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J Am Coll Cardiol, 1996; 28:1770-1774 © 1996 by the American College of Cardiology Foundation |
Department of Internal Medicine, University of Michigan, Ann Arbor 48109-0022, USA.
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 approximately 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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