title: Electrocardiographic predictors in the ESVEM trial: unsustained ventricular tachycardia, heart period variability, and the signal-averaged electrocardiogram.
abstract: Sudden death remains a major problem because the causes are uncontrolled and accurate predictors have not been identified. However, new forms of electrocardiographic (ECG) analyses may provide prognostic information. The Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial provides a unique perspective to this issue because baseline and follow-up data were prospectively acquired on a relatively large sample of patients who were homogeneous with respect to sustained ventricular tachyarrhythmias, frequent ectopic activity, and inducible sustained ventricular tachyarrhythmias. Although analysis of the large amount of ECG data collected is in progress, initial studies have provided information about unsustained ventricular tachycardia (VTu), heart period (R-R) variability, and the signal-averaged ECG. VTu has been reported to have prognostic implications in several disorders, but its clinical significance in patients with sustained ventricular tachyarrhythmias is unknown. The significance of VTu recorded in the baseline (antiarrhythmic drug-free) 48-hour ECG recording in ESVEM study patients was examined; no variable representing the presence of VTu, the frequency of VTu events, or the duration of the longest episode of VTu was a significant predictor of arrhythmia recurrence, arrhythmic death, or all-cause mortality, although a trend was present for worse all-cause mortality in patients with VTu. R-R variability provides powerful prognostic information after acute myocardial infarction (AMI) and in patients with chronic ischemic heart disease. In general, R-R variability decreases dramatically at the time of AMI and recovers somewhat during the year after infarction. Although most patients in the ESVEM trial had chronic ischemic heart disease, R-R variability, which has been determined in about three fourths of the patients, was much lower than that reported in patients 1 year after MI. Instead, the mean values were closer to the more depressed values observed shortly after MI. This suggests a greater degree of autonomic dysfunction in patients with sustained ventricular tachyarrhythmias, frequent ventricular ectopic activity, and low ejection fractions, as compared with that for patients with chronic ischemic heart disease in general. Signal-averaged ECGs have also been shown to predict arrhythmic events in patients with ischemic heart disease. In a subset of the ESVEM patients, antiarrhythmic drugs that block sodium channels were found to prolong the filtered, signal-averaged QRS duration, especially the late potential portion. This correlated with prolongation of the cycle length of induced ventricular tachycardia. Sotalol appeared to have a differential effect on the signal-averaged ECG; the signal-averaged QRS shortened slightly in patients in whom induction of VT was suppressed by sotalol, whereas it appeared to lengthen slightly in patients in whom VT remained inducible despite sotalol. This suggests that sotalol may affect conduction in diseased tissue in some patients, and that this may affect suppression of ventricular arrhythmia induction by programmed stimulation.
authors.affiliation: Cardiac Electrophysiology Program, University of Pittsburgh Medical Center, PA 15213-2585, USA.
authors.forename: K P
authors.initials: KP
authors.lastname: Anderson
authors.forename: J T
authors.initials: JT
authors.lastname: Bigger
authors.forename: R A
authors.initials: RA
authors.lastname: Freedman
mesh_terms: D000889:Anti-Arrhythmia Agents / Q000494:pharmacology / Q000627:therapeutic use; D002986:Clinical Trials as Topic; D016757:Death, Sudden, Cardiac / Q000209:etiology*; D004562:Electrocardiography / Q000379:methods; D006801:Humans; D011379:Prognosis; D012307:Risk Factors; D012815:Signal Processing, Computer-Assisted; D013015:Sotalol / Q000494:pharmacology / Q000627:therapeutic use; D015996:Survival Rate; D017180:Tachycardia, Ventricular / Q000188:drug therapy / Q000401:mortality* / Q000503:physiopathology
chemical_list: D000889:Anti-Arrhythmia Agents; D013015:Sotalol