Interaction of inhomogeneities of repolarization with anisotropic propagation in dog atria. A mechanism for both preventing and initiating reentry.

Having found the regional differences in right atrial action potentials shown in an accompanying article, we tested two seemingly paradoxical hypotheses: 1) The spatial pattern of repolarization provides a protective mechanism against reentry, and 2) repolarization inhomogeneities interact with anisotropic discontinuous propagation to produce reentry. Measurement of multidimensional refractory periods demonstrated an anisotropic distribution within large bundles with the longest refractory periods in the medial upper crista terminalis (sinus node area), a distribution similar to that of action potential durations. Also, discontinuities of repolarization were found at muscle bundle junctions. Early premature impulses originating in the sinus node area propagated throughout the right atrial preparations without conduction disturbances or reentry. Conversely, early premature impulses that originated at sites distal to the sinus node area resulted in localized conduction block at multiple sites, which frequently produced complex conduction changes and reentry. The critical nature of the site of origin of a premature impulse in initiating reentry was related to locations where the steepest repolarization gradients occurred: within anisotropic bundles in the direction of highest axial resistance (across fibers) and at muscle bundle junctions that represented localized discontinuities of axial resistance. The multiple conduction abnormalities at localized sites interacted to produce different types of reentry at a larger size scale (25 mm2 to several cm2). In each case, neither repolarization inhomogeneities (leading circle concept) nor anisotropic discontinuous propagation was the only "mechanism" involved. That is, reentry at a macroscopic size scale occurred as a result of a combined repolarization-anisotropic discontinuous propagation mechanism.