Functional characteristics of retrograde conduction in a pacing model of "endless loop tachycardia".
A pacing model was designed that stimulated "endless loop tachycardia," a complication found in the new generation of DDD (atrioventricular [AV] universal) pacemakers. The functional characteristics of the train of ventricular impulses simulating endless loop tachycardia were studied during both AV sequential pacing and basic ventricular drive. AV sequential pacing, by causing a decrease in ventriculoatrial (VA) conduction time of the first beat of the endless loop tachycardia, was associated with a decrease in the cycle length at which VA block occurred in 9 of 12 patients. The site of block was the His-Purkinje system in 4 of these 12 patients and the AV node in the remaining 8. At a cycle length with 1:1 VA conduction, a steady state VA conduction time was achieved in 2 to 4 beats (VA conduction time accommodation). The pattern of such accommodation depended on the site (His-Purkinje system versus AV node) of the maximal conduction delay. The steady state VA conduction time itself was altered with AV sequential pacing in patients showing His-Purkinje system delay, but not in patients with AV nodal delay. The results suggest that in most patients, the cycle length of VA block and the longest steady state VA conduction time will depend on the retrograde conduction time of the first beat of the tachycardia. In addition, pharmacologic measures to prevent or terminate endless loop tachycardia will have to take into account the fact that both the His-Purkinje system and the AV node can be the site of initial block.
D001283:Atrioventricular Node / Q000503:physiopathology*; D002036:Bundle of His / Q000503:physiopathology; D002304:Cardiac Pacing, Artificial / Q000009:adverse effects*; D004562:Electrocardiography; D005260:Female; D006327:Heart Block / Q000503:physiopathology; D006329:Heart Conduction System / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008955:Models, Cardiovascular; D013610:Tachycardia / Q000209:etiology / Q000503:physiopathology*