원저 : 발작성 상심실성 빈맥 환자에 대한 항부정맥 약물작용 기전과 약물반응 예측에 관한 연구

In this study, the effects of antiarrhythmic drugs on the reentrant pathway in paroxysmal supraventricular tachycardia (PSVT) were evaluated by observing the changes of conduction block cycle length. And this study was aimed to determine whether the drug responses could be predicted by characterizing the reentry path- way. Seventy-three patients with clinically documented PSVT without preexcitation were carried on electro-physiologic studies between November, 1986 and April 1990 in Severance Hospital, Yonsei University were reviewed. The study group included 35 males and 38 females with ages ranging from 16 to 67 years (mean±SD:40±15). The mean duration of symptom was 10.9±9.5 years. They had experienced paroxysmal tachycardia once per week to once in 6 months (mean frequency: 5 per year). All patients had structurally normal heart except the 2 Ebstein`s anomaly. The induction of tachycardia and the determination of mechanism of PSVT were performed by baseline electrophysiologic study in drug free status, The effects of drugs were assessed by the intravenous administration of procainamide 20 mg/kg, flecainide 2 mg/kg, verapamil 0.15 mg/kg, digoxin 0.75 mg, and digoxin 0,75 mg plus propranolol 0.15 mg/kg. The response to drug was defined as the not-induced SVT or the induction of nonsustained SVT after drug administration. 1) Fourty-nine patients had atrioventricular (AV) reentrant tachycardia using concealed bypass tract(CBT) and twenty-four patients had atrioventricular nodal reentrant tachycardia. In AV reetry using CBT, procainamide prevented induction of sustained tachycardia in 38 of 45 patients (84%), flecainide in 23 of 30 patients(77%), verapamil in 34 of 39 patients(87%), digoxin in 4 of 17 patients (23%), and digoxin plus propranolol in 7 of 14 patients(50%), In AV nodal reentry, procainamide prevented induction of sustained tachycardia in 19 of 22 patients (86%), flecainide in 9 of 10(90%), verapamil in 20 of 22 patients(91%), digoxin in 10 of 17 patients(59%), and digoxin plus propranolol in 9 of 13 patients(69%). 2) In AV reentry using CBT, procainamide and flecainide induced significant prolongation of the ventriculoatrial block cycle length (VABCL) in responder group. Also the atriventricular block cycle length (AVBCL) was prolonged significantly, but not increased above the tachycardia cycle length. Verapamil, digoxin and digoxin plus propranolol showed significant prolongation of AVBCL, but not of VABCL. 3) In AV nodal reentry, procainamide and flecainide induced significant prolongation of VABCL in responder group, and AVBCL was also prolonged but not increased above the tachycardia cycle length. Verapamil, digoxin and digoxin plus propranolol induced significant prolongation of both AVBCL and VABCL in responder group. 4) In patients with AV reentry, there was no significant difference of baseline VA block cycle length between responders and non-responders for procainamide and flecainide. But the patients having the 260 millisecond or more of block cycle length were all responded to procainamide except 1 case and all to flecainide. 5) The procainamide and flecainide had a strong concordant relationship in drug response for AV reentry(p<0. 001). With the avove results, it is noted that the procainamide and flecainide prevent induction of reentrant supraventricular tachycardia by selectively depressing the conduction over retrograde pathway of reentry circuits in responders with AV reentry using CBT and AV nodal reentry. Also it is noted that the verapamil, digoxin and digoxin plus propranolol prevented induction of SVT by depressing the conduction over antegrade pathway in responders with AV reentry using CBT, and over antegrade (AV nodal slow) and retrograde (AV nodal fast) pathways in responders with A V nodal reentry. And it can be suggested that the baseline block cycle length of accessory pathway has a limited value in predicting the drug responses in AV reentry using CBT. Also it is noted that in AV r