PubMed Health⌕ Search

Biomedical subjects

Jacques Billette

Publications and source records attributed to Jacques Billette.

8 recordsLinked to original sources
PubMed2006

Unified rate-dependent atrioventricular nodal function: consistent recovery and fatigue properties revealed with S1S2S3 protocols and different recovery indexes.

BACKGROUND: Rate-dependent nodal properties are commonly assessed with premature protocols performed at different basic rates. Because characteristics of responses differ with recovery time index, the true nature of nodal rate-dependent properties is elusive. OBJECTIVES: The purpose of this study was to reveal consistent nodal rate-dependent properties regardless of selected recovery index. METHODS: With S(1)S(2)S(3) protocols, we independently varied basic and pretest cycle lengths and thereby distinguished cumulative from noncumulative effects of rate on nodal conduction time in rabbit heart preparations. Nodal responses to 30 basic and pretest cycle length combinations (five with identical basic and pretest cycles as in standard protocols) were analyzed using both atrial (AA) and His-atrial (HA) intervals as recovery index. RESULTS: AA and HA curves had an identical shape for any of 30 steady-state conditions. When assessed with constant pretest cycle lengths, cumulative effects (fatigue) of shortened basic cycle lengths were also independent of recovery index. Shortening of pretest cycle length at fixed basic rates led to apparent inhibitory and facilitatory effects when assessed with AA and HA curves, respectively. These effects vanished when a single long cycle was inserted after the pretest cycle. In all responses including those obtained with standard protocols, combined effects of basic and pretest cycle lengths set nodal conduction time. CONCLUSION: S(1)S(2)S(3) protocols reveal consistent nodal recovery and fatigue properties regardless of recovery index used. Changes in nodal function curves arising from the use of different recovery indexes mainly depend on pretest effects. This study provides a new approach to a unified interpretation of nodal recovery and fatigue properties.

Analysis of Variance↗
PubMed2006

Concealed conduction in nodal dual pathways: depressed conduction, prolonged refractoriness, or reset excitability cycle?

BACKGROUND: Concealed conduction is recognized as a major determinant of atrioventricular (AV) nodal filtering properties, but little is known about the underlying mechanisms. OBJECTIVES: The purpose of this study was to consistently elicit concealed conduction through the AV node and to determine the involvement of slow and fast pathways in resultant changes in nodal function. METHODS: The concealment zone (nodal effective refractory period minus nodal functional refractory period of atrium) was determined in six rabbit heart preparations with and without a conditioning cycle (10 ms longer than nodal effective refractory period). Nodal function curves were constructed for concealed cycle lengths selected within the concealment zone. Experiments were repeated after slow pathway ablation. RESULTS: When assessed with a blocked beat alone, a narrow concealment zone (22 +/- 12 ms, n = 3) was observed in 50% of the preparations. In contrast, when assessed with a blocked beat preceded by a conducted conditioning beat, a wider concealment zone (77 +/- 47 ms, n = 6, P <.03) was observed in all preparations. Increases in the concealed cycle length resulted in graded increases in the nodal effective refractory period and nodal functional refractory period and graded rightward shifts of the recovery curve as a whole, consistent with resetting of the excitability cycle in the slow and fast pathways. These effects were analogous to those expected from a conducted beat. Slow pathway ablation widened the concealment zone but failed to alter fast pathway resetting. CONCLUSION: Our approach reveals a wide concealment zone consistently displayed in all preparations. Concealed conduction acts as a resetting mechanism of the excitability cycle in the slow and fast pathways similar to that expected from a conducted beat.

Analysis of Variance↗
PubMed2005

Atrioventricular conduction in mammalian species: hemodynamic and electrical scaling.

OBJECTIVES: The purpose of this study was to investigate scaling of the duration of late diastolic left ventricular (LV) filling in relation to AV conduction time (delay) (PR interval on the ECG) in mammals. BACKGROUND: From mouse to whale, AV delay increases 10-fold, whereas body mass increases one million-fold. The apparent "mismatch" results from scaling of AV delay versus body and heart mass. METHODS: We measured (1) mitral orifice diameter in 138 postmortem hearts of 48 mammalian species weighing between 17 g and 250 kg and (2) transmitral diastolic flow using magnetic resonance imaging (MRI) recordings of 10 healthy human individuals. (3) We visually inspected early and late diastolic LV filling. (4) We developed two physical models to explain scaling of late diastolic LV filling time. RESULTS: (1) Diameter of the mitral orifice proportionally relates to heart length (third root of heart mass). (2) Atrial contraction starts at a fixed instant (+/- 80%) of the (normalized) cardiac cycle and contributes 31% +/- 5% to LV filling. (3) MRI shows that during diastole, the left atrium (LA) and LV form a single space. (4) The physical models relate the duration of late diastolic LV filling directly to heart length, the third root of heart mass. CONCLUSIONS: (1) Late diastolic (LV) filling time scales with heart length (third root of heart mass). (2) No "mismatch" exists between AV delay and heart size. (3) Knowledge of the actual starting time of atrial contraction may contribute to better treatment of patients with heart failure. (4) The findings suggest that in evolution of mammalian species, hemodynamics commands electrical behavior of the heart.

Animals↗
PubMed2003

Role of compact node and posterior extension in direction-dependent changes in atrioventricular nodal function in rabbit.

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.

Animals↗
PubMed2002

What is the atrioventricular node? Some clues in sorting out its structure-function relationship.

The anatomic and functional substrate underlying AV nodal rate-dependent and dual pathway properties remains highly controversial. This article focuses on some factors that impair the understanding of the AV nodal structure-function relationship and some clues toward sorting it out. A definition of the AV node that applies to both anatomic and functional studies, an orthogonal topographic representation of nodal structures, and the integration of rate-dependent and dual pathway behavior of the AV node are proposed as primary steps toward a better understanding of the AV nodal structure-function relationship. Further fact-based information is the key to the sorting out of this puzzle.

Atrioventricular Node↗