title: Effects of class I and III antiarrhythmic drugs on ventricular tachycardia-interrupting critical paced cycle length with rapid pacing.
abstract: The most common mechanism of sustained ventricular tachycardia (VT) is re-entry with an excitable gap, but the electrophysiologic properties and response to antiarrhythmic drugs in the area of slow conduction are not yet fully known. The purpose of this study was to assess the effects of a class I antiarrhythmic drug (procainamide) and class III agents (amiodarone, E-4031, and MS-551) on re-entrant VT using the width of the zone of entrainment. The cycle length (CL) of VT (VTCL), the block CL that was the longest paced CL that interrupted the VT, and the width of the zone of entrainment, defined as the difference between VTCL and block CL, were compared before and after treatment with antiarrhythmic drugs. The VTCL was prolonged significantly from 308+/-63 to 410+/-77 msec after procainamide (p<0.005) but was not changed after the administration of the class III agents: from 294+/-50 to 292+/-13 msec after amiodarone, and from 305+/-47 to 313+/-31 msec after E-4031 or MS-551 (p=NS). The block CL was prolonged from 255+/-61 to 331+/-70 msec after procainamide (p <0.01), from 256+/-20 to 260+/-25 msec after amiodarone, and unchanged after E-4031 or MS-551 (253+/-31 msec before and 270+/-43 msec after) (p=NS). The width of the zone of entrainment as a representative of the width of the excitable gap was changed from 52+/-26 to 79+/-35 msec (p<0.05) after procainamide, whereas it was unchanged after amiodarone (48+/-7 msec before and 43+/-7 msec after) and after E-4031 or MS-551 (50+/-10 msec before and 40+/-9 msec after). Therefore, amiodarone, E-4031, and MS-551 did not affect VTCL and block CL whereas procainamide increased these parameters. The excitable gap substituting as the zone of entrainment was increased by procainamide but slightly reduced by amiodarone, E-4031, and MS-551. The effects of these antiarrhythmic drugs on the excitable gap of re-entrant VT were variable and should be examined further.
authors.affiliation: First Department of Internal Medicine, Niigata University School of Medicine, Japan.
authors.forename: N
authors.initials: N
authors.lastname: Naitoh
authors.forename: T
authors.initials: T
authors.lastname: Washizuka
authors.forename: K
authors.initials: K
authors.lastname: Takahashi
authors.forename: Y
authors.initials: Y
authors.lastname: Aizawa
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000638:Amiodarone / Q000494:pharmacology* / Q000627:therapeutic use*; D000889:Anti-Arrhythmia Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D002648:Child; D004594:Electrophysiology; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D010880:Piperidines / Q000494:pharmacology* / Q000627:therapeutic use*; D011725:Pyridines / Q000494:pharmacology* / Q000627:therapeutic use*; D011744:Pyrimidinones / Q000494:pharmacology* / Q000627:therapeutic use*; D017180:Tachycardia, Ventricular / Q000188:drug therapy* / Q000503:physiopathology*
chemical_list: D000889:Anti-Arrhythmia Agents; D010880:Piperidines; D011725:Pyridines; D011744:Pyrimidinones; C063968:E 4031; C076259:nifekalant; D000638:Amiodarone