2 1 ATRIOVENTRICULAR-BLOCK DURING ATRIOVENTRICULAR NODE REENTRANT TACHYCARDIA/

Citation
Kc. Man et al., 2 1 ATRIOVENTRICULAR-BLOCK DURING ATRIOVENTRICULAR NODE REENTRANT TACHYCARDIA/, Journal of the American College of Cardiology, 28(7), 1996, pp. 1770-1774
Citations number
7
Categorie Soggetti
Cardiac & Cardiovascular System
ISSN journal
07351097
Volume
28
Issue
7
Year of publication
1996
Pages
1770 - 1774
Database
ISI
SICI code
0735-1097(1996)28:7<1770:21ADAN>2.0.ZU;2-E
Abstract
Objectives. The purpose of this study was to determine the incidence a nd to clarify the mechanism of 2:1 atrioventricular (AV) block during AV node reentrant tachycardia induced in the electrophysiology laborat ory. Background. In patients with 2:1 AV block during AV node reentran t tachycardia, the absence of a His bundle potential in the blocked be ats has been considered evidence of intranodal, lower common pathway b lock. Methods. In consecutive patients with AV node reentrant tachycar dia, 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 tachyc ardia. A His bundle deflection was present in the blocked beats in eig ht patients and absent in five. Patients with 2:1 AV block had a short er tachycardia cycle length than did patients without such block (mean +/- SD 312 +/- 32 vs. 353 +/- 55 ms, p < 0.01). Atropine did not alte r the 2:1 block in any patient. In every patient, a single ventricular extrastimulus introduced during the tachycardia converted the 2:1 blo ck to 1:1 conduction, Conclusions. The incidence of induced 2:1 AV blo ck during AV node reentrant tachycardia is similar to 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, regardles s of the presence or absence of a His bundle potential in blocked beat s, 2:1 block during AV node reentrant tachycardia is due to functional infranodal black. (C) 1996 by the American College of Cardiology