Myocardial fibrosis is an integral component of most forms of heart failure. Clinical and computational studies have reported that spatial fibrosis pattern and fibrosis amount play a significant role in ventricular arrhythmogenicity. This study investigated the effect of the spatial distribution of fibrosis and fibrosis amount on the electrophysiology and mechanical performance of the human ventricles.
View Article and Find Full Text PDFThe KCNH2 L532P mutation is an alteration in the I channel that is associated with short QT syndrome and atrial fibrillation in zebrafish. In preliminary studies, the electrophysiological effects of the hERG L532P mutation were investigated using a mathematical model in a single-cell and 2D sheet medium. The objective of this study was to quantify the effects of the KCNH2 L532P mutation on the 3D ventricular electrophysiological behavior and the mechanical pumping responses.
View Article and Find Full Text PDFBackground: Atrial arrhythmia is a cardiac disorder caused by abnormal electrical signaling and transmission, which can result in atrial fibrillation and eventual death. Genetic defects in ion channels can cause myocardial repolarization disorders. Arrhythmia-associated gene mutations, including gene mutations, which are one of the most common genetic disorders, have been reported.
View Article and Find Full Text PDFThe understanding of cardiac arrhythmia under genetic mutations has grown in interest among researchers. Previous studies focused on the effect of the D172N mutation on electrophysiological behavior. In this study, we analyzed not only the electrophysiological activity but also the mechanical responses during normal sinus rhythm and reentry conditions by using computational modeling.
View Article and Find Full Text PDFBackground And Aims: Although it is important to analyze the hemodynamic factors related to the right ventricle (RV) after left ventricular assist device (LVAD) implantation, previous studies have focused only on the alteration of the ventricular shape and lack quantitative analysis of the various hemodynamic parameters. Therefore, we quantitatively analyzed various hemodynamic parameters related to the RV under normal, heart failure (HF), and HF incorporated with continuous flow LVAD therapy by using a computational model.
Methods: In this study, we combined a three-dimensional finite element electromechanical model of ventricles, which is based on human ventricular morphology captured by magnetic resonance imaging (MRI) with a lumped model of the circulatory system and continuous flow LVAD function in order to construct an integrated model of an LVAD implanted-cardiovascular system.
This study hypothesized that a left ventricular assist device (LVAD) shortens the electromechanical delay (EMD) by mechanical unloading. The goal of this study is to examine, by computational modeling, the influence of LVAD on EMD for four heart failure (HF) cases ranging from mild HF to severe HF. We constructed an integrated model of an LVAD-implanted cardiovascular system, then we altered the Ca transient magnitude, with scaling factors 1, 0.
View Article and Find Full Text PDFMitral valve regurgitation (MR) causes blood to flow in two directions during contraction of the left ventricle (LV), that is, forward into the aorta and backward into the left atrium (LA). In aortic valve regurgitation (AR), leakage occurs from the aorta into the LV during diastole. Our objective is to analyze the contribution of a left ventricular assist device (LVAD) to MR and AR for the following two different cannulation sites: from the LA to the aorta (LAAO) and from the LV to the aorta (LVAO).
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