Effects of anisotropy on the development of cardiac arrhythmias associatedwith focal activity

The anisotropy that normally exists in the myocardium may be either enhance d in peri-infarction zones by loss of lateral cell connections or reduced b y redistribution of gap junctions. To test how the degree of anisotropy aff ects the development of ectopic focal activity, we carried out computer sim ulations in which a model of an ectopic focus is incorporated as the centra l element of a two-dimensional sheet of ventricular cells. At low values of intercellular coupling conductance (G(c)), the focus region is spontaneous ly active, but the limited intercellular current How inhibits propagation. At high G(c), automaticity is suppressed by the loading effects of the surr ounding cells. At intermediate G(c), the ectopic activity may propagate int o the sheet. In the case of isotropic coupling, the minimum size of the foc us region for propagation to occur (in terms of number of collaborating cel ls within the focus) is as small as approximately ten cells, and this numbe r decreases with increasing anisotropy. Thus, the presence of anisotropy fa cilitates the development of ectopic focal activity. We conclude that the r emodeling that occurs in pori-infarction zones may create a substrate that either facilitates (enhanced anisotropy) or inhibits (reduced anisotropy) t he development of cardiac arrhythmias associated with ectopic focal activit y.