DIFFERENTIAL EFFECT OF ESMOLOL ON THE PAST AND SLOW AV NODAL PATHWAYSIN PATIENTS WITH AV NODAL REENTRANT TACHYCARDIA

Introduction: AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting (''slow'') pathway and retrograde conduction over a rapidly conducting (''fast'') pathway. A variety of drugs, such as beta blockers, digitalis, and calcium chann el blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways re spond in a quantitatively different manner to drugs such as beta-adren ergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refr actoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. Methods and Results: Thirteen patients with di scontinuous AV nodal conduction properties and typical AVNRT were stud ied. Anterograde and retrograde AV nodal functional assessment was per formed at baseline and following steady-state drug infusion of intrave nous esmolol at a dose of 500 mu g/kg for 1 minute, 150 mu g/kg per mi nute for the next 4 minutes, followed by a continuous maintenance infu sion of 50 to 100 mu g/kg per minute. The anterograde effective refrac tory period of the fast pathway increased from 381 +/- 75 msec at base line to 453 +/- 92 msec during the infusion of esmolol (P = 0.003). Th e anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 +/- 26 msec to 310 +/- 17 msec (P = 0. 005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 +/- 59 msec) was significantly greater than the change in anterograde effective refrac tory period of the slow pathway (+21 +/- 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased f rom 276 +/- 46 msec to 376 +/- 61 msec during esmolol infusion (P = 0. 03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion . In contrast to the effects of esmolol on refractoriness, the AH inte rval during anterograde slow pathway conduction prolonged to a far gre ater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). Conclusion: The beta-adr energic antagonist, esmolol, has a quantitatively greater effect on an terograde refractoriness of the fast than the slow AV nodal pathway. H owever, the effects on conduction intervals during AVNRT are greater i n the anterograde slow pathway than in the retrograde fast pathway. Th ese observations suggest that the fast and slow pathways may have diff erential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinica lly useful method for demonstrating slow pathway conduction in some in dividuals with AVNRT.