Electrical Excitability of Atrioventricular Nodal Cells

Merideth, John; Méndez, Carlos; Mueller, William J.; Moe, Gordon K.

doi:10.1161/01.res.23.1.69

Cited by 153 publications

(63 citation statements)

References 16 publications

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“…Another possibility is that the supernormal response would propagate slowly through partially refractory tissue, and would be blocked eventually because it would fall outside the window of supernormality of the more At first glance, our results seem to contradict the classical microelectrode studies of Merideth et al 5 These authors studied recovery of excitability in the isolated rabbit AV node but did not demonstrate supernormality during repolarization. Yet, it should be kept in mind that although Merideth et a15 constructed a recovery of excitability curve from the N region of the AV node, they limited their study to scanning the diastolic interval with intracellular stimuli; they did not attempt to determine whether these cells were excitable during the repolarization phase.…”

Section: Potential Limitationscontrasting

confidence: 89%

Wenckebach periodicity in single atrioventricular nodal cells from the rabbit heart.

et al. 1990

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Previous studies have suggested that Wenckebach periodicity in cardiac tissues may occur because of discontinuous propagation across junctional areas in which there is high intercellular resistivity or different cell types. Under these conditions, the impulse may stop altogether at a given junction, or may renew its propagation but only after a step delay imposed by the diastolic time-dependent recovery in the excitability of cells distal to that junction. Accordingly, Wenckebach periodicity in the atrioventricular node may be explained in terms of electrotonically mediated delay in the activation of the nodal cells. To test this hypothesis, we have studied recovery of excitability, and susceptibility to rate-dependent activation failure in single myocytes isolated from the adult rabbit atrioventricular node. Recordings were obtained by using the patch technique in the whole-cell, current clamp configuration. Repetitive stimulation of single atrioventricular nodal myocytes with depolarizing current pulses of critical amplitude yielded frequency-dependent stimulus response patterns that ranged from 1:1, through various Wenckebachlike periodicities (e.g., 5:4 and 4:3) to 2:1 and 3:1. Both typical and atypical Wenckebach structures were demonstrated, as well as "complex" patterns (e.g., reverse Wenckebach or alternating Wenckebach) previously ascribed to multiple levels of block. The diastolic recovery of excitability curve, determined by application of repetitive stimuli at cycle lengths that were longer than the action potential duration, showed a monotonic function with a refractory period outlasting the action potential duration (i.e., postrepolarization refractoriness). Abbreviation of the stimulation cycle length to values below those of the action potential duration revealed the existence of a period of supernormal excitability during the repolarizing phase of the action potential. In either case, the stimulus response patterns obtained were a direct consequence of the shape of the recovery of excitability curve. The monotonic portion of the recovery curve was fitted to an empirical equation that when iterated reproduced the stimulus response patterns observed in the atrioventricular nodal cell. Our data demonstrate that recovery of excitability after an action potential is indeed a function of the diastolic interval, and that this slow process sets the conditions for the development of Wenckebach periodicity in the atrioventricular node. (Circulation 1990;82:2201-2216 The atrioventricular (AV) node of the heart normally prevents high-frequency atrial impulses from reaching the ventricles, and thus prevents severe life-threatening arrhythmias. Indeed, repetitive discharge of the atria can lead to periodic From the

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Section: Potential Limitationscontrasting

confidence: 89%

Wenckebach periodicity in single atrioventricular nodal cells from the rabbit heart.

et al. 1990

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“…This mechanism would therefore depend on N ceUs becoming inexcitable at short cycle lengths. It has indeed been shown that in N ceUs recovery of excitability occurs at a later time than completion of repolarization (125). This delayed recovery of excitability may be crucial in explaining failure of A Vnodal conduction of premature or successive rapid impulses.…”

Section: A Decremental Conduction Versus Electrotonic Transmissionmentioning

confidence: 99%

“…In only one study has the refractory period of A Vnodal cells been determined, by applying stimulating current through an intracellular microelectrode and, after a short latency, recording from the same microelectrode (125). It was indeed demonstrated that inthe N zone recovery of excitability was delayed and lagged behind full repolarization.…”

Section: Nature Of Lnward Gurrent In a Vnodal Gellsmentioning

confidence: 99%

Morphology and electrophysiology of the mammalian atrioventricular node

Meijler

Janse

1988

Physiological Reviews

203

146

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The AV node of those mammalian species in which it has been thoroughly investigated (rabbit, ferret, and humans) consists of various cell types: transitional cells, midnodal (or typical nodal cells), lower nodal cells, and cells of the AV bundle. There are at least two inputs to the AV node, a posterior one via the crista terminalis and an anterior one via the interatrial septum, where atrial fibers gradually merge with transitional cells. The role of a possible third input from the left atrium has not been investigated. Since the transition from atrial fibers to nodal fibers is gradual, it is very difficult to define the "beginning" of the AV node, and gross measurements of AV nodal length may be misleading. Histologically, the "end" of the AV node is equally difficult to define. At the site where macroscopically the AV node ends, at the point where the AV bundle penetrates into the membranous septum, typical nodal cells intermingle with His bundle cells. A conspicuous feature, found in all species studied, is the paucity of junctional complexes, most marked in the midnodal area. The functional counterpart of this is an increased coupling resistance between nodal cells. An electrophysiological classification of the AV nodal area, based on transmembrane action potential characteristics during various imposed atrial rhythms (rapid pacing, trains of premature impulses), into AN (including ANCO and ANL), N, and NH zones has been described by various authors for the rabbit heart. In those studies in which activation patterns, transmembrane potential characteristics, and histology have been compared, a good correlation has been found between AN and transitional cells, N cells and the area where transitional cells and cells of the beginning of the AV bundle merge with midnodal cells, and NH cells and cells of the AV bundle. Dead-end pathways correspond to the posterior extension of the bundle of lower nodal cells and to anterior overlay fibers. During propagation of a normal sinus beat, activation of the AN zone accounts for at least 25% of conduction time from atrium to His bundle, the small N zone being the main source of AV nodal delay. Cycle length-dependent conduction delay is localized in the N zone. Conduction block of premature atrial impulses can occur both in the N zone and in the AN zone, depending on the degree of prematurity. Several factors determining AV nodal conduction delay have been identified.(ABSTRACT TRUNCATED AT 400 WORDS)

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“…Preto the expected responses of phase 4 depolarvious studies in rabbits showed that such rapid atrial ) those interventions. These results, together pacing most likely blocked in the N region of the AV previous results on recordings of diastolic node.8 9 Thus the pause after rapid atrial pacing and om the sinus node, ectopic atrial pacemakers, underdrive of the His bundle in figure 1 is most consisjunction, and the ventricles'-5 suggest that the tent with a pacemaker location in the N or AN region. slope recorded from the AV junction indeed However, the AN location (coronary sinus ostial loca-)hase 4 activity of the junction.…”

Section: Discussionmentioning

confidence: 66%

Recording of diastolic slope with catheters during junctional rhythm in humans.

Hariman¹,

Gomes

El‐Sherif

1984

Circulation

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Junctional diastolic slopes were recorded in 11 of 15 patients (73.3%) with junctional rhythm that occurred spontaneously, after intravenous administration of atropine (1 mg), or during carotid sinus massage. The diastolic slopes were recorded through a unipolar lead consisting of a terminal of an electrode catheter placed in the His bundle area paired with an indifferent terminal on the superior vena cava. The slope of these diastolic deflections averaged -0.18 ± 0.06 mV/sec (mean -+ SD). Overdrive atrial and ventricular stimulations were followed by slowing of the junctional rate and decrease in the diastolic slope. Strong negative correlations (r values from -.71 to -.95) were found between the junctional cycle lengths and the diastolic slopes after atrial or ventricular pacing. Carotid sinus massage decreased the junctional rate and the junctional diastolic slope, whereas atropine increased the junctional rate and the junctional diastolic slope. Since prolongation of junctional cycle lengths after atrial pacing did not depend on frequency of impulse penetration into the His bundle, we postulate that the junctional pacemaker responsible for the junctional rhythm in some of our patients was in the N region of the AV node. Application of this recording method should help in the identification and characterization of automatic junctional pacemakers. Circulation 69, No. 3, 485-491, 1984.DIFFERENTIATION between automatic and reentrant arrhythmias is frequently done in the electrophysiologic laboratory by evaluating the response of the rhythm to electrical stimulation. For example, overdrive suppression is considered a hallmark of an automatic rhythm caused by phase 4 depolarization. On the other hand, differentiation between triggered rhythm, a form of automatic rhythm, and reentrant rhythm cannot be made with certainty because both rhythms can be initiated and terminated by electrical stimuli. Phase 4 depolarization, a marker of automatic activity, can be extracellularly recorded from the junctional area in dogs with junctional rhythm.' In this article we describe application of this technique in patients with junctional rhythm. MethodsFifteen men with junctional rhythm were used for the study (table 1). Junctional rhythm in these patients was characterized as a rhythm with a P wave occurring within or immediately after the QRS complex and with a QRS configuration and HV interval identical to those during sinus rhythm or atrial pacing. The patients' ages averaged 66.7 + 10.9 years (mean + SD). Twelve patients had an underlying clinical diagnosis of sick sinus syndrome, two had junctional rhythm after treatment with digitalis and propranolol, and one had escape junctional rhythm associated with myocardial infarction of the inferior wall (table 1). Seven of the patients had a stable junctional rhythm during the study, five had a junctional rhythm after intravenous administration of 1 mg of atropine, and three had reproducible junctional rhythm during carotid sinus massage.Electrophysiologic studies were p...

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Electrical Excitability of Atrioventricular Nodal Cells

Cited by 153 publications

References 16 publications

Wenckebach periodicity in single atrioventricular nodal cells from the rabbit heart.

Wenckebach periodicity in single atrioventricular nodal cells from the rabbit heart.

Morphology and electrophysiology of the mammalian atrioventricular node

Recording of diastolic slope with catheters during junctional rhythm in humans.

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