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  • 1
    Electronic Resource
    Electronic Resource
    350 Main Street , Malden , MA 02148-5018 , USA , and 9600 Garsington Road , Oxford OX4 2DQ , UK . : Blackwell Science Inc
    Journal of cardiovascular electrophysiology 14 (2003), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Introduction: AV nodal conduction properties differ in the anterograde versus the retrograde direction. The underlying substrate remains unclear. We propose that direction-dependent changes in AV nodal function are the net result of those occurring in the slow and fast pathways. Methods and Results: Anterograde and retrograde AV nodal properties were determined with a premature protocol before and after posterior extension (slow pathway) ablation, and before and after upper compact node (fast pathway) ablation. Each ablation was performed in a different group of six rabbit heart preparations. In control, nodal minimum conduction time (NCTmin) and effective refractory period (ERPN) typically were longer, and maximum conduction time (NCTmax) was shorter in the retrograde compared to the anterograde direction. Posterior extension ablation prolonged anterograde ERPN from 91 ± 10 ms to 141 ± 15 ms (P 〈 0.01) and shortened NCTmax from 150 ± 13 ms to 82 ± 7 ms (P 〈 0.01) but did not affect retrograde conduction. Thus, the posterior extension normally contributes to the anterograde but not retrograde recovery curve. Compact node ablation prolonged anterograde conduction (NCTmin increased from 57 ± 2 ms to 73 ± 7 ms, P 〈 0.01) but did not alter ERPN and NCTmax. This ablation abolished retrograde conduction in two preparations and resulted in retrograde slow pathway conduction in four, the latter being interrupted by posterior extension ablation. Thus, the compact node accounts for the baseline of the recovery curve in both directions. Ablation of the compact node results in anterograde slow pathway conduction over the entire cycle length range and may result in retrograde slow pathway conduction. Conclusion: Direction-dependent properties of the AV node arise from those of the compact node-based fast pathway and posterior extension-based slow pathway. Normal AV node has bidirectional dual pathways. (J Cardiovasc Electrophysiol, Vol. 14, pp. 1342-1350, December 2003)
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Selective Slow Nodal Pathway Model. Introduction: The properties and substrates of slow and fast AV nodal pathway remain unclear. This applies particularly to the slow pathway (SP), which is largely concealed by fast pathway (FP) conduction. We designed a new FP ablation approach that exposes the SP over the entire cycle length range and allows for its independent characterization and ablation. Methods and Results: Premature stimulation was performed before and after FP ablation with 5.4 ± 1.9 lesions (300-μm diameter each; overall lesion size 1.4 ± 0.5 mm) targeting the junction between perinodal and compact node tissues in seven rabbit heart preparations. The resulting SP recovery curve and control curve had the same maximum nodal conduction time (165 ± 22 msec vs 164 ± 24 msec; P = NS) and effective refractory period (101 ± 10 msec vs 100 ± 9 msec; P = NS). The two curves covered the same cycle length range. However, the SP curve was shifted up with respect to control one at intermediate and long cycle lengths and thus showed a longer minimum nodal conduction time (81 ± 15 msec vs 66 ± 10 msec; P 〈 0.01) and functional refractory period (180 ± 11 msec vs 170 ± 12 msec; P 〈 0.05). The SP curve was continuous and closely fitted by a single exponential function. Small local lesions (2 ± 1) applied to the posterior nodal extension resulted in third-degree nodal block in all preparations. Conclusion: The posterior nodal extension can sustain effective atrial-His conduction at all cycle lengths and account for both the manifest and concealed portion of SP. Slow and FP conduction primarily arise from the posterior extension and compact node, respectively.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: AV Nodal Conduction and Dual Pathways. Introduction: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. Methods and Results: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (〈300 μm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 ± 16 ms to 123 ± 11 msec (P 〈 0.01) and prolonged the effective refractory period from 104 ± 6 msec to 119 ± 11 msec (P 〈 0.01) without affecting A2H2 min (55 ± 9 msec vs 55 ± 8 msec; P = NS) and functional refractory period (174 ± 7 msec vs 175 ± 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. Conclusion: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Journal of cardiovascular electrophysiology 10 (1999), S. 0 
    ISSN: 1540-8167
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Functional Origin of AV Nodal Reentry. Introduction: The circuitry underlying AV nodal reentry remains debated. We developed a model of AV nodal reentry and assessed the role of nodal inputs, compact node, and its posterior nodal extension (PNE) in this phenomenon. Methods and Results: A fine scanning of short coupling interval range with an atrial premature heat consistently initiated slow-fast AV nodal reentrant heats that occurred 37 ± 31 msec (mean ± SD) after His-bundle activation in 11 of 16 consecutive rabbit heart preparations. The repeated testing (〉40 times) of a chosen coupling interval within reentry window (6 ± 9 msec, n = 11) yielded reentrant intervals that varied by 2 ± 1 msec (mean SD for 40 heats ± SD, n = 11). The breakthrough point of reentrant activation, as assessed from four perinodal sites, varied in different preparations from diffuse (4) to anterior (1), medial (3), or posterior (3); mean reentrant interval did not differ between perinodal sites. Antegrade perinodal activation pattern did not differ at reentrant versus nonreentrant coupling intervals and thus was not a primary determinant of reentry. A PNE ablation (n = 4) interrupted the slow pathway conduction and prevented reentry without affecting antegrade perinodal activation or fast pathway conduction. Conclusion: A reproducible model of AV nodal reentrant beats was developed and used to study underlying circuitry. The AV nodal reentry involves unaltered antegrade perinodal activation, slow PNE conduction and retrograde broad invasion of perinodal tissues starting at a preparation-dependent breakthrough point. A PNE ablation abolishes the reentry.
    Type of Medium: Electronic Resource
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