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...
We calculated the wavelength of the atrial impulse in chronically instrumented conscious dogs by measuring both conduction velocity and refractory period: wavelength = refractory period X conduction velocity. Implantation of multiple stimulating and recording electrodes allowed wavelength determination at four different areas: the right and left parts of Bachmann's bundle and the free walls of the right and left atria. During programmed electrical stimulation, three types of arrhythmias were observed: rapid repetitive responses, atrial flutter, and atrial fibrillation. During normal rhythm, the wavelength of the atrial impulse varied between 14 and 18 cm. Premature beats had a shorter wavelength, depending on the degree of prematurity. Premature beats that evoked rapid repetitive responses showed a critical shortening of the wavelength below 12.3 cm. Episodes of atrial flutter were induced at a wavelength below 9.7 cm, while fibrillation occurred at wavelengths shorter than 7.8 cm. We correlated the induction of these arrhythmias with the values of refractory period, conduction velocity, and wavelength during control and during administration of several drugs. Intravenous administration of acetylcholine shortened the wavelength by 30-40%, mainly because of refractory period shortening. Both propafenone and lidocaine had strong but opposite effects on refractoriness and conduction and, consequently, little effect on the wavelength. Quinidine markedly prolonged the refractory period, but prolongation of wavelength was less because of a simultaneous decrease in conduction velocity. d-Sotalol also increased refractory period, but because it had no appreciable effect on conduction velocity, this drug was the most effective in prolongation of wavelength. Linear discriminant analysis of the data showed that the refractory period and the conduction velocity each were poor parameters to predict the occurrence of the different arrhythmias (predictive value 48% and 38%, respectively). The combination of both properties, however, as expressed in the wavelength, was a more reliable index that predicted the induction of the different arrhythmias correctly in 75% of the cases. We conclude that the wavelength is a useful parameter for evaluating antiarrhythmic drugs.
The isolated left atrium of the rabbit, which showed no spontaneous activity, was electrically driven for 20 beats with a cycle length of 500 msec. Tachycardia could be repeatedly initiated by the application of a single adequately timed stimulus shortly after the refractory period of the last basic beat. After the termination of the tachycardia, either spontaneously or artificially by a properly timed stimulus, this procedure was repeated. The number of beats of these tachycardias varied from just one (coupled extrasystole) to many hundreds. Surface electrograms were recorded at about 300 different sites. From the moments of activation of these sites, the spread of activation during regular driving and during the premature beat and the subsequent tachycardia could be determined. In contrast to the radial spread of the activation during basic rhythm, the impulse of the premature beat was propagated in a circular pathway. This circus movement was maintained during tachycardia. These results show that even in a small area of atrial muscle containing no anatomical obstacle the impulse can be entrapped in a circus movement. This circus movement was the underlying mechanism of the arrhythmia. KEY WORDS unidirectional blocksurface electrogram atrial premature beats initiation and termination of tachycardia reentry• From the many investigations that have been done to explain the mechanism underlying flutter and fibrillation of the heart, two alternative hypotheses have emerged: that of ectopic impulse formation and that of circus movement.
Periods of tachycardia were induced in isolated segments (15 X 15 mm) of rabbit left atrium by local application of a properly timed premature stimulus. We used a special device for multiple synchronous microelectrode recordings of responses of more than 100 fibers during the initiation of tachycardia. We clearly demonstrated circus movement of the impulse through a small area of atrial muscle as the underlying mechanism. The premature impulse was conducted antegrade in only one direction, whereas in the other directions antegrade conduction failed. The local responses of the fibers in the blocked area served as a temporary obstacle for return of the premature impulse. When these fibers recovered their excitability before extinction of the premature impulse, they were reentered in a retrograde direction, and the impulse traveled in a circular route. During the propagation of a premature beat, local block, which set the stage for circus movement, was caused by nonuniform recovery of excitability of the atrium. We related the spread of activation of a premature impulse to the naturally occurring spatial dispersion in refractory periods and found that local conduction block invariably was associated with an area of delayed restoration of excitability. Artificial induction of differences in refractory periods by regional application of carbamylcholine made it clear that a disparity in refractory periods of only 11-6 msec between adjacent areas may be sufficient to cause local conduction block of a properly timed premature impulse.
We measured the wavelength of the cardiac impulse, defined as the distance traveled by the depolarization wave during the functional refractory period, in isolated narrow strips of rabbit atrium. During control, wavelength was 42 mm during pacing with 2 Hz, and was 28 mm at the maximum pacing rate; early premature beats had a wavelength as short as 23 mm. Administration of carbamylcholine (4 X 10(-7) g/ml) shortened the wavelength to 21 mm during 2 Hz, 18 mm at the maximum pacing rate Fmax, and 16 mm during an early premature impulse, respectively. The effects of epinephrine (6 X 10(-7) M) were strongly rate dependent. At slow heart rates, epinephrine clearly prolonged the wavelength (58 mm), whereas, during maximum pacing, wavelength remained unchanged (28 mm). Hypokalemia (2 mM) decreased the length of the impulse at all stimulation frequencies. Moderate hyperkalemia (5.6 and 7.0 mM) did not modify wavelength because refractoriness and conduction velocity were affected proportionally. Above 7.0 mM potassium, the wavelength became progressively prolonged because of the development of post-repolarization refractoriness. Cooling to 27 degrees C resulted in a slight lengthening of the impulse. At lower temperatures, however, wavelength prolonged significantly because of a relatively strong prolongation of the refractory period. In separate experiments in 15 X 20 mm segments of atrium, reentrant tachyarrhythmias were induced and the circuit size compared with the wavelength. The size of intraatrial circuits was similar to the magnitude of the measured wavelength during maximum pacing. Carbamylcholine and hypokalemia, both of which shorten the impulse length, also clearly decreased the size of reentrant circuits. Cooling to 27 degrees C, which affects both refractoriness and conduction velocity, only slightly prolonged the wavelength; accordingly, the size of reentrant circuits at 27 degrees C was only slightly longer than at 37 degrees C. These experiments emphasize the importance of the wavelength of the cardiac impulse in relation to the occurrence of intramyocardial reentry.
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