In patients vulnerable to sustained ventricular tachycardia(VT) may be found low amplitude, high frequency waveforms in the terminal QRS complex of the electrocardiogram called ventricular late potentials, which are continuous with the QRS complex and persist for tens of milliseconds into the ST segment.

Pathophysiological Basis Of Late Potentials

They appear to arise form small areas of structurally abnormal myocardium (heart muscle) in which ventricular activation is delayed and asynchronous. When surviving heart fibers are separated by connective tissue, heterogenous activation patterns may occur. The result is a low- amplitude, fragmented local electrogram. This activity can be recorded in most patients with remote myocardial infarction (heart attack), but is detected at fewer recording sites and is of shorter duration in infarction patients without clinical VT.
Late potentials imply that the substrate for reentry is present, and then be precipitated by such triggers as premature ventricular beats, myocardial ischemia (lack of oxygen), electrolyte imbalance (like low potassium), or autonomic nervous system instability.
Healthy volunteers rarely have abnormal SAECGs. Patients with sustained, inducible monomorphic VT after myocardial infarction have abnormal SAECGs in 79 to 92% of cases. Late potentials occur more frequently and are of greater duration in patients with monomorphiic sustained VT than in patients with ventricular fibrillation, a rhythm less associated with conduction delay.

TECHNIQUE

Using a Butterworth filter multiple samples of a repeating wave form are averaged to exclude randomly occurring noise, having excluded ectopic ventricular beats and excessively noisy beats. After signal averaging, the ECG is high-pass filtered to reduce the low-frequency signals contained in the QRS complex and ST segment.This is necessary because the repolarization phases of the action potential produces slowly changing and lower frequency signals that interfer with the measurement of microvolt signals corresponding to the delayed depolarization of small areas of myocardium (figure 143).

Figure 143 click to enlarge	Figure 144 click to enlarge

Frequency domain analysis using a Fourier transform is another means to extract diagnostic high frequency content from the SAECG (figure144). The analysis of multiple segments may allow better separation between noise and late potential.

VENTRICULAR LATE POTENTIALS

Common criteria defining of a late potential include the following:
1) the filtered QRS complex is longer than 114ms,
2) the terminal filtered QRS complex remains below 40 microvolt for more than 38ms, and
3) there is less than 20microvolt of signal in the last 40ms of the filtered QRS complex.

Late potentials are not present universally in patients with recurrent VT. In some instances the fragmented activity may be too brief or the late potential may be masked by bundle branch block. The signal amplitude may be too low to be differentiated from noise. Delayed fragmented electrical activity is probably related to reentry ventricular arrhythmias. Other potential electrophysiologic mechanisms of VT, such as increased automaticity or triggere activity, may not be associated with late potentials. Patients with VT in the absence of structural heart disease rarely have late potentials.

Prognostic Value of late potentials after acute myocardial infarction.

Several studies in post myocardial infarction patients have shown an increased likelihood of spontaneous VT or sudden cardiac death in patients who have an abnormal SAECG. Abnormal SAECGs are found in 26 to 40% of postmyocardial infarction patients when the recording is made prior to hospital discharge.

Fourteen to 29% of patients recovering from myocardial infarction with abnormal SAECGs will experience sustained VT during the first year, compared to 0.8 to 4.5% of those with a normal recording.
A majority of patients who have an abnormal SAECG do not develop a serious arrhythmia.

The negative SAECG coupled with normal left ventricular function suggests less need for concern about arrhythmias and less need for ambulatory monitoring and drug therapy of of ventricular ectopy. Patients with abnormal SAECGs are more prone to inducible, sustained monomorphic VT, ventricular fibrillation, or sudden death.

Reference:Walter,P.,MD,Hurst's The Heart,8th Edition,Technique of Signal- Averaged Electrocardiography,pp.893-896.