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J Am Coll Cardiol, 1993; 22:1541-1547
© 1993 by the American College of Cardiology Foundation
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Experimentally created atrioventricular node reentrant tachycardia in the dog: evidence of a brake system for nodal reentry in the anterior interatrial septum

FY Lin, HM Lo, and JJ Cheng

Department of Surgery, College of Medicine, National Taiwan University, Taipei, Republic of China.

OBJECTIVES. The purpose of the study was to investigate the hypothesis that nodal approaches of both anterior and posterior atrial input sites of the atrioventricular (AV) node contribute to part of the circuit of AV node reentrant tachycardia. Thus, tachycardia might be elicited by a premature atrial impulse that arrived at the AV node through one input site while blocked at another. BACKGROUND. Atrioventricular node reentrant tachycardia is the most common supraventricular tachycardia in humans, yet the exact pathway of the reentrant circuit is unknown. METHODS. In eight dogs, an operation that blocked atrial impulses from the anterior input site to the AV node was performed through a right thoracotomy with the inflow occlusion method. The right atrial free wall and the anterior atrial septum between the sinoatrial node and the AV node were completely divided, whereas the tissues within the triangle of Koch remained intact. Thus, atrial impulses were blocked from the anterior input site in the right atrium and the atrial septum and were conducted only through the left atrial free wall to the posterior atrial septum into the AV node. RESULTS. In a baseline electrophysiologic study before operation, dual AV conduction pathways were demonstrated in seven of eight dogs, but none of the seven had inducible AV node reentrant tachycardia. A repeat study 1 week postoperatively revealed that 1) both PR and AH intervals were prolonged during sinus rhythm (p < 0.01); 2) anterograde and retrograde conduction of the AV node showed no significant changes; and 3) AV node reentrant tachycardia was induced in four dogs (50%), of which three had sustained tachycardia. CONCLUSIONS. These results are compatible with the hypothesis that both nodal approaches of atrial input sites of the AV node contribute to part of the circuit of AV node reentrant tachycardia. They also confirm Moe's hypothesis of the existence of a brake system that prevents sustained AV node reentry. Our data suggest that the brake system is located in the anterior atrial septum.


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