EFFECTS OF PHARMACOLOGICAL AUTONOMIC BLOCKADE ON DUAL ATRIOVENTRICULAR NODAL PATHWAYS PHYSIOLOGY IN PATIENTS WITH SLOW-FAST ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA

The purpose of this study was to investigate the atrioventricular AV n odal physiology and the inducibility of AV nodal reentrant tachycardia (AVNRT) under pharmacological autonomic blockade (AB). Seventeen cons ecutive patients (6 men and 11 women, mean age 39 +/- 17 years) with c linical recurrent slow-fast AVNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and pro pranolol (0.2 mg/kg). in baseline, all 17 patients could be induced wi th AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71 %) of 17 patients still demonstrated A V nodal duality. AVNRT bec ame noninducible in 7 of 12 nonisoproterenol dependent patients and re mained noninducible in all 5 isoproterenol dependent patients. The sin us cycle length (801 +/- 105 ms vs 630 +/- 80 ms, P < 0.005) and AV bl ocking cycle length (365 +/- 64 ms vs 338 +/- 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and funct ional refractory period of the fast pathway (369 +/- 67 ms vs 305 +/- 73 ms, P < 0.005; 408 +/- 56 ms vs 350 +/- 62 ms, P < 0.005) and the s low pathway (271 +/- 30 ms vs 258 +/- 27 ms, P < 0.01; 344 +/- 60 ms v s 295 +/- 50 ms, P < 0.005) likewise became significantly shortened. H owever the ventriculoatrial blocking cycle length (349 +/- 94 ms vs 32 6 +/- 89 ms, NS) and effective refractory period of retrograde fast pa thway (228 +/- 38 ms vs 240 +/- 80 ms, NS) remained unchanged after au tonomic blockade. Pharmacological AB unveiling the intrinsic AV nodal physiology could result in the masking of AV nodal duality and the dec reased inducibility of clinical AVNRT.