This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Takahashi, N. Articles by Zipes, D. P. Search for Related Content PubMed PubMed Citation Articles by Takahashi, N. Articles by Zipes, D. P.

Circulation, Vol 70, 495-505, Copyright © 1984 by American Heart Association

ARTICLES

Overdrive suppression of conduction in the canine His-Purkinje system after occlusion of the anterior septal artery

N Takahashi, RF Gilmour Jr and DP Zipes

The purpose of these experiments was to determine whether overdrive suppression of conduction (OSC), i.e., transient worsening of conduction or development of atrioventricular block after cessation of rapid pacing, could be produced in the canine His-Purkinje system damaged by ligation of the anterior septal coronary artery and to investigate the responsible mechanism. We found that OSC occurred in vivo after rapid ventricular and His bundle pacing but not after atrial pacing, and that it occurred in vitro after rapid pacing from the left bundle branch but not after pacing from the proximal His bundle. OSC was related to the duration and cycle length of pacing. Lidocaine increased while verapamil reduced the duration of OSC in vivo. The mechanism responsible for the unidirectionality of OSC is not clear but is probably related to the geometry of the atrioventricular junction and the anterograde versus the retrograde activation sequence. Changes in regional myocardial blood flow, autonomic tone, hemodynamic variables, or ventricular function do not appear to be required to produce OSC, based on the demonstration of the phenomenon in vitro. The data suggest a time- and rate-dependent change in factors affecting conduction such as excitability or cell-to-cell coupling, possibly due to accumulation of intracellular cations such as calcium.