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B Thibault

Publications and source records attributed to B Thibault.

22 records · Page 2Linked to original sources
PubMed1996

Atrioventricular junctional tissue. Discrepancy between histological and electrophysiological characteristics.

BACKGROUND: Previous work has demonstrated that cells with AV nodal-type action potentials are not confined to Koch's triangle but may extend along the AV orifices. The aim of this study was to examine the histological and electrophysiological characteristics of this tissue. METHODS AND RESULTS: Studies were performed in isolated, blood-perfused dog and pig hearts. Microelectrode recordings revealed cells with nodal-type action potentials around the tricuspid and mitral valve rings. These cells were found within 1 to 2 mm of the valve annuli. A zone of cells with intermediate action potentials, approximately 1 cm wide, separated cells with nodal-type action potentials from cells with atrial-type action potentials in the body of the atria. In cells with nodal-type action potentials, adenosine caused a reduction in action potential amplitude (49 +/- 2 versus 33 +/- 2 mV, mean +/- SE; P < .001), upstroke velocity (2.5 +/- 0.2 versus 2.0 +/- 0.2 V/s, P < .05), and duration (150 +/- 4 versus 96 +/- 8 ms, P < .001). The light microscopic appearance of AV junctional cells was similar to that of myocytes in the body of the atrium. A polyclonal antibody raised against connexin-43 bound to atrial and ventricular tissue but not to the AV junctional tissue or AV nodal region. The absence of connexin-43 correlated with the sites of cells with nodal-like action potentials. With pacing techniques, the AV junctional tissue in the region of the posterior AV nodal approaches could be electrically dissociated from atrial, AV nodal, and ventricular tissue. AV nodal echoes were induced with ventricular pacing in three dog hearts. In each case, retrograde conduction was through the slow pathway, and anterograde conduction was through the fast pathway. During echoes, activation of AV junctional cells preceded atrial activation during retrograde slow pathway conduction, but these cells were not activated during anterograde fast pathway conduction. CONCLUSIONS: AV junctional cells around both annuli are histologically similar to atrial cells but resemble nodal cells in their cellular electrophysiology, response to adenosine, and lack of connexin-43. The light microscopic appearance of AV junctional cells is a poor guide to their action potential characteristics. The AV junctional cells in the posterior AV nodal approaches appear to participate in slow pathway conduction. These cells may be the substrate of the slow "AV nodal" pathway.

Action Potentials↗
PubMed1996

Electrophysiology of the A-V node in relation to A-V nodal reentry.

During A-V nodal reentry the impulse is supposed to travel through two distinct pathways in the A-V nodal junction, called slow and fast pathways. Clinically, catheter ablation of these pathways has been very successful in abolishing A-V nodal reentrant tachycardias. So-called double potentials have been used as a marker for the slow pathway, and the occurrence of accelerated junctional rhythms (AJR) following ablation is an indicator of successful destruction of the slow pathway. In Langendorff, blood-perfused porcine and canine hearts, extensive mapping of extracellular potentials, combined with microelectrode recordings, was carried out to answer the following questions: 1) what is the origin of double extracellular potentials? 2) what causes post-ablation AJR? 3) what is the activation pattern of the AV junction during ventricular echoes? 1) Two types of double potentials were found: a low-frequency component followed by a high-frequency deflection, the LH potential was caused by asynchronous activation of the sinus septum above the coronary sinus and the region between the coronary sinus orifice and tricuspid annulus, where the L component is a far field potential. HL potentials (high-frequency deflection followed by a low frequency component) were caused by asynchronous activation of atrial cells and cells with AV nodal characteristics at the same location. These cells were present around the entire tricuspid annulus, and were not part of the compact node. The proximity of LH potentials to the slow pathway is probably serendipity, HL potentials could represent the slow pathway. 2) Two types of AJR could be initiated both by application of radiofrequency energy and by heat: a regular rhythm that progressively accelerated and an irregular rhythm. The discrete sites where heat application induced AJR did not correlate with areas showing double potentials, nor with exit regions during ventricular pacing. They were close to the compact node and the underlying mechanism was accelerated phase 4 depolarization in single or multiple foci, the latter accounting for irregular AJR. The association between presence of AJR and successful slow pathway ablation is probably also serendipity. 3) During ventricular pacing, two separate areas of earliest atrial activity were found. When ventricular echoes were induced by premature stimulation, the retrograde impulse activated both atrial exit sites and still returned in the ventricles as an echo. Thus, no evidence was found that atrial tissue forms part of the reentrant circuit.

Animals↗