The purpose of this study was to compare the atrial-His intervals generated during programmed atrial stimulation in patients with and without dual atrioventricular nodal physiology and with and without inducible atrioventricular nodal reentrant tachycardia. Programmed atrial stimulation at a basic-drive cycle length of 500 to 600 msec was performed in 180 patients. The minimum atrial-His interval was defined as the atrial-His interval of the basic-drive beats. The maximum atrial-His interval was defined as the longest A2H2 interval. The criterion for dual atrioventricular nodal physiology was an increment of 50 msec in the A2H2 interval in association with a 10 msec decrement in the A1A2 interval. The minimum atrial-His interval was significantly shorter (106 +/- 34 msec vs 116 +/- 29 msec; p < 0.05) and the maximum atrial-His interval significantly longer (304 +/- 101 msec vs 222 +/- 56 msec; p < 0.001) in the 87 patients who had atrioventricular nodal reentry than in the 93 patients who did not. Among the 87 patients who had atrioventricular nodal reentry, the maximum atrial-His interval was significantly longer in 53 patients who had dual atrioventricular nodal physiology than in 34 patients who did not (340 +/- 105 msec vs 249 +/- 62 msec; p < 0.001). Among the 66 patients who had dual atrioventricular nodal physiology, the maximum atrial-His interval was significantly longer in 53 patients who had atrioventricular nodal reentry than in 13 patients who did not (340 +/- 105 msec vs 268 +/- 61 msec; p < 0.01). The insensitivity of the conventional dual atrioventricular nodal physiology criterion for the detection of dual atrioventricular nodal pathways is in part attributable to a lesser degree of slowing of conduction in the slow pathway relative to the fast pathway in some patients who have atrioventricular nodal reentry. The inability to demonstrate atrioventricular nodal reentry despite the presence of dual atrioventricular nodal physiology in some persons may be attributable in part to an inadequate degree of conduction delay in the slow pathway.