch‐induced CV slowdown on the re‐entry formation in a 2D myocardium sample. The model describes myocardial electrophysiology using a simple phenomenological model, 26 passive and active stress, actin–myosin interaction, Ca 2+ dynamics in the cytoplasm and sarcoplasmic reticulum, and its interaction with regulatory proteins that control the actin‐myosin interaction.…”

Mechanical stress concealed force enhancement and ionic transient membrane potential and metabolism in akinesia of stress cardiomyopathy

“…The second phase is considered to actuate the spontaneous myogenic force that responds to instantaneous lengthening tolerance. Stretch-activated ionic channels play an important role in this force enhancement event [69] , which is considered the energy consumption period…”