Garcia-Civera R, Sanjuan R, Morell S, Ferrero J A, Miralles L, Llavador J, Lopez-Merino V
Pacing Clin Electrophysiol. 1984 Jul;7(4):649-55. doi: 10.1111/j.1540-8159.1984.tb05591.x.
Electrophysiologic studies were performed in 10 patients with atrioventricular (A-V) nodal reentrant paroxysmal supraventricular tachycardias (PSVT), before and after intravenous administration of propafenone (1.5 mg/kg). All patients utilized an A-V nodal slow pathway for anterograde conduction and an A-V nodal fast pathway for retrograde conduction of the reentrant impulse. Propafenone depressed retrograde fast pathway conduction which was manifested by: 1) complete V-A block at all ventricular paced cycle lengths after propafenone in 3 cases; 2) increase in mean +/- SD of ventricular paced cycle length producing V-A block from less than 308 +/- 37 ms to 432 +/- 63 ms in the remaining 7 patients. Nine of the 10 patients had induction of sustained PSVT before propafenone. In 7 of the 9, PSVT could not be induced or sustained after propafenone, reflecting depression of the retrograde fast pathway conduction with either absence of atrial echoes (5 patients) or induction of nonsustained PSVT, with termination occurring after the QRS (2 patients). In 1 patient, single atrial echoes were induced before propafenone but none were noted after the drug. In only 2 patients was a sustained PSVT inducible after propafenone. In conclusion, propafenone inhibited induction of sustained A-V nodal reentrant PSVT in most patients, reflecting depression of retrograde A-V nodal fast pathway conduction.
对10例房室（A-V）结折返性阵发性室上性心动过速（PSVT）患者在静脉注射普罗帕酮（1.5mg/kg）前后进行了电生理研究。所有患者在折返冲动的前向传导中利用A-V结慢径路，在逆向传导中利用A-V结快径路。普罗帕酮抑制逆向快径路传导，表现为：1）3例患者在注射普罗帕酮后，在所有心室起搏周期长度时均出现完全性室房（V-A）阻滞；2）其余7例患者中，产生V-A阻滞的心室起搏周期长度的平均±标准差从小于308±37ms增加到432±63ms。10例患者中有9例在注射普罗帕酮前可诱发持续性PSVT。在这9例中的7例中，注射普罗帕酮后不能诱发或维持PSVT，这反映了逆向快径路传导受到抑制，表现为无房性回波（5例患者）或诱发非持续性PSVT，在QRS波之后终止（2例患者）。1例患者在注射普罗帕酮前可诱发单个房性回波，但用药后未发现。仅2例患者在注射普罗帕酮后可诱发持续性PSVT。总之，普罗帕酮在大多数患者中抑制了持续性A-V结折返性PSVT的诱发，这反映了A-V结逆向快径路传导受到抑制。
