Anisotropic shortening in the wavelength of electrical waves promotes onset of electrical turbulence in cardiac tissue: An in silico study.

Several pathological conditions introduce spatial variations in the electrical properties of cardiac tissue. These variations occur as localized or distributed gradients in ion-channel functionality over extended tissue media. Electrical waves, propagating through such affected tissue, demonstrate distortions, depending on the nature of the ionic gradient in the diseased substrate. If the degree of distortion is large, reentrant activity may develop, in the form of rotating spiral (2d) and scroll (3d) waves of electrical activity. These reentrant waves are associated with the occurrence of lethal cardiac rhythm disorders, known as arrhythmias, such as ventricular tachycardia (VT) and ventricular fibrillation (VF), which are believed to be common precursors of sudden cardiac arrest. By using state-of-the-art mathematical models for generic, and ionically-realistic (human) cardiac tissue, we study the detrimental effects of these ionic gradients on electrical wave propagation. We propose a possible mechanism for the development of instabilities in reentrant wave patterns, in the presence of ionic gradients in cardiac tissue, which may explain how one type of arrhythmia (VT) can degenerate into another (VF). Our proposed mechanism entails anisotropic reduction in the wavelength of the excitation waves because of anisotropic variation in its electrical properties, in particular the action potential duration (APD). We find that the variation in the APD, which we induce by varying ion-channel conductances, imposes a spatial variation in the spiral- or scroll-wave frequency ω. Such gradients in ω induce anisotropic shortening of wavelength of the spiral or scroll arms and eventually leads to instabilitites.