The effect of myocardial action potential duration on cardiac pumping efficacy: a computational study

Da Un Jeong,Ki Moo Lim

doi:10.1186/s12938-018-0508-2

Abstract

Background and aimsAlthough studies on the relation between arrhythmias and the action potential duration (APD) have been carried out, most of them are based only on electrophysiological factors of the heart and lack experiments that consider cardiac mechanical and electromechanical characteristics. Therefore, we conducted this study to clarify the relevance of the shortening of APD of a cell in relation to the mechanical contraction activity of the heart and the associated risk of arrhythmia.MethodsThe human ventricular model used in this study has two dynamic characteristics: electrophysiological conduction and mechanical contraction. The model simulating electrophysiological characteristics was consisted of lumped parameter circuit that can mimic the phenomenon of ion exchange through the cell membrane of myocyte and consisted of 214,319 tetrahedral finite elements. In contrast, the model simulating mechanical contraction characteristics was constructed to mimic cardiac contraction by means of the crossbridge of a myofilament and consisted of 14,720 hermite-based finite elements to represent a natural 3D curve of the cardiac surface. First, we performed a single cell simulation and the electrophysiological simulation according to the change of the APD by changing the electrical conductivity of the IKs channel. Thus, we confirmed the correlation between APD and intracellular Ca2+ concentration. Then, we compared mechanical response through mechanical simulation using Ca2+ data from electrical simulation.ResultsThe APD and the sum of the intracellular Ca2+ concentrations showed a positive correlation. The shortened APD reduced the conduction wavelength of ventricular cells by shortening the plateau and early repolarization in myocardial cells. The decrease in APD reduced ventricular pumping efficiency by more than 60% as compared with the normal group (normal conditions). This change is caused by the decline of ventricular output owing to reduced ATP consumption during the crossbridge of myofilaments and decreased tension.ConclusionThe shortening of APD owing to increased electrical conductivity of a protein channel on myocardial cells likely decreases the wavelength and the pumping efficiency of the ventricles. Additionally, it may increase tissue sensitivity to ventricular fibrillation, including reentry, and cause symptoms such as dyspnea and dizziness.

Highlights

Background and aims studies on the relation between arrhythmias and the action potential duration (APD) have been carried out, most of them are based only on electrophysiological factors of the heart and lack experiments that consider cardiac mechanical and electromechanical characteristics
Abnormality of the protein channels inside the cell membrane directly affects the movement of ions entering and exiting the cell, thereby changing the action potential duration (APD) [3]
We recently developed image-based three-dimensional ventricular electromechanical models, that can quantitatively compare the energy consumed by electrophysiological phenomena during mechanical beating [9,10,11]

Summary

Introduction

Background and aims studies on the relation between arrhythmias and the action potential duration (APD) have been carried out, most of them are based only on electrophysiological factors of the heart and lack experiments that consider cardiac mechanical and electromechanical characteristics. We conducted this study to clarify the relevance of the shortening of APD of a cell in relation to the mechanical contraction activity of the heart and the associated risk of arrhythmia. Changes in AP may cause abnormal transmembrane currents in myocardial cells, which in turn may cause cardiac arrhythmias and other heart diseases. Abnormality of the protein channels inside the cell membrane directly affects the movement of ions entering and exiting the cell, thereby changing the action potential duration (APD) [3]. This is because the K+ channel plays an important role in determining the repolarization of the cell’s AP. Prolonged APD can induce torsades de pointes tachycardia, leading to cardiac death [5, 6]

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Discussion

Conclusion