Electrocardiographic signal-averaging during atrial pacing and effect of cycle length on the terminal QRS in patients with and without inducible ventricular tachycardia

doi:10.1016/0002-9149(90)90511-X

The American Journal of Cardiology

Volume 66, Issue 15, 1 November 1990, Pages 1095-1098

https://doi.org/10.1016/0002-9149(90)90511-X Get rights and content

Abstract

Electrocardiographic signal-averaging during sinus rhythm (61 to 99 beats/man) and atrial pacing (100 to 171 beats/min) were performed to determine the effect of heart rate on late potentials in 15 patients without (group 1) and 7 patients with (group 2) inducible sustained ventricular tachycardia (VT). In sinus rhythm (79 ± 12 vs 77 ± 12 beats/min, difference not significant), the duration of the low-amplitude signal <40 μV was longer in group 2 than group 1 (43 ± 21 vs 26 ± 8 ms, p = 0.034) and more patients had late potentials (57 vs 7%, p = 0.021), but QRS duration (121 ± 32 vs 98 ± 19 ms) and terminal voltage (33 ± 33 vs 50 ± 26 ms) were not significantly different.

With atrial pacing in group 1 (128 ± 16 beats/ min), 3 patients developed a simultaneous decrease in terminal voltage and an increase in terminal QRS duration consistent with a late potential, but mean total and terminal durations were unchanged. Terminal voltage increased (50 ± 26 to 59 ± 40) but not significantly. With atrial pacing in group 2 (119 ± 12 beats/min) all patients either had a late potential or developed a simultaneous decrease in terminal voltage and an increase in terminal QRS duration (p = 0.001 vs group 1). Root mean square voltage decreased (33 ± 23 to 22 ± 23) and became significantly different from group 1 (p = 0.017). Mean QRS duration, root mean square terminal voltage and low-amplitude terminal QRS duration, however, were unchanged. At rates from 61 to 171 beats/min, the signal-averaged electrocardiogram is largely independent of heart rate, but there is a trend toward a decrease in terminal voltage and an increase in low-amplitude terminal QRS duration in patients with inducible VT. This may be the result of decremental conduction in arrhythmogenic tissue.

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2016, Journal of Electrocardiology
Citation Excerpt :
Previous studies in animals employing ECG [26] and invasive HV interval measurement [27] did not show a decrease in QRS duration or intraventricular conduction time during incremental supraventricular pacing. Two studies [28,29] in humans with and without structural heart disease, employing signal averaged electrocardiography for precise determination of QRS duration, also failed to show shortening of the QRS during incremental atrial pacing. Thus, the QRS change we observed during spontaneous change in heart rate must not be a result of the change in heart rate per se.
Existence of a relationship between the electrocardiographic QRS interval duration and the diurnally varying heart rate, of consistent sign and magnitude, is controversial and the relationship has not been fully characterized in normal populations.
We analyzed the QRS-RR interval relationship in 884 Holter recordings in 410 normal subjects participating in 5 clinical trials.
The slope of the linear regression of QRS on RR was positive in 93% of subjects with an average slope of 0.0125, which indicates an increase in QRS duration of 1.25 msec for an increase in RR interval of 100 msec. The increase was 15% larger in women than in men. Age had no significant effect on the slope.
In two populations of normal subjects we observed a robust, direct relationship between the spontaneously changing RR interval and intraventricular conduction time represented by the duration of the QRS interval. As heart rate increases, QRS duration decreases. The change is larger in women. These observations have important physiological and clinical implications.
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Sudden cardiac death occurs in up to 30% of patients with cardiac pacemakers, caused by ventricular arrhythmias, but in these patients noninvasive risk stratification with Holler, exercise, or standard signal-averaged electrocardiogram is limited. This study investigated whether late potential analysis during cardiac pacing is applicable. In 50 postinfarction patients with documented sustained ventricular tachycardia (VT) and in 50 patients without VT, late potential analysis during sinus rhythm was compared with the corresponding patient's analysis during temporary pacing. During sinus rhythm late potentials were seen in 48 of 50 patients with VT and in 2 of 50 patients without VT. No significant changes were observed during atrial pacing. Modified QRS alignment for signal averaging, QRS endpoint definition, and adjusted cutoff values for abnormality in time and frequency domain analysis allowed retrieval of all late potentials observed during sinus rhythm even in ventricular-paced beats and retrograde conduction. By application of an adjusted analyis to 100 selected patients with permanent pacemakers (50 patients with a history of VT, 50 patients without VT) late potentials were detectable in 44 of 50 patients with VT and in 4 of 50 without VT (sensitivity 88%, specificity 92%). Thus, considering that varying pacing modes, ventricular-paced beats, and retrograde conduction do require modifications of standard late potential analysis, this is an applicable mode for noninvasive risk stratification even in patients with cardiac pacemakers.
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1996, Journal of the American College of Cardiology
This study sought to evaluate the behavior of late potentials on the body surface by signal averaging during programmed stimulation and to correlate the findings with the cycle length of induced ventricular tachycardia.
Clinically relevant late potentials may be concealed within the QRS complex and may be missed by the conventional signal-averaged electrocardiogram (SAECG). In contrast, some late potentials may arise from dead-end pathways or pathways not capable of supporting sustained ventricular tachycardia (VT). It has been shown that durations of late potentials in sinus rhythm correlate poorly with VT cycle length.
Signal-averaged electrocardiography during sinus rhythm, right ventricular pacing (S1) and introduction of a right ventricular extrastimulus (S2) was performed in 95 patients: 11 patients with a structurally normal heart and no inducible VT (Group I); 44 with a previous myocardial infarction (MI) and no inducible monomorphic VT (Group II); and 40 with a previous MI and inducible monomorphic VT (Group III).
The best subset of SAECG variables and the best cut points for each variable to differentiate between patients with and without VT were first established for each rhythm studied. Total duration of the filtered QRS complex (QRSD) was found to be the only independent predictor of inducibility of VT. When late potentials were defined for these criteria (QRSD ≥113, ≥178 and ≥168 ms for the SAECG during sinus rhythm, S1 and S2, respectively), there was no difference in the incidence of false positive (16% vs. 18%) or false negative (30% vs. 26%) late potentials between sinus rhythm and S1. During S2, there were significantly fewer false positive late potentials (11% vs. 16%) and fewer false negative late potentials (17% vs. 30%) than with sinus rhythm. Compared with sinus rhythm, 31% of the false positive late potentials detected during sinus rhythm were lost, whereas 43% of the false negative late potentials became detectable after S2, resulting in improved sensitivity (83% vs. 70%), specificity (89% vs. 84%) and predictive accuracy (86% vs. 77%, p < 0.05). Among the patients with VT, QRSD during S2 achieved the best correlation with VT cycle length (r = 0.74) and was the only independent predictor of VT cycle length when all SAECG variables were considered.
Late potentials revealed by ventricular extrastimuli but concealed during sinus rhythm may be clinically relevant and may explain some of the false negative late potentials and reduced sensitivity of the conventional SAECG in predicting VT. In contrast, those late potentials that are detected during sinus rhythm but lost after ventricular extrastimuli are often clinically irrelevant and may account for the false positive late potentials and reduced specificity of the conventional SAECG.
Analysis of alternans in late potentials: Correlations between epicardial and body surface recordings
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The methodical performance of the signal-averaged electrocardiogram is strongly influenced by the beat-to-beat reproducibility of late potentials (LPs). Especially at higher heart rates, epicardial recordings from infarct regions show progressive beat-to-beat prolongations with alternating conduction block. To analyze the influence of beat-to-beat-alternans of LPs on the signal-averaging process, epicardial and body surface recordings were studied at different heart rates and extrastimulation. Epicardial and body surface recordings were obtained from dogs with 4-day postligation of the left anterior descending coronary artery (Harris model). Body surface potentials were averaged in different modes to a final noise level of 0.3 μV (rms) and digitally bandpass filtered (40–250 Hz). Modulation of the heart rate was performed by atrial or His-bundle pacing and by atrial premature extrastimulation. Pacing up to heart rates close to 180 beats/min produced no significant changes in the duration of LPs in epicardial and averaged body surface recordings; however, at higher pacing rates, considerable prolongation of LPs with different patterns in the epicardial leads was observed. In these cases, averaging of all beats revealed only a slight prolongation of LPs, as seen from the body surface. Selective averaging of beats with prolonged epicardial LPs showed the prolongation or absence of LPs, as seen in the epicardial recordings. Similar observations were made using an atrial extrastimulation technique, whereby the average of the premature beats was compared to the average of all normal sinus beats. Selective beat averaging of body surface potentials can unmask the prolongation of LPs due to atrial pacing or extrastimulation, as seen in recordings from the infarcted epicardium. The evidence of this modulation of LPs may improve the positive predictive value of the signal-averaged electrocardiogram.
Variation in late potentials and the reproducibility of their measurement
1993, Progress in Cardiovascular Diseases
Atrial flutter causes pseudo late potentials on signal-averaged electrocardiogram
1993, The American Journal of Cardiology
Signal-averaged electrocardiography (SAECG) is a useful tool for determining which patients are at risk for sustained ventricular tachycardia.^1–3 In patients at risk for sustained ventricular tachycardia, SAECG often shows high-frequency and low-amplitude electrical activity at the terminal portion of the QRS complex.^4–6 This electrical activity is thought to be due to slow conduction in scarred or abnormal ventricular myocardial tissue and is usually not apparent on the standard 12-lead surface electrocardiogram.^7–10 During atrial flutter, flutter waves may occur before, during or after ventricular systole. Atrial flutter waves that occur during ventricular diastole frequently appear as “sawtooth” waves on the standard 12-lead electrocardiogram, particularly in the inferior limb or anterior chest leads. However, atrial flutter waves that occur during ventricular systole may be obscured by the QRS complex. To test the hypothesis that atrial flutter waves that coincide with the terminal portion of the QRS complex cause low-amplitude electrical activity and thus result in a pseudo late potential on the electrocardiogram, we performed SAECG in 9 patients during atrial flutter and normal sinus rhythm.

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Electrocardiographic signal-averaging during atrial pacing and effect of cycle length on the terminal QRS in patients with and without inducible ventricular tachycardia

Abstract

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

Am J Cardiol

J Am Coll Cardiol

Am Heart J

J Am Coll Cardiol

Am J Cardiol

Quantitative analysis of the-high-frequency components of the terminal portion of the body surface QRS in normal subjects and in patients with ventricular tachycardia

Circulation

Body surface detection of delayed depolarizations in patients with recurrent ventricular tachycardia and left ventricular aneurysym

Circulation