The mechanism of unidirectional retrograde atrioventricular (AV) @entity616 remains largely unknown. In this study, factors determining the reversal of the unidirectional block by @entity3897 were evaluated in 12 @entity1 who had no demonstrable ventriculoatrial (VA) conduction during ventricular pacing. Six @entity1 demonstrated 1:1 VA conduction after @entity3897 (group I), while the remaining six @entity1 continued to show @entity616 (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 @entity3897 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 less than 0.004). The onset of VA conduction appeared to correlate with the improvement of antegrade conduction. The ratio of these two effects of @entity3897 (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 @entity3897 (1.2 +/- 0.3), reflecting a relatively greater decrease in sinus cycle length. Three of six group I @entity1 redeveloped @entity616 at maximal effect of @entity3897 . The results suggest a functional and dynamic nature of the unidirectional AV @entity616 , possibly caused by vagal influence exaggerating the well-known directional asymmetry of AV nodal conduction in @entity1 .(ABSTRACT TRUNCATED AT 250 WORDS)

Unidirectional retrograde atrioventricular XXXX in @entity1 : determinants of reversibility by vagal antagonism.

@entity1 :: ('9606', 'Species') :: ['patients', 'man'] @entity3897 :: ('MESH:D001285', 'Chemical') :: ['atropine'] @entity616 :: ('MESH:D006327', 'Disease') :: ['nodal block', 'VA block']
@entity616 :: (MESH:D006327,Disease) :: ['nodal block']
