Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle.

Abstract

SUMMARY In small pieces of rabbit atrial myocardium, sustained periods of circus movement tachycardia were produced by the induction of a single properly timed premature impulse. By use of multiple intracellular and extracellular electrodes the spread of activation during the tachycardia could be analyzed accurately. Because in the present experiments there was no gross anatomical obstacle for the impulse to circulate around, we paid special attention to phenomena occurring in the center of the circus movement. We found that in the absence of an inexcitable central obstacle the center of a circus movement was invaded by multiple centripetal wavelets which converged in the very center of the circuit. On the basis of these observations we developed a new model of circulating excitation in cardiac tissue. The properties of this model (referred to as the "leading circle concept") were compared with the behavior of circus movement around the anatomical obstacle. It turned out that both types of circus movement tachycardia responded differently to changes in basic electrophysiological properties such as conduction velocity and refractory period. For example, addition of carbamylcholine to the tissue bath caused a marked acceleration of the leading circle tachycardia, whereas circus movement in a ring of atrial tissue was hardly affected. On the other hand, depression of conduction velocity by exposure to moderate concentrations of tetrodotoxin had a more pronounced effect on circus movement in the ring preparations than on tachycardias based on a leading circle mechanism. Finally we suggest the use of the strength-interval curve -after some modification -to describe and predict the behavior of a leading circle tachycardia.IN OUR SERIES of papers on circus movement in rabbit atrial muscle 1 ' 2 we were able to show that in a small piece of atrial myocardium the induction of a properly timed premature beat can force the impulse to conduct in a circuitous route and thus set the stage for a period of tachycardia. We gathered evidence that the naturally existing nonuniform recovery of excitability in the atrium was of major importance for the occurrence of unidirectional block of the premature impulse, which, of course, is a prerequisite for the onset of circus movement. Furthermore, by use of a technique for synchronous multiple microelectrode recordings we obtained detailed information about the cellular responses during the initiation of the circus movement.2 However, thus far no conclusive model of circus movement in the absence of an anatomical obstacle could be derived. This was due mainly to a lack of information about what happens in the center of a circulating impulse. In most studies on circus movement and reentry, the model introduced by Mines 3 in 1913 has been used. This model is based on observations in ring-shaped strips of cardiac tissue and implicitly supposes the presence of some kind of gross anatomical obstacle. However, in many cases of tachycardia, as in our experimental studies, circus movement witho...

Inducibility of atrial fibrillation during electrophysiologic evaluation is associated with increased dispersion of atrial refractoriness

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Antiarrhythmic and Electrophysiologic Effects of Flecainide on Acutely Induced Atrial Fibrillation in Healthy Horses

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Split atrial activity in a man with Brady-Tachy syndrome.

“…In the ventricle, local reentry is considered to be the most probable mechanism for tachycardias (Josephson and Seides 1979) and local conduction delay was documented in canine heart (El-Sherif et al 1977) and in man (Josephson et al 1978). As for atrial tachycardias, Wydham et al (1980) suggested triggered activity to be one of the mechanisms, but reentry is also proposed (Allessie et al 1977;Pastelin et al 1978; Watson and Josephson 1980;Boineau et al 1980), and a conduction delay is shown to be a major predisposing factor for the development of atrial flutter (Leier et al 1978). In this report we observed peculiar split atrial activity which suggests some defects of conductivity in the atrium of a man with brady-tacky syndrome.…”