Abstract
This study investigated the involvement of ventricular focal activity and dispersion of repolarization in LQT2 models at rapid rates. The Luo-Rudy dynamic model was used to simulate ventricular tissues. LQT2 syndrome due to genetic mutations was modeled by modifying the conductances of delayed rectifier potassium currents. Cellular automata was employed to generate virtual tissues coupled with midmyocardial (M) cell clusters. Simulations were conducted using grid-based computation. Under LQT2 conditions, early after-depolarizations (EADs) occurred first at the border of the M refractory zone in epicardium coupled with M clusters, but spiked off from endocardial cells in endocardium coupled with M clusters. The waveform of EADs was affected by the topological distribution of M clusters. Our results explain why subepicardial and subendocardial cells could exhibit surprisingly EADs when adjacent to M cells and suggest that phase 2 EADs are responsible for the onset of Torsade de Pointes at rapid ventricular pacing.
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Wang, C., Krause, A., Nugent, C., Dubitzky, W. (2005). Focal Activity in Simulated LQT2 Models at Rapid Ventricular Pacing: Analysis of Cardiac Electrical Activity Using Grid-Based Computation. In: Oliveira, J.L., Maojo, V., MartÃn-Sánchez, F., Pereira, A.S. (eds) Biological and Medical Data Analysis. ISBMDA 2005. Lecture Notes in Computer Science(), vol 3745. Springer, Berlin, Heidelberg. https://doi.org/10.1007/11573067_31
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DOI: https://doi.org/10.1007/11573067_31
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-540-29674-4
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