Until recently only two types of media have been considered to provide the nonuniformities necessary to initiate cardiac reentry: (1) continuous isotropic media with intrinsic repolarization inhomogeneities; and (2) continuous isotropic media free of inhomogeneities in which repolarization nonuniformities are introduced transiently. The purpose of this article is to establish cellular coupling as a basis for arrhythmias by placing a new type of inhomogeneity, nonuniform anisotropy due to sparse side-to-side coupling between cells, in an overall perspective with the other nonuniformities that lead to reentry. Review of experimental and theoretical models of reentry leads to the following picture: with slowed conduction, reentrant circuits diminish in size and the nonuniformities necessary for reentry are provided by nonuniform anisotropy. Repolarization nonuniformities create functionally different pathways for reentrant circuits of relatively large size (> 30-50 mm(2)). Nonuniform anisotropic cellular coupling, which is associated with underlying microfibrosis, makes it possible for reentry to occur in small areas (< 10-15 mm(2)). A general property found in nonuniform anisotropic bundles is the presence of functionally different pathways in the absence of intrinsic repolarization inhomogeneities-one of fast longitudinal conduction with a longer refractory period, and another of ''very slow'' transverse conduction with a shorter refractory period. Since it is not known if nonuniform anisotropy exists in the AV node, the best known structure with small reentrant circuits, we performed microscopic extracellular measurements in the AV node of the rabbit. The transitional zone of the AV node was found to have markedly nonuniform anisotropic conduction properties. The analysis provides the view that functionally different pathways of small reentrant circuits, including those of the AV node, need to be reevaluated in terms of the role of nonuniform anisotropic cellular coupling.
