Atrial reentry around an anatomic barrier with a partially refractory excitable gap. A canine model of atrial flutter.

Abstract

We have characterized, in dogs, a model of inducible regular atrial tachycardia that resembles atrial flutter. The model involves creating a Y-shaped lesion comprised of an intercaval incision and a connected incision across the right atrium. It is suitable for serial studies of the effects of pacing or antiarrhythmic drugs in chronically instrumented animals studied in the awake state for at least several months. The postoperative cycle length of the induced tachycardia varies from 143 to 188 msec, depending on the size of the dog. The tachycardia cycle length was consistent for each dog, and the rhythm--once induced--was very stable until terminated by pacing. The mechanism of the tachycardia was reentry due to circus movement based on the ability to induce and terminate it by premature impulses or overdrive, the ability to reset the tachycardia by single premature stimuli, the pattern of entrainment during overdrive stimulation, and the ability to terminate the tachycardia by interrupting the conduction pathway. The window of reset determined by the range of coupling intervals of premature stimuli that were able to enter and reset the tachycardia ranged from 56 to 82 msec. There appears to be incomplete recovery of excitability by the end of the excitable gap as evidenced by the fact that even late premature impulses that enter the reentrant circuit conduct more slowly than the tachycardia impulse, and because stimulation of muscarinic receptors that shortens the duration of the action potential and refractoriness also reduces the cycle length of the tachycardia. Epicardial and endocardial activation mapping during tachycardia showed the reentrant pathway does not merely encircle the lesion, particularly over the left atrial epicardium near the intercaval lesion. Rather, the impulse appears to travel around the atrial tissue just above the tricuspid ring, including a portion that travels through the right side of the lower intraatrial septum. Thus, the model involves circus movement around an anatomic barrier through normal tissue that contains no depressed segments. During the circus movement, there is a relatively long excitable gap during which there is incomplete recovery of excitability. This model should be useful for studies of the mechanism of antiarrhythmic drug action and the responses to premature stimulation in this particular subclass of reentrant rhythms, and for comparison with the behavior and responses of other forms of reentry.

Effect of procainamide and N-acetylprocainamide on atrial flutter: studies in vivo and in vitro.

“…figure 6 in Frame et al . 3) This suggests that the cycle length of the flutter is equal to the FRP. The wave length of functional refractoriness thus may be constantly adjusted in terms of the cycle length and vice versa.…”

“…Recently we modified this preparation and studied the mechanism for this type of flutter in detail. 3 We made a Y-shaped lesion, whichconsisted ofan intercaval incision and a contiguous one that branched toward the right atrial appendage. This rendered the atria more susceptible to persistent flutter than did the intercaval lesion alone.…”

“…Furthermore, there is a partially excitable gap in the circus path and thus the rhythm can be entrained by programmed stimulation. 3 In this preparation of atrial flutter the path for circus movement is provided by electrophysiologically normal tissue4' 5; the reentrant impulse propagates in an anatomically discrete circuit and the arrhythmia can be studied over the long term in conscious animals. The preparation is thus suitable for study of the mechanism of action of antiarrhythmic agents.…”

Atrial fibrillation with Wolff-Parkinson-White syndrome

“…Thus, it is possible that in patients with WPW syndrome, the increased structural heterogeneity created by the presence of the AP may play a role in the generation and maintenance of atrial reentry. 32 In experimental studies of the canine heart model of WPW syndrome, structural differences in the AP apparently affected refractoriness and conduction properties of the AP. 33 It was postulated that the AP is the result of an embriologic fault in the formation of fibrous tissue separating the atria and the ventricles .…”

A quantitative evaluation of refractoriness within a reentrant circuit during ventricular tachycardia. Relation to termination.

“…The cycle length of these tachycardias should be dependent on both the path length as defined by the anatomical barrier and the refractory state of the tissue supporting the reentrant impulse. 10,11 Ventricular extrastimuli introduced during clinical sustained uniform ventricular tachycardia frequently results in the advancement of the tachycardia. This suggests that in those tachycardias due to reentry, an excitable gap exists within the tachycardia circuit.…”