Characteristics, Circuit, Mechanism, and Ablation of Reentry in the Rabbit Atrioventricular Node

Lin, Long-Yau; Billette, Jacques; Martel, Karyne; Wang, Jun; Medkour, Djamila

doi:10.1111/j.1540-8167.1999.tb01266.x

Cited by 12 publications

(21 citation statements)

References 50 publications

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“…We have earlier presented the reentry pathway for the retrograde-induced ventricular echo phenomenon 10 ; now we have extended our findings to the more clinically relevant anterogradely-induced AV nodal reentry. Our data are consistent with the electrode mapping data of AV nodal reentry from Billette's group 9,25,26 and the optical imaging data of canine AV nodal reentry from Zipes group. 6 Our results provide support for the dual-pathway electrophysiology theory by presenting images of the two AV nodal conduction pathways.…”

supporting

confidence: 80%

Cx43 and Dual-Pathway Electrophysiology of the Atrioventricular Node and Atrioventricular Nodal Reentry

Nikolski

Jones²,

Lancaster³

et al. 2003

Circulation Research

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Fluorescent imaging has revealed that posterior nodal extensions provide the anatomical substrate for the dual-pathway electrophysiology of the atrioventricular (AV) node during normal conduction and reentry. The reentry can be intranodal, or as well as the posterior nodal extensions, it can involve an endocardial layer of atrial/atrial-nodal (A/AN) cells as part of the AV nodal reentry (AVNR) circuit. Using fluorescent imaging with a voltage-sensitive dye and immunolabeling of Cx43, we mapped the electrical activity and structural substrate in 3 types of AVNR induced by premature atrial stimulation in 8 rabbit hearts. In 6 cases, the AVNR pathway involved (1) a fast pathway (FP), (2) the A/AN layer, and (3) a slow pathway (SP). In 4 cases, reentry took the path (1) SP, (2) A/AN layer, and (3) FP. In 2 cases, reentry was intranodal, propagating between the 2 posterior nodal extensions. Immunolabeling revealed that the FP and SP are formed by Cx43-expressing bundles surrounded by tissue without Cx43. Cx43-expressing posterior nodal extensions are the substrate of AVNR during both intranodal and extranodal reentry.

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supporting

confidence: 80%

Cx43 and Dual-Pathway Electrophysiology of the Atrioventricular Node and Atrioventricular Nodal Reentry

Nikolski

Jones²,

Lancaster³

et al. 2003

Circulation Research

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“…Normal dual pathways are observed in human, rabbit, porcine, and canine hearts (4,26,28,30,36,43,49,50,60,71) and show FP and SP conduction ranges and refractory periods analogous to those of patients suffering from an AV nodal reentrant tachycardia. However, the normal dual pathways yield a smoother recovery curve at the transition from FP to SP than that of these patients (36,50,60).…”

Section: Dual Pathway Origin Of Rate-dependent Av Nodal Functionmentioning

confidence: 98%

“…However, the normal dual pathways yield a smoother recovery curve at the transition from FP to SP than that of these patients (36,50,60). They can nonetheless be interrupted with ablation lesions (4,26,36,43,44,60,71). The typical target of a SP ablation is the crista terminalis input to the AV node, while the target of FP ablation is the interatrial septum input.…”

Section: Dual Pathway Origin Of Rate-dependent Av Nodal Functionmentioning

confidence: 99%

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Integrated rate-dependent and dual pathway AV nodal functions: principles and assessment framework

Billette

Tadros

2014

American Journal of Physiology-Heart and Circulatory Physiology

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The atrioventricular (AV) node conducts slowly and has a long refractory period. These features sustain the filtering of atrial impulses and hence are often modulated to optimize ventricular rate during supraventricular tachyarrhythmias. The AV node is also the site of a clinically common reentrant arrhythmia. Its function is assessed for a variety of purposes from its responses to a premature protocol (S 1S2, test beats introduced at different cycle lengths) repeatedly performed at different basic rates and/or to an incremental pacing protocol (increasingly faster rates). Puzzlingly, resulting data and interpretation differ with protocols as well as with chosen recovery and refractory indexes, and are further complicated by the presence of built-in fast and slow pathways. This problem applies to endocavitary investigations of arrhythmias as well as to many experimental functional studies. This review supports an integrated framework of rate-dependent and dual pathway AV nodal function that can account for these puzzling characteristics. The framework was established from AV nodal responses to S 1S2S3 protocols that, compared with standard S 1S2 protocols, allow for an orderly quantitative dissociation of the different factors involved in changes in AV nodal conduction and refractory indexes under rate-dependent and dual pathway function. Although largely based on data from experimental studies, the proposed framework may well apply to the human AV node. In conclusion, the rate-dependent and dual pathway properties of the AV node can be integrated within a common functional framework the contribution of which to individual responses can be quantitatively determined with properly designed protocols and analytic tools. atrioventricular node; functional assessment; conduction; refractory period; pretest cycle length; recovery; facilitation; fatigue THE ATRIOVENTRICULAR (AV) node generates a delay between atrial and His bundle activation that helps optimize ventricular filling and blood pumping. The AV node also has rate-dependent conduction and refractory properties accounting for the filtering of atrial impulses during supraventricular tachyarrhythmias. The optimization of this filtering to control the ventricular rate constitutes a cornerstone of atrial fibrillation therapy (3). Another consistent feature of the normal AV node is its built-in fast pathway (FP) and slow pathway (SP) (29,36,45,50,60,73). In some human hearts, SP and FP interplay to result in a clinical arrhythmia known as AV nodal reentrant tachycardia, the most common form of paroxysmal supraventricular tachycardia that can now be successfully cured by ablation therapy (24,34,59,61). These properties are obviously sensitive to autonomic tone (54 -57), itself modulated by conditions such as rest, exercise, pregnancy, stress, diseases, drugs, etc. However, the basic AV nodal physiology and its assessment tools remain debated. Their understanding is the primary goal of this review.The understanding of AV nodal function remains indeed challenging. Zip...

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“…Although mapping studies have clearly established that anterograde and retrograde activation largely result in mirror images, the substrate underlying slow and fast pathway involvement remains undetermined 28,29 . There is growing evidence that the compact node and posterior extension play a critical role in slow and fast pathways 30–33 . Dye mapping studies support this view and establish both their anterograde and retrograde activation patterns 9,10 .…”

Section: Introductionmentioning

confidence: 99%

Role of Compact Node and Posterior Extension in Direction‐Dependent Changes in Atrioventricular Nodal Function in Rabbit

Reid

Billette

Khalifé

et al. 2003

Cardiovasc electrophysiol

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Characteristics, Circuit, Mechanism, and Ablation of Reentry in the Rabbit Atrioventricular Node

Cited by 12 publications

References 50 publications

Cx43 and Dual-Pathway Electrophysiology of the Atrioventricular Node and Atrioventricular Nodal Reentry

Cx43 and Dual-Pathway Electrophysiology of the Atrioventricular Node and Atrioventricular Nodal Reentry

Integrated rate-dependent and dual pathway AV nodal functions: principles and assessment framework

Role of Compact Node and Posterior Extension in Direction‐Dependent Changes in Atrioventricular Nodal Function in Rabbit

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