The Effects of Type I Antiarrhythmic Drugs on the Signal-Averaged Electrocardiogram in Patients with Malignant Ventricular Arrhythmias

• Published in: Pacing and clinical electrophysiology 1992-10, Vol.15 (10), p.1445-1453
• Main Authors: GREENSPON, ARNOLD J., KIDWELL, GREGORY A., DeCARO, MATTHEW, HESSEN, SCOTT
• Format: Article
• Language: English
• Subjects: Anti-Arrhythmia Agents - pharmacology; Anti-Arrhythmia Agents - therapeutic use; antiarrhythmic drugs; Cardiac Pacing, Artificial; electrocardiography; Electrocardiography - methods; Electrophysiology; Female; Heart Conduction System - drug effects; Humans; Male; Middle Aged; Signal Processing, Computer-Assisted; signal-averaged electrocardiogram; Tachycardia, Ventricular - diagnosis; Tachycardia, Ventricular - drug therapy; Tachycardia, Ventricular - physiopathology; ventricular arrhythmias
• ISSN: 0147-8389; 1540-8159
• DOI: 10.1111/j.1540-8159.1992.tb02917.x

The effects of type I antiarrhythmic drugs on the signal‐averaged electrocardiogram (SAECG) were analyzed in 58 patients with inducible sustained monomorphic ventricular tachycardia. SAECGs were acquired before and after drug therapy. A total of 99 drug trials were analyzed (mean 1.7 per patient). Analysis of temporal domain parameters included the duration of the QRS complex (QHSD), the high frequency total duration of the filtered QRS complex (HFTD), the duration of the signal under 40 μV (D40), initial QRS (HFTD minus D40), and the root mean square amplitude (RMSA)of the terminal 40 msec of the QRS signal. Changes in temporal parameters failed to predict drug efficacy. There were, however, type‐specific drug effects on the SAECG. With the exception of type IB drugs, all drugs increased the QRSD, HFTD, and D40. Type IC drugs caused more prolongation of the QRSD and HFTD than type IA, IB, and the combination of IA + IB drugs. Prolongation of the HFTD was related to prolongation of the late potential and the initial portion of the QRS complex. A preferential effect of these drugs on the late potential was not observed. Type IC drugs also caused more prolongation of ventricular tachycardia cycle length than type IA or IB drugs. However, the increase in ventricular tachycardia cycle length did not correlate with a change in the SAECG. In summary, type I antiarrhythmic drugs cause a global slowing of ventricular activation. Although analysis of the SAECG following drug therapy was not useful for predicting drug efficacy, drug induced changes in the SAECG may be helpful for categorizing antiarrhythmic agents.