Quantitation of dynamic AV nodal properties and application to predict rate-dependent AV conduction

Abstract

A number of functional properties of the atrioventricular (AV) node have been described in response to changes in the atrial input rate. The purpose of this study was 1) to develop quantitative descriptors of these properties, and 2) to determine whether they can account for rate-dependent changes in AV nodal conduction. The delay in AV nodal conduction of single premature beats (recovery) was found to be an exponential function of coupling interval with a time constant of 66 +/- 2 (+/- SE) ms. A single abbreviated (facilitation) cycle did not alter the time constant of recovery or basal conduction for a subsequent beat but shifted its recovery curve to the left to an extent exponentially related to the facilitation cycle length. The induction of a tachycardia with HA interval fixed so as to control the recovery and facilitation variables resulted in a first-order onset of AV conduction slowing (fatigue). The fatigue process had a time constant in the range of 70 beats and a magnitude that was a decaying exponential function of HA interval. An equation incorporating quantitative descriptors of recovery, facilitation, and fatigue accurately predicted rate-dependent changes in AH interval. We conclude that 1) the AV nodal properties of recovery, facilitation, and fatigue are amenable to quantitative characterization, and 2) rate-dependent changes in AV nodal conduction time can be well described in terms of these underlying properties.

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

“…While ERPN increases with basic rates (14,16,70), FRPN shortens (13,14,16,20,25,51), so that the significance of these changes remains confounding. The dependence of A 2 H 2 on the preceding cycle length is similarly expressed at all BCL (41,54,66). However, a short BCL (Fig.…”

“…For instance, these properties account for transient responses to linear ramp increase and decrease in cycle length inducing hysteresis in AV nodal conduction time (12,75). These properties also quantitatively account for a variety of other rate-induced AV nodal responses including Wenckebach cycles (54,62,68,74). A recent study also provides analytical and modeling data supporting their involvement in human supraventricular tachyarrhythmias (46).…”

“…One factor is the fatigue property that increases nodal conduction time with the magnitude and duration of the fast rate (11,40,41,52). Fatigue develops rapidly during the first minute of a fast rate and has usually reached a steady state after 5 min (11,54). Mean maximum fatigue measured in the flat portion of the curve increases A 2 H 2 by up to 12 ms in rabbit and dog hearts (11,20,41,54).…”

“…Fatigue develops rapidly during the first minute of a fast rate and has usually reached a steady state after 5 min (11,54). Mean maximum fatigue measured in the flat portion of the curve increases A 2 H 2 by up to 12 ms in rabbit and dog hearts (11,20,41,54). Although fatigue remains to be selectively characterized in humans, it is expected to be analogous to that of other species (62).…”

Atrioventricular nodal reverse facilitation in connexin40-deficient mice

“…[12][13][14][15][16][17][18][19][20][21][22] Microelectrode recording studies have shown that the proximal, rather than distal, AV node plays a critical role in the generation of facilitation. 23,24 Based on our previous study 11 that Cx40-deficient mice display impaired AV nodal conduction, we hypothesize that Cx40-deficient mice display altered patterns of AV nodal facilitation compared with wild-type controls.…”