2017 IEEE 17th International Conference on Bioinformatics and Bioengineering (BIBE) (2017)
Oct 24, 2017 to Oct 26, 2017
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 (IKr) 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.
bioelectric phenomena, biological tissues, biomechanics, cardiology, cellular biophysics, diseases, drugs, fatigue, muscle, potassium
L. Aydin et al., "Is Central Origin of Muscle Fatigue Distinguished Solely in Finger Tapping Performance?," 2017 IEEE 17th International Conference on Bioinformatics and Bioengineering (BIBE), Washington, DC, 2018, pp. 542-547.