title: Selective prolongation of QRS late potentials by sodium channel blocking antiarrhythmic drugs: relation to slowing of ventricular tachycardia. Electrophysiologic Study Versus Electrocardiographic Monitoring Trial (ESVEM) Investigators.
abstract: Sodium channel blocking antiarrhythmic drugs have preferential effects on diseased, slowly conducting myocardium, and slowing of tachycardia caused by these drugs may result primarily from further prolongation of conduction time in slowly conducting tissue. In patients with sustained ventricular tachycardia, late potentials detected by signal-averaged electrocardiography (ECG) are thought to arise from slowly conducting ventricular myocardium. This study tested the hypothesis that sodium channel blocking drugs selectively prolong the late potential, or terminal low amplitude signal, portion of the signal-averaged QRS complex and that prolongation of the late potential would correlate with slowing of ventricular tachycardia. Fifty-six drug trials in 32 patients with spontaneous and inducible ventricular arrhythmias were studied. Prolongation of the late potential (11 +/- 15 ms) was significantly greater than prolongation of the initial portion of the QRS complex (4 +/- 9 ms) (p = 0.01). Selective prolongation of the late potential by drugs resulted in significantly greater QRS prolongation detectable by signal-averaged ECG than by standard ECG (p less than 0.0001). In 40 trials in which ventricular tachycardia remained inducible during drug therapy, the increase in induced tachycardia cycle length correlated strongly with the increase in late potential duration (p = 0.005) but not with change in the initial portion of the QRS complex. These data suggest that in patients with ventricular tachycardia, sodium channel blocking antiarrhythmic drugs have preferential effects on slowly conducting tissue and that drug effect on slowly conducting tissue contributes to prolongation of ventricular tachycardia cycle length.
authors.affiliation: Department of Internal Medicine, University of Utah School of Medicine, Salt Lake City.
authors.forename: R A
authors.initials: RA
authors.lastname: Freedman
authors.forename: J S
authors.initials: JS
authors.lastname: Steinberg
mesh_terms: D000368:Aged; D000889:Anti-Arrhythmia Agents / Q000627:therapeutic use*; D001145:Arrhythmias, Cardiac / Q000503:physiopathology; D004562:Electrocardiography; D005260:Female; D006329:Heart Conduction System / Q000187:drug effects; D006801:Humans; D008297:Male; D008875:Middle Aged; D015222:Sodium Channels / Q000187:drug effects; D013610:Tachycardia / Q000188:drug therapy* / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents; D015222:Sodium Channels