Modeling and simulation of transmural cellular electromechanical properties in heart failure

In this paper, we present a simulation study of transmural cellular electromechanical properties in heart failure based on a integrated and refined heart cell model of Luo-Rudy II model and modified Hunter-McCullochter Keurs mechanical model. The results show that prolonged action potential duration (APD) and APD rate-adaptation are more obviously transmurally heterogeneous in heart failure than those in control hearts. The results suggest that the differences of the electrical responses between failing cells and normal cells can cause slowing relaxation of the Ca²⁺ transient, and the difference of the Ca²⁺-TnC concentrations between fast and slow myocytes in failing hearts is smaller than in nonfailing hearts. It results in a decrease of force, which might diminish the role of mechanoelectric feedback, and then induce an increase of transmural APD gradient that might cause arrhythmia in heart failure. These results are in good accordance with experimental findings reported in the literatures and this electromechanical cardiac cell model might be very useful for further modeling and simulation of heart failure at both the tissue and the whole organ levels