OPTICAL MAPPING OF ATRIOVENTRICULAR NODE REVEALS A CONDUCTION BARRIERBETWEEN ATRIAL AND NODAL CELLS

The mechanisms responsible for atrioventricular (AV) delay remain uncl ear, in part due to the inability to map electrical activity by conven tional microelectrode techniques. In this study, voltage-sensitive dye s and imaging techniques were refined to detect action potentials (APs ) from the small cells comprising the AV node and to map activation fr om the ''compact'' node. Optical APs (124) were recorded from 5 x 5 mm (similar to 0.5-mm depth) AV zones of perfused rabbit hearts stained with a voltage-sensitive dye. Signals from the node exhibited a set of three spikes; the first and third (peaks I and III) were coincident w ith atrial (A) and ventricular (V) electrograms, respectively. The sec ond spike (peak II) represented the firing of midnodal (N) and/or lowe r nodal (NH) cell APs as indicated by their small amplitude, propagati on pattern, location determined from superimposition of activation map s and histological sections of the node region, dependence on depth of focus, and insensitivity to tetrodotoxin (TTX). AV delays consisted o f tau(1) (49.5 +/- 6.59 ms, 300-ms cycle length), the interval between peaks I and II (perhaps AN to N cells), and tau(2) (57.57 +/- 5.15 ms ), the interval between peaks II and III (N to V cells). The conductan ce time across the node was 10.33 +/- 3.21 ms, indicating an apparent conduction velocity (Theta(N)) of 0.162 +/- 0.02 m/s (n = 9) that was insensitive to TTX. In contrast, tau(1) correlated with changes in AV node delays (measured with surface electrodes) caused by changes in he art rate or perfusion with acetylcholine. The data provide the first m aps of activation across the AV node and demonstrate that Theta(N) is faster than previously presumed. These findings are inconsistent with theories of decremental conduction and prove the existence of a conduc tion barrier between the atrium and the AV node that is an important d eterminant of AV node delay.