TY - JOUR
T1 - 2:1 atrioventricular block during atrioventricular node reentrant tachycardia
AU - Man, K. Ching
AU - Brinkman, Karin
AU - Bogun, Frank
AU - Knight, Bradley
AU - Bahu, Marwan
AU - Weiss, Raul
AU - Goyal, Rajiva
AU - Harvey, Mark
AU - Daoud, Emile G.
AU - Strickberger, S. Adam
AU - Morady, Fred
PY - 1996
Y1 - 1996
N2 - Objectives. The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory. Background. In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block. Methods. In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed. Results. Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean ± SD 312 ± 32 vs. 353 ± 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction. Conclusions. The incidence of induced 2:1 AV block during AV node reentrant tachycardia is ∼10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.
AB - Objectives. The purpose of this study was to determine the incidence and to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laboratory. Background. In patients with 2:1 AV block during AV node reentrant tachycardia, the absence of a His bundle potential in the blocked beats has been considered evidence of intranodal, lower common pathway block. Methods. In consecutive patients with AV node reentrant tachycardia, the incidence of 2:1 AV block and the response to atropine and a single ventricular extrastimulus was observed. Results. Persistent 2:1 AV block occurred in 13 of 139 patients with AV node reentrant tachycardia. A His bundle deflection was present in the blocked beats in eight patients and absent in five. Patients with 2:1 AV block had a shorter tachycardia cycle length than did patients without such block (mean ± SD 312 ± 32 vs. 353 ± 55 ms, p < 0.01). Atropine did not alter the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 block to 1:1 conduction. Conclusions. The incidence of induced 2:1 AV block during AV node reentrant tachycardia is ∼10%. The lack of a response to atropine and the consistent conversion of 2:1 block to 1:1 conduction by a ventricular extrastimulus indicate that, regardless of the presence or absence of a His bundle potential in blocked beats, 2:1 block during AV node reentrant tachycardia is due to functional infranodal block.
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U2 - 10.1016/S0735-1097(96)00415-9
DO - 10.1016/S0735-1097(96)00415-9
M3 - Article
C2 - 8962565
AN - SCOPUS:0030339821
VL - 28
SP - 1770
EP - 1774
JO - Journal of the American College of Cardiology
JF - Journal of the American College of Cardiology
SN - 0735-1097
IS - 7
ER -