COMPARISON OF ATRIAL-HIS INTERVALS IN PATIENTS WITH AND WITHOUT DUAL ATRIOVENTRICULAR NODAL PHYSIOLOGY AND ATRIOVENTRICULAR NODAL REENTRANTTACHYCARDIA

The purpose of this study was to compare the atrial-His intervals gene rated during programmed atrial stimulation in patients with and withou t dual atrioventricular nodal physiology and with and without inducibl e atrioventricular nodal reentrant tachycardia. Programmed atrial stim ulation 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 a trial-His interval of the basic-drive beats. The maximum atrial-His in terval was defined as the longest A2H2 interval. The criterion for dua l atrioventricular nodal physiology was an increment of 50 msec in the A2H2 interval in association with a 10 msec decrement in the A1A2 int erval. The minimum atrial-His interval was significantly shorter (106 +/- 34 msec vs 116 +/- 29 msec; p < 0.05) and the maximum atrial-His i nterval 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 atriove ntricular nodal reentry, the maximum atrial-His interval was significa ntly longer in 53 patients who had dual atrioventricular nodal physiol ogy than in 34 patients who did not (340 +/- 105 msec vs 249 +/- 62 ms ec; p < 0.001). Among the 66 patients who had dual atrioventricular no dal physiology, the maximum atrial-His interval was significantly long er in 53 patients who had atrioventricular nodal reentry than in 13 pa tients who did not (340 +/- 105 msec vs 268 +/- 61 msec; p < 0.01). Th e insensitivity of the conventional dual atrioventricular nodal physio logy criterion for the detection of dual atrioventricular nodal pathwa ys is in part attributable to a lesser degree of slowing of conduction in the dow pathway relative to the fast pathway in some patients who have atrioventricular nodal reentry. The inability to demonstrate atri oventricular nodal reentry despite the presence of dual atrioventricul ar nodal physiology in some persons may be attributable in part to an inadequate degree of conduction delay in the slow pathway.