Circus Movement within the AV Node as a Basis for Supraventricular Tachycardia as Shown by Multiple Microelectrode Recording in the Isolated Rabbit Heart

Janse, Michiel J.; Capelle, F J van; Freud, Gerrit E.; Durrer, D

doi:10.1161/01.res.28.4.403

Cited by 184 publications

(37 citation statements)

References 22 publications

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“…Alternatively, another experimental study provided evidence in favor of an intra-AV nodal reentry circuit. 8 Also, some recent descriptions of the AV node have suggested that the slow and fast pathways exist within the AV node. 9,10 Clinically, Josephson and Miller 11 proposed the concept of intra-AV nodal reentry.…”

Section: Discussionmentioning

confidence: 99%

Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia

et al. 1999

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Background-The exact boundaries of the reentry circuit in atrioventricular nodal reentrant tachycardia (AVNRT) have not been convincingly defined. Methods and Results-To define the tachycardia circuit, single extrastimuli were delivered during AVNRT to 8 sites of the right intra-atrial septum: 3 arbitrarily divided sites of the AV junction extending from the His bundle (HB) site to the coronary sinus ostium (CSOS) (sites S, M, and I) and the superior (S-CSOS), inferior (I-CSOS), posterior (P-CSOS), and posteroinferior (PI-CSOS) portions of the CSOS and the CSOS in 18 patients. The mean tachycardia cycle length (TCL) was 368Ϯ52 ms. Retrograde earliest atrial activation was observed at the HB site in all patients. The longest coupling intervals of single extrastimuli that reset AVNRT at sites S, M, I, I-CSOS, CSOS, S-CSOS, P-CSOS, and PI-CSOS were 356Ϯ51, 356Ϯ51, 355Ϯ52, 357Ϯ51, 318Ϯ47, 305Ϯ53, 311Ϯ56, and 312Ϯ56 ms, respectively, and the following return cycles at these sites were 368Ϯ52, 368Ϯ53, 367Ϯ53, 367Ϯ53, 407Ϯ66, 431Ϯ73, 415Ϯ55, and 412Ϯ56 ms, respectively. The longest coupling intervals at sites S, M, I, and I-CSOS did not differ from each other and were longer than those at CSOS and S-, P-, and PI-CSOS (PϽ0.0001). The return cycles at sites S, M, I, and I-CSOS did not differ from the TCL, whereas those at CSOS and S-, P-, and PI-CSOS were longer than the TCL (PϽ0.0001). Conclusions-The perinodal atrium extending from the HB site to I-CSOS was involved in the tachycardia circuit. I-CSOS was thought to be the entrance of the slow pathway. (Circulation. 1999;100:621-627.)

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Section: Discussionmentioning

confidence: 99%

Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia

et al. 1999

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“…Further experiments using the superfused rabbit AV junction have demonstrated echo beats and even sustained supraventricular arrhythmia within the posterior-inferior right atrium, with the reentrant pathway contained either within or partially outside of Koch's triangle. [5][6][7][8] Little information concerning the anatomic site and functional basis for echo beats and sustained supraventricular arrhythmia has been provided, a result of a complicated 3-dimensional anatomy and the absence of an accepted definition for the dimensions and location of the AV node. Both the mechanism and the site for AVNRT in humans have been presumed to be intra-AV nodal for 20 to 30 years, with a paucity of clinical data supporting this hypothesis.…”

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confidence: 99%

Longitudinal Dissociation Within the Posterior AV Nodal Input of the Rabbit

Patterson

Scherlag

1999

Circulation

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Background-Longitudinal dissociation of an anatomic pathway into 2 electrophysiologically distinct pathways has been hypothesized as a basis for localized AV nodal reentry and supraventricular arrhythmias. Methods and Results-Extracellular bipolar and intracellular microelectrodes were used to record activation in the superfused rabbit AV junction. A subset of rabbit hearts (nϭ19 of 72) demonstrated dissociation of the posterior AV nodal input into Ն2 functional pathways. Antegrade AH conduction was maintained by a pathway just inferior to the tendon of Todaro. Rate-dependent conduction block was observed in a second pathway just superior to the tricuspid annulus, allowing retrograde activation of the distal portion of the inferior posterior AV nodal input and leading to the formation of apparent "dead-end" pathways. The superior (antegrade) and inferior (retrograde) pathways were separated by a band of well-polarized but poorly excitable transitional cells. Additional decreases in the atrial cycle length progressively increased the AH interval, further delaying retrograde activation of the inferior pathway, and progressively moved the site of conduction block in the inferior pathway proximally, thus extending the length of the retrograde conduction pathway and allowing circus movement within the transitional cells of the posterior AV nodal connection. Conclusions-Longitudinal

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“…Activation times for intracellular recording were determined at the point of .Tnax. 16 Resting membrane potential was obtained from a DC amplified action potential signal (total IOOX) and stored on a memory oscilloscope. If resting membrane potential deviated by more than 5 mV, the experiment was not used for the determination of action potential variables since we noted some variability inVmax.…”

Section: Methodsmentioning

confidence: 99%

The effects of procainamide on conduction in anisotropic canine ventricular myocardium.

Kadish¹,

Spear²,

Levine

et al. 1986

Circulation

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Although conduction velocity in cardiac tissue is dependent on fiber orientation, the influence of commonly used antiarrhythmic agents on conduction longitudinal and transverse to such fibers is unknown. We evaluated the effects of procainamide on conduction velocity and intracellular potentials in vitro during conduction longitudinal and transverse to fiber orientation in epicardial strips obtained from areas of uniform fiber orientation from 15 adult mongrel dogs. Ventricular epicardial strips demonstrated marked anisotropy. At a pacing cycle length of 1000 msec, mean conduction velocity longitudinal to fiber orientation averaged 0.602 + 0.051 m/sec and mean conduction velocity transverse to fiber orientation was 0.186 + 0.024 m/sec, resulting in a ratio of longitudinal to transverse conduction velocities of (OL/T) 3.27 ± 0.38. After the addition of procainamide, conduction velocity decreased to 0.532 + 0.062 m/sec longitudinal to fiber orientation and to 0.174 ± 0.023 m/sec transverse to fiber orientation resulting in a decrease of OL/T to 3.09 ± 0.37 (p < .05 vs control). Before the addition of procainamide, when pacing at progressively shorter cycle lengths, conduction velocity longitudinal to fiber orientation was relatively unchanged, whereas conduction velocity transverse to fiber orientation decreased resulting in an increase in OL/T. After the addition of procainamide, conduction velocity at shorter pacing cycle lengths decreased both longitudinal and transverse to fiber orientation demonstrating the well-known use-dependent effect of procainamide. However, in contrast to control conditions, conduction velocity longitudinal to fiber orientation was slowed by a greater extent than the conduction transverse to fiber orientation, resulting in an even greater decrease in OL/T. To investigate the effect of differences in drug binding during propagation in different directions, we examined conduction velocity during alternations in pacing direction and compared it with velocity during steady-state pacing. At a pacing cycle length of 1000 msec, no difference was observed between the initial conduction velocity after changing pacing directions and the steady-state conduction velocity. At pacing cycle lengths shorter than 1000 msec, when changing from transverse to longitudinal conduction, there was an initial drop in normalized conduction velocity that was present on the first beat of longitudinal conduction; however, with continued pacing in a longitudinal direction there was a further decrease in conduction velocity. We conclude from the above findings that: (1) procainamide has nonhomogeneous effects on conduction in anisotropic ventricular muscle; conduction velocity longitudinal to fiber orientation is depressed by a greater extent than transverse to it; and (2) differences in drug binding depending on propagation direction and/or an effect of procainamide on junctional resistivity may be responsible for the directional differences in the effects of procainamide we observed. Circulation 74, No. 3...

show abstract

Circus Movement within the AV Node as a Basis for Supraventricular Tachycardia as Shown by Multiple Microelectrode Recording in the Isolated Rabbit Heart

Cited by 184 publications

References 22 publications

Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia

Electrophysiological Delineation of the Tachycardia Circuit in Atrioventricular Nodal Reentrant Tachycardia

Longitudinal Dissociation Within the Posterior AV Nodal Input of the Rabbit

The effects of procainamide on conduction in anisotropic canine ventricular myocardium.

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