We examined the electrophysiologic characteristics and mechanisms of verapamil-sensitive atrial tachycardia (AT) originating from the atrioventricular (AV) annulus in 18 patients. AT originated from the AV node vicinity (AV nodal AT, 10 patients) and the area distant from the AV node (non-AV nodal AT, 8 patients). There was no significant difference in the tachycardia cycle length between AV nodal and non-AV nodal AT. For both types of AT, tachycardia was inducible by atrial extrastimulation with an inverse relation between the coupling and the postpacing intervals. A single extrastimulus delivered from the earliest atrial activation site reset both ATs with an inverse relation between the coupling interval and return cycle. Also no significant difference was observed in the percentage of the excitable gap to tachycardia cycle length between AV nodal and non-AV nodal AT. Concealed entrainment was observed by rapid atrial pacing delivered from the earliest atrial activation site for both ATs. These findings suggest that these ATs are due to reentry. Intravenous administration of verapamil (2.5 to 5 mg) and adenosine triphosphate (5 mg) terminated AT in all patients. AT was successfully ablated at the earliest atrial activation site in all patients. It was shown that this form of AT in which a calcium channel-dependent substrate is involved arises not only from the vicinity of the AV node but also along the AV annulus with common electrophysiologic characteristics. These suggest the presence of a distinct entity of tachycardia more appropriately classified as verapamil-sensitive AV annular AT.