Calcium oscillations and ectopic beats in virtual ventricular myocytes and tissues: Bifurcations, autorhythmicity and propagation

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. © Springer-Verlag Berlin Heidelberg 2005.