Ajmaline is a well-known atrioventricular (AV) node depressant agent, but its effects on functional properties of the AV node and on experimental AV re-entrant
tachycardia have not been explored. The aims of the present study were (1) to determine whether
ajmaline administration modifies the rate-dependent properties of the AV node and (2) to correlate these changes with the actions of
ajmaline on an in vitro model of AV re-entrant
tachycardia. Selective stimulation protocols and mathematical formulations were used to quantify independently AV node recovery, facilitation, and
fatigue in 10 isolated rabbit AV nodes.
Ajmaline decreased facilitation and
fatigue and had no significant effect on AV node recovery. The most important effect of
ajmaline was rate-induced prolongation of AV node effective refractory period, resulting in a greater increase in
tachycardia cycle length. AV re-entrant
tachycardia was sustained when AV effective refractory period divided to
tachycardia cycle length was less than 1,
ajmaline suppressed AV re-entrant
tachycardia by increasing the slope of the AV effective refractory period divided to
tachycardia cycle length versus
tachycardia rate relation, causing the critical ratio of 1 to be attained at a slower rate. A mathematical model incorporating quantitative descriptors of recovery, facilitation, and
fatigue accounted for changes in nodal conduction time, AV effective refractory period,
tachycardia cycle length, and AV effective refractory period divided to
tachycardia cycle length under all conditions. It can be concluded that (1)
ajmaline increases AV conduction time, decreases AV node
fatigue, and facilitation, without altering AV node recovery. (2)
Ajmaline significantly prolongs AV effective refractory period in a rate-dependent manner. (3) These changes play a role in
ajmaline's actions on experimental AV re-entrant
tachycardia.
Ajmaline's ability to terminate re-entrant
supraventricular tachycardia may be due, at least in part, to its ability to amplify the rate-induced prolongation of the nodal refractory period.