D172N KCNJ2 Mutation Effect on Electromechanical Activation in the Heart a Simulation Study

D172N KCNJ2 Mutation Effect on Electromechanical Activation in the Heart a Simulation Study

썸네일 Challenge 애게서 업로드 하였습니다. 19. 7. 4 오후 4:43
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Nowadays, it is known that the cause of electrical instability or arrhythmia in the heart is due to alteration or mutation in the ion channels. The goal of this study is to computationally analyze the effect of D172N KCNJ2 mutation in the electromechanical activation of the ventricle. We used a well-developed electromechanical ventricular model which combined electrophysiological model with the myofilament sliding to mimic “excitation-contraction” in myocardium with the addition of the D172N mutation model embedded. We compared three cases including ten Tusscher model, wild-type (WT), heterozygous WT/D172N, and Homozygous D172N mutation conditions. The results show that the electrical wavelength of WT/D172N was shortened, and it shortened further under the D172N mutation condition. The wavelength shortening impact to the contractility which lowering the left ventricular and aortic pressures, ejection fraction, and cardiac output. The electrical wavelength shortening due to D172N mutation can be investigated further and can possibly be treated with an appropriate potassium conduction block.
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19. 7. 4 오후 4:47
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Nowadays, it is known that the cause of electrical instability or arrhythmia in the heart is due to alteration or mutation in the ion channels. The goal of this study is to computationally analyze the effect of D172N KCNJ2 mutation in the electromechanical activation of the ventricle. We used a well-developed electromechanical ventricular model which combined electrophysiological model with the myofilament sliding to mimic “excitation-contraction” in myocardium with the addition of the D172N mutation model embedded. We compared three cases including ten Tusscher model, wild-type (WT), heterozygous WT/D172N, and Homozygous D172N mutation conditions. The results show that the electrical wavelength of WT/D172N was shortened, and it shortened further under the D172N mutation condition. The wavelength shortening impact to the contractility which lowering the left ventricular and aortic pressures, ejection fraction, and cardiac output. The electrical wavelength shortening due to D172N mutation can be investigated further and can possibly be treated with an appropriate potassium conduction block.
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