In summary, we have found a close association between the stress of A-V nodal conduction and the occurrence of atrial dispersion or aberration. We could not explain atrial dispersion on the basis of incomplete recovery of atrial activity, slowing of atrial conduction, or the occurrence of atrial fusion. We postulate that the phenomenon of dispersion of atrial activation is related to the functional dissociation within the A-V node seen during situations which stress A-V conduction. This phenomenon may represent a mechanism whereby a second area of turnaround other than the A-V node is involved in reentry atrial tachyarrhythmias. Indeed, such a mechanism could provide a physiological basis for the concept of the atrial bridge being involved in supraventricular tachycardias and reciprocal beating
