Mechanisms of the dynamics of reentry in a fibrillating myocardium. Developing a genes-to-rotors paradigm.

Abstract

Because the myocardium was considered to behave structurally as a continuous medium, for many years attention focused on spatial variations in the membrane properties, which allow some cells to recover excitability faster as the mechanism for reentry.1 This mechanism still holds its place as a major underlying cause of many arrhythmias; eg, the long-QT syndrome.2 In the early 1980s, a second general mechanism was introduced with evidence that propagation in the myocardium is discontinuous because of the discrete nature of cells, which results in anisotropic differences in conduction attributable to the anisotropic distribution of the intercellular connections.3 4 Additional evidence quickly accumulated that resistive discontinuities at a larger size scale delay wavefront movement at locations where there is an abrupt change in fiber orientation.5 6 The underlying mechanism of anisotropic resistive discontinuities is that they alter electrical loading of the active membrane.3 4 5 During the last decade, a third type of reentrant mechanism produced by the geometrical shape of excitation waves has received considerable attention. These mechanisms do not “depend on any peculiarities of the cardiac muscle and may be demonstrated in any excitable medium” (page 631). Previously, cardiac electrical events were described for a reentrant path2 8 9 10 or the vortex of reentrant wavefronts (leading circle theory).11 Presently, reentrant wavefront dynamics are described in terms of wavefront curvature, rotors, spiral waves, and scroll waves.12 13 14 15 16 These studies demonstrated that an intrinsic heterogeneity of the myocardium is not necessarily required for reentry to be maintained. For example, if a small area is stimulated within the tail of the broad wavefront of repolarization, a critical point is established that …