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 A V nodal physiology and the inducibility of A V nodal reentrant tachycardia (A VNRT) under pharmacological autonomic blockade (AB). Seventeen consecutive patients (6 men and 11 women, mean age 39 ± 17 years) with clinical recurrent slow-fast A VNRT received electrophysiological study before and after pharmacological AB with atropine (0.04 mg/kg) and propranolol (0.2 mg/kg). In baseline, all 17 patients could be induced with AVNRT, 5 were isoproterenol-dependent. After pharmacological AB, 12 (71%) of 17 patients still demonstrated A V nodal duality. AVNRT became noninducible in 7 of 12 nonisoproterenol dependent patients and remained noninducible in all 5 isoproterenol dependent patients. The sinus cycle length (801 ± 105 ms vs 630 ± 80 ms, P < 0.005) and AV blocking cycle length (365 ± 64 ms vs 338 ± 61 ms, P < 0.005) became shorter after AB. The antegrade effective refractory period and functional 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 slow pathway (271 ± 30 ms vs 258 ± 27 ms, P 0.01; 344 ± 60 ms vs 295 ± 50 ms, P < 0.005) likewise became significantly shortened. However, the ventriculoatrial blocking cycle length (349 ± 94 ms vs 326 ± 89 ms, NS) and effective refractory period of retrograde fast pathway (228 ± 38 ms vs 240 ± 80 ms, Ns) remained unchanged after autonomic blockade. Pharmacological AB unveiling the intrinsic A V nodal physiology could result in the masking of A V nodal duality and the decreased inducibility of clinical A VNRT.