title: Electropharmacologic effects of class I and class III antiarrhythmia drugs on typical atrial flutter: insights into the mechanism of termination.
abstract: BACKGROUND
  Acute effects of class I and class III antiarrhythmia drugs on the reentrant circuit of typical atrial flutter are not fully studied. Furthermore, the critical electrophysiologic determinants of flutter termination by antiarrhythmia drugs are not clear.
  
  
  RESULTS
  The study population consisted of 36 patients (mean age, 53+/-17 years) with clinically documented typical atrial flutter. A 20-pole "halo" catheter was positioned around the tricuspid annulus. Incremental pacing was performed to measure the conduction velocity along the isthmus and lateral wall, and extrastimulation was performed to evaluate atrial refractory period in the baseline state and after intravenous infusion of ibutilide, propafenone, and amiodarone. Efficacy of these drugs in conversion of typical atrial flutter and patterns of termination were also determined. Ibutilide significantly increased the atrial refractory period and decreased conduction velocity in the isthmus at short pacing cycle length. It terminated atrial flutter in 8 (67%) of 12 patients after prolongation of flutter cycle length due to increase (86+/-19%) of conduction time in the isthmus. Propafenone predominantly decreased conduction velocity with use dependency and significantly increased atrial refractory period, but it only converted atrial flutter in 4 (33%) of 12 patients. Amiodarone had fewer effects on atrial refractory period and conduction velocity than did ibutilide and propafenone, and it terminated atrial flutter in only 4 (33%) of 12 patients. Termination of typical atrial flutter was due to failure of wave front propagation through the isthmus, which occurred with cycle length oscillation, abruptly without variability of cycle length, or after premature activation of the reentrant circuit.
  
  
  CONCLUSIONS
  Ibutilide, with a unique increase in atrial refractoriness, was more effective in conversion of atrial flutter than were propafenone and amiodarone.
authors.affiliation: Department of Medicine, National Yang-Ming University, School of Medicine, Veterans General Hospital-Taipei, Taiwan, ROC.
authors.forename: C T
authors.initials: CT
authors.lastname: Tai
authors.forename: S A
authors.initials: SA
authors.lastname: Chen
authors.forename: A N
authors.initials: AN
authors.lastname: Feng
authors.forename: W C
authors.initials: WC
authors.lastname: Yu
authors.forename: Y J
authors.initials: YJ
authors.lastname: Chen
authors.forename: M S
authors.initials: MS
authors.lastname: Chang
mesh_terms: D000328:Adult; D000368:Aged; D000638:Amiodarone / Q000008:administration & dosage / Q000494:pharmacology*; D000704:Analysis of Variance; D000889:Anti-Arrhythmia Agents / Q000008:administration & dosage / Q000145:classification / Q000494:pharmacology*; D001282:Atrial Flutter / Q000188:drug therapy / Q000503:physiopathology*; D016275:Atrial Function / Q000187:drug effects* / Q000502:physiology; D006328:Cardiac Catheterization; D004594:Electrophysiology / Q000379:methods; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D008875:Middle Aged; D011405:Propafenone / Q000008:administration & dosage / Q000494:pharmacology*; D013449:Sulfonamides / Q000008:administration & dosage / Q000494:pharmacology*
chemical_list: D000889:Anti-Arrhythmia Agents; D013449:Sulfonamides; C067192:ibutilide; D011405:Propafenone; D000638:Amiodarone