Key result
In a numerical model of human ventricular tissue, suppression of the inward rectifier potassium current (IK1) substantially increased the critical anisotropy ratio required for waveblock formation.
In a computational model of human ventricular tissue, suppression of the inward rectifier potassium current (IK1) was identified as the most effective way to prevent waveblock at areas of abrupt change in anisotropy.
IK1 suppression may raise arrhythmia thresholds in anisotropic models; leaves open experimental validation before any therapeutic consideration.
Waveblock formation is the main cause of reentry. We have performed a comprehensive numerical modeling study of block formation due to anisotropy in Ten Tusscher and Panfilov (2006) ionic model for human ventricular tissue. We have examined the border between different areas of myocardial fiber alignment and have shown that blockage can occur for a wave traveling from a transverse fiber area to a longitudinal one. Such blockage occurs for reasonable values of the anisotropy ratio (AR): from 2.4 to 6.2 with respect to propagation velocities. This critical AR decreases by the suppression of INa and ICa, slightly decreases by the suppression of IKr and IKs, and substantially increases by the suppression of IK1. Hyperkalemia affects the block formation in a complex, biphasic way. We provide examples of reentry formation due to the studied effects and have concluded that the suppression of IK1 should be the most effective way to prevent waveblock at the areas of abrupt change in anisotropy.
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Kudryashova et al. (2015) studied Cardiac arrhythmias (Waveblock formation). Suppression of ionic currents (INa, ICa, IKr, IKs, IK1) and hyperkalemia vs. Normal conditions was evaluated on Critical anisotropy ratio (AR) for waveblock formation. In a numerical model of human ventricular tissue, suppression of the inward rectifier potassium current (IK1) substantially increased the critical anisotropy ratio required for waveblock formation.
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