title: Drug response at electropharmacologic study in patients with ventricular tachyarrhythmias: the importance of ventricular refractoriness.
abstract: The clinical and electrophysiologic predictors of successful antiarrhythmic drug therapy for patients with inducible ventricular tachycardia were evaluated in 59 consecutive patients undergoing serial electropharmacologic trials. Structural heart disease was less frequently present in patients for whom effective therapy was found (p less than 0.05). The presence of coronary artery disease and a history of prior myocardial infarction were significantly more frequently present in patients for whom antiarrhythmic drug therapy could not be found (p less than 0.05). The corrected QT interval and ventricular effective refractory period measured at a pacing cycle length of 400 ms were significantly shorter in responders compared with nonresponders (QT interval 428 +/- 52 versus 460 +/- 59 ms; ventricular effective refractory period 237 +/- 28 versus 254 +/- 24 ms; (p less than 0.05). In addition, the interelectrogram coupling interval of the ventricular extrastimulus initiating ventricular tachycardia was significantly shorter in responders compared with nonresponders (223 +/- 37 versus 251 +/- 33 ms; p = 0.003). Logistic regression analysis identified a short ventricular interelectrogram coupling interval (p less than 0.01) and absence of prior myocardial infarction (p less than 0.05) as the only independent predictors of antiarrhythmic drug suppression of the induction of ventricular tachycardia. Greater drug-induced increments in the ventricular effective and functional refractory periods were observed in responders than in nonresponders as was the shortest ventricular interelectrogram coupling interval. Thus, baseline electrophysiologic measurements identify patients with inducible ventricular tachycardia who are likely to respond to antiarrhythmic drug therapy. Furthermore, these patients demonstrate greater drug-induced electrophysiologic changes.
authors.affiliation: Department of Medicine, University of Calgary, Alberta, Canada.
authors.forename: A M
authors.initials: AM
authors.lastname: Gillis
authors.forename: D G
authors.initials: DG
authors.lastname: Wyse
authors.forename: H J
authors.initials: HJ
authors.lastname: Duff
authors.forename: L B
authors.initials: LB
authors.lastname: Mitchell
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D002304:Cardiac Pacing, Artificial; D003327:Coronary Disease / Q000503:physiopathology; D004562:Electrocardiography; D004594:Electrophysiology; D005069:Evaluation Studies as Topic; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects* / Q000503:physiopathology; D006801:Humans; D008297:Male; D008875:Middle Aged; D012032:Refractory Period, Electrophysiological / Q000187:drug effects; D012044:Regression Analysis; D013610:Tachycardia / Q000175:diagnosis / Q000188:drug therapy*
chemical_list: D000889:Anti-Arrhythmia Agents