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Clinical applications of the signal-averaged electrocardiogram: Overview

Sanjiv M Narayan, MD, PhD
Michael E Cain, MD
Section Editor
Ary L Goldberger, MD
Deputy Editor
Brian C Downey, MD, FACC


Over 300,000 individuals succumb to sudden cardiac death per year in the United States alone, with the single biggest cause being ventricular tachycardia (VT) or ventricular fibrillation (VF) [1]. (See "Pathophysiology and etiology of sudden cardiac arrest".)

The signal-averaged electrocardiogram (SAECG) is a noninvasive technique that enables detection of the pathophysiology underlying reentrant arrhythmias such as VT. It was one of the first clinically applicable and mechanistically based surrogates for sudden death and is a prototype for other such indices. It has been applied to identify individuals at risk for sudden cardiac death, particularly in the context of coronary artery disease, acute myocardial infarction, and left ventricular dysfunction (table 1) [2-5]. (See "Incidence of and risk stratification for sudden cardiac death after acute myocardial infarction".)

In patients with the substrates for VT, slow conduction through myocardium disrupted by inflammation, edema, fibrosis, or scar tissue results in electrical potentials that extend beyond the activation time of normal surrounding myocardium, but which are too small for detection on the surface ECG. The SAECG uses computerized averaging of ECG complexes during sinus rhythm to facilitate the detection of these small microvolt level signals, which occur later than rapid ventricular activation and are termed late potentials. (See "Technical aspects of the signal-averaged electrocardiogram".)

A broad overview of the settings in which the SAECG may be of value (table 2) and of the relationship between late potentials detected by SAECG and ventricular tachycardia (table 3) is presented here. The data supporting the use of SAECG in specific clinical settings are discussed separately.


Late potentials are low-amplitude, high frequency signals that are thought to reflect slow and fragmented myocardial conduction (figure 1). This abnormal conduction, which may occur in regions of prior infarction, nonischemic scar, or fibrosis, provides a substrate for reentrant VT (figure 2) [6,7]. Accordingly, the prevalence of late potentials in patients with documented VT and coronary artery disease ranges from 70 to 92 percent and the predictive value of late potentials for VT increases with the number of other clinical risk factors [8,9]. Late potentials are present in 6 percent of asymptomatic normal subjects, but their incidence increases progressively when examining patients with a recent myocardial infarction (MI) without VT, patients with a remote MI who have not had VT, and patients with a remote MI who have had sustained monomorphic VT.


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Literature review current through: Sep 2016. | This topic last updated: Sep 7, 2016.
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