Unidirectional retrograde atrioventricular nodal block in man: Determinants of reversibility by vagal antagonism

Abstract

The mechanism of unidirectional retrograde atrioventricular (AV) nodal block remains largely unknown. In this study, factors determining the reversal of the unidirectional block by atropine were evaluated in 12 patients who had no demonstrable ventriculoatrial (VA) conduction during ventricular pacing. Six patients demonstrated 1:1 VA conduction after atropine (group I), while the remaining six patients continued to show VA block (group II). During the control study there was no significant difference in the sinus cycle length and AH interval between the two groups. The percent decrease in sinus cycle length after atropine was also similar in groups I and II (i.e., 23 ± 12 and 26 ± 6, respectively). The effect on antegrade AV nodal conduction (i.e., the percent decrease in AH interval), however, was significantly greater in group I (24 ± 9) as compared to group II (9 ± 5) ( p<0.004). The onset of VA conduction appeared to correlate with the improvement of antegrade conduction. The ratio of these two effects of atropine (i.e., percent decrease in AH interval to percent decrease in sinus cycle length) was higher when VA conduction was first demonstrated in group I (2.3 ± 1.1) than at the maximal effect of atropine (1.2 ± 0.3), reflecting a relatively greater decrease in sinus cycle length. Three of six group I patients redeveloped VA block at maximal effect of atropine. The results suggest a functional and dynamic nature of the unidirectional AV nodal block, possibly caused by vagal influence exaggerating the well-known directional asymmetry of AV nodal conduction in man. Greater improvement in retrograde AV nodal conduction relative to the decrease in sinus cycle length may determine the reversibility of the retrograde conduction block with atropine. This may explain why the latter phenomenon is demonstrable in some patients and not in others.