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J Am Coll Cardiol, 1999; 34:570-577
© 1999 by the American College of Cardiology Foundation
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Double component action potentials in the posterior approach to the atrioventricular node: do they reflect activation delay in the slow pathway?

Jacques M. T. de Bakker, PhDa* {dagger}, Peter Loh, MDa* {dagger}, M.élèze Hocini, MDa* {dagger}, Bernard Thibault, MDa* {dagger} and Michiel J. Janse, MDa* {dagger}

a Department of Experimental Cardiology, Academic Medical Center, Amsterdam, The Netherlands
* Interuniversity Cardiology Institute of the Netherlands, Utrecht, The Netherlands
{dagger} Heart Lung Institute, University of Utrecht, Utrecht, The Netherlands



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Figure 1 Upper tracing: extracellular recording from the His bundle region. Middle tracing: action potentials with a double upstroke recorded in the posterior aspect of the AV node during basic stimulation (S1) with a cycle length of 500 ms followed by an early coupled stimulus (S2). The heart was stimulated from a posterior site. Lower tracings: Action potentials recorded after a premature stimulus with a coupling interval of 1) 310, 2) 290 and 3) 280 ms, respectively. Delay between the first and the second component of the action potential increased and the amplitude of the second component decreased with prematurity. Delay between the stimulus and the first upstroke remained virtually the same. Activation evoked after the extra of 280 ms was blocked toward His. This presents a rather exceptional case. Inset: schematic drawing of the AV junctional area, showing the recording site. A = atrial deflection; CFB = central fibrous body; CS = orifice of coronary sinus; H = His deflection; ME = microelectrode; TT = Tendon of Todaro; TVA = tricuspid valve annulus; V = ventricular deflection.

 


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Figure 2 Upper tracing: extracellular electrogram from the His bundle region. Lower tracings are action potentials recorded from the same endocardial site after the last basic stimulus (S1) and an early coupled stimulus (S2). The tracing marked superficial shows the action potential from a cell located in a superficial layer (directly beneath the endocardium). The tracing marked deep shows the action potential from a cell located at a deeper level. Both tracings show double components during basic stimulation (S1), but the notch in the superficial tracing (bold arrow) becomes more distinct after the premature stimulus (S2). The main (first) component of the action potentials of the superficial tracing has a low upstroke velocity. The timing corresponds with the first, low amplitude deflection of the action potentials from the deeper tracing (open arrow). The main (second) component of the deeper tracing has a high amplitude and fast upstroke velocity. The timing corresponds with the notches marked by the bold arrow in the superficial tracing. The inset shows the endocardial location of the microelectrode. The dips following the bold arrows are artifacts caused by the reference of the microelectrode. Abbreviations as in Figure 1.

 


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Figure 3 Section from the area beneath the endocardial site where the microelectrode from Fig. 2 was impaled. The section was cut perpendicular to the tricuspid valve annulus. The arrow indicates the insertion site. The area consists of strands of myocardial cells widely separated by connective tissue (light areas). Most cells are deprived of cross striation, indicative of transitional cells. A = atrium; E = endocardium; V = ventricle. Scale 0.5 mm.

 


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Figure 4 Tracings are intracellular recordings made during cooling of the anterior area of the AV junction (Panel A). This area was the atrial exit during retrograde conduction. Recordings were made during posterior stimulation at three instants during the cooling procedure: 1) baseline, no cooling, 2) 30 s of cooling, 3) 60 s of cooling. A double component is present during baseline (tracing 1). Delay between the first and second components of the action potential increases with cooling. Delay between the stimulus and the first component remains the same. The inset shows the location of the cooling probe and the recording electrode. The distance between the center of the cooling probe and the endocardial site where the microelectrode was impaled was 5 mm. The tracing, marked His, shows the extracellular electrogram from a site overlying the bundle of His and was made 90 s after starting the cooling procedure (Panel B). At this level of cooling Wenckebach periodicity occurred. The lower tracing (ME) shows the microelectrode recording in the posterior region. Note that the two components do not change with the Wenckebach periodicity. Abbreviations as in Figure 1.

 


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Figure 5 Schematic drawings illustrating how double component action potentials may arise. An activation front (arrows) that passes a discontinuity, being a high resistance gap (panel a), or a site with impedance mismatch (panel b) generates double component action potentials at sites before (1) and after (2) the discontinuity (panel c). Because this process is active, at least one of the components has a large (suprathreshold) amplitude. When activation blocks at the discontinuity, only one deflection remains (panel d). A weak coupling between bundles (panel e) or summation of activation in branching structures (panel f) also gives rise to double component action potentials. When the wave fronts (arrows) are propagating in these structures, the configuration of the generated action potentials is similar to those that arise at high resistance gaps or sites with a load mismatch. When, however, wave fronts are dying, double component action potentials with subthreshold amplitudes may arise (panel h). 1 and 2 indicate recording sites.

 




 
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