Key result
Reduction of intercellular conductance in a midmyocardial island in the presence of LQTS2 can cause a non-sustained reentrant arrhythmia, which is prolonged by hyperkalaemic conditions.
In a 2D computational cardiac tissue model, regional cellular uncoupling combined with LQTS2 and hyperkalaemia facilitates the initiation and prolongation of reentrant arrhythmias.
Regional uncoupling may promote reentry in LQTS2 models; hypothesis-generating and leaves open human relevance.
Ischemia in presence of drug induced long QT syndrome 2 (LQTS2) predisposes the tissue to Torsade de pointes (TdP). Reentrant arrhythmias occurring during phase 1B of ischemia have been primarily associated with areas of cellular uncoupling and hyperkalaemia. This study aims to investigate how a region of lowered gap junction conductance (GJC) in presence of LQTS2 can initiate a TdP. Here, a discrete grid of 250x100 cells interconnected using GJCs is taken representing a portion of the transmural wall with anisotropic conduction velocities. LQTS2 is introduced by reducing the potassium current (I Kr ) of all cells to 50%. An ischemic zone is located almost in the centre of the mid myocardium layer in the form of an elliptic inhomogeneity with varying percentage reduction of GJC compared to the surrounding. Results show that reduction of intercellular conductance in a midmyocardial island can cause a non-sustained reentrant arrhythmia to develop due to premature pacing beats. Addition of hyperkalaemic conditions in the ischemic zone has the effect of prolonging the arrhythmia.
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Priya et al. (2017) studied Long QT syndrome 2 (LQTS2) and ischemia. Regional cellular uncoupling (lowered gap junction conductance) and hyperkalaemia was evaluated on Initiation of Torsade de pointes / reentrant arrhythmia. Reduction of intercellular conductance in a midmyocardial island in the presence of LQTS2 can cause a non-sustained reentrant arrhythmia, which is prolonged by hyperkalaemic conditions.
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