Abstract
One mechanism for the onset of arrhythmias is abnormal impulse initiation such as ventricular ectopic beats. These may be caused by abnormal calcium (Ca2 + ) cycling. The Luo-Rudy model was used to simulate the dynamics of intracellular Ca2 + ([Ca2 + ]i) handling and the initiation of ectopic beats in virtual ventricular myocytes and tissues. [Ca2 + ]i in the reduced Ca2 + handling equations settles to a steady state at low levels of intracellular sodium ([Na + ]i), but oscillates when [Na + ]i is increased. These oscillations emerge through a homoclinic bifurcation. In the whole cell, Ca2 + overload, brought about by inhibition of the sodium-potassium pump and elevated [Na + ]i, can cause autorhythmic depolarisations. These oscillations interact with membrane currents to cause action potentials that propagate through one dimensional virtual tissue strands and two dimensional anisotropic virtual tissue sheets.
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Benson, A.P., Holden, A.V. (2005). Calcium Oscillations and Ectopic Beats in Virtual Ventricular Myocytes and Tissues: Bifurcations, Autorhythmicity and Propagation. In: Frangi, A.F., Radeva, P.I., Santos, A., Hernandez, M. (eds) Functional Imaging and Modeling of the Heart. FIMH 2005. Lecture Notes in Computer Science, vol 3504. Springer, Berlin, Heidelberg. https://doi.org/10.1007/11494621_31
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DOI: https://doi.org/10.1007/11494621_31
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