High-frequency QRS Research Articles

Possible late potentials in 4 dogs with sustained ventricular tachycardia.

Signal-averaged electrocardiograms (SAEKGs) were performed on 4 dogs with sustained ventricular tachycardia. Quantitative and qualitative analyses of SAEKGs were consistent with the presence of late potentials. Two of the 4 dogs subsequently died suddenly, and ventricular tachycardia and ventricular fibrillation were observed in 1 dog. High-frequency QRS durations (75-90 milliseconds), duration of low amplitude (less than 40 microV) signals during the terminal QRS complex (LAS40) (28-40 milliseconds), root mean square voltages of the terminal 40 milliseconds of the QRS complex (RMS40) (124-6.5 microV), and root mean square voltages of the terminal 30 milliseconds of the QRS complex (RMS30) (13-2.1 microV) differed from results obtained in 68 of 70 control dogs. Echocardiographic data suggested dilated cardiomyopathy in 2 dogs and the cause of the arrhythmia in 2 dogs was not determined. The SAEKG may be a useful adjunct in identifying a subset of dogs with ventricular tachyarrhythmias that are at high risk for sustained ventricular tachycardia and sudden death. The sensitivity, specificity, and predictive accuracies of the technique remain to be determined.

Decrease in the high frequency QRS components depending on the local conduction delay.

The high frequency components contained in the QRS complex (HF-QRS) are a powerful indicator for the risk of sudden cardiac death. However, it is controversial whether conduction delay increases or decreases the HF-QRS. In 21 anesthetized, open-chest dogs, the right atrium was constantly paced. A cannula was inserted into the left anterior descending artery and flecainide, lidocaine or disopyramide was infused to slow the local conduction. Sixty unipolar electrograms were recorded from the entire ventricular surface and were signal-averaged. Data were filtered (30-250 Hz) by using fast-Fourier transform. The HF-QRS was calculated by integrating the filtered QRS signal. Activation time (AT; dV/dt minimum) was delayed and the HF-QRS was reduced in the area perfused by flecainide, lidocaine or disopyramide. The percent increase in AT closely correlated the percentage decrease in the HF-QRS; the correlation coefficients were 0.75, 0.83 and 0.76 for flecainide, lidocaine and disopyramide infusion, respectively, (p<0.001). Decrease in the HF-QRS linearly correlated with the local conduction delay. This study proved that conduction delay decreases the HF-QRS, and that the HF-QRS is a potent indicator of disturbed local conduction.

Conditions of significant relation between high frequency QRS potentials and cardiac index in open heart surgery

Conditions of significant relation between high frequency QRS potentials and cardiac index in open heart surgery

Analysis of high frequency QRS potential during exercise testing in patients with coronary artery disease and in healthy subjects.

High resolution ECG waveforms from leads V3, V4, V5, and V6 were analyzed in two groups of male subjects before, during, and following treadmill exercise testing. Group A included 32 coronary artery disease (CAD) patients, with arteriographically proven > 75% obstruction of at least two main coronary arteries, and group B included 30 healthy subjects, without history or symptoms of CAD. Signal averaging and filtering techniques were used in order to enhance the signal-to-noise ratio of the recorded ECG. The averaged QRS waveforms were filtered between 150 and 250 Hz. QRS complexes of the four leads were combined to form a "precordial average complex" (PAC). The PAC signals were examined for each subject at different stages of the exercise test and two parameters were computed: the root mean square (RMS) voltage; and the peak amplitude. The values of RMS and peak amplitudes measured at each stage of the exercise test were normalized to the values at rest. Normalized RMS (NRMS) values at peak exercise, immediately after peak exercise, and during the recovery phase were found to be higher for the healthy subjects than for the CAD group (1.17 +/- 0.31 vs 0.94 +/- 0.26, P < 0.008 at peak exercise, 1.13 +/- 0.24 vs 0.84 +/- 0.19, P < 0.001 after peak exercise, 1.08 +/- 0.22 vs 0.94 +/- 0.17, P < 0.007 during recovery). Cut-off NRMS value of one had a sensitivity of 81.3% and a specificity of 70.0% in differentiating CAD patients from healthy subjects in the examined groups. Normalized peak amplitude (NAMP) values exhibited similar behavior, with higher values for the healthy subjects than for the CAD group (1.23 +/- 0.48 vs 0.94 +/- 0.36, P < 0.03 at peak exercise, 1.20 +/- 0.34 vs 0.83 +/- 0.28, P < 0.001 after peak exercise, 1.10 +/- 0.29 vs 0.94 +/- 0.23, P < 0.02 during recovery). Specificity of 73.3% and sensitivity of 71.8% were found using a postpeak NAMP cut-off value of 1. In conclusion, the present study shows that using high frequency ECG may contribute to identifying patients with CAD. Further studies in larger groups of patients are required to better define the true predictive value of the method described for the diagnosis of CAD.

Signal-averaged ECG prior to and serially after thrombolytic therapy for acute myocardial infarction.

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7-10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 +/- 11.3 ms and 93.4 +/- 8.0 ms vs 103.3 +/- 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 +/- 29.1 microV and 58.6 +/- 44.7 microV vs 44.4 +/- 35.5 microV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.

High frequency QRS electrocardiography in the detection of reperfusion following thrombolytic therapy.

The hypothesis that an increase in the amplitude (root-mean-square voltage) of the high frequency (150-250 Hz) components of the QRS complex occurs with successful reperfusion following thrombolytic therapy in acute myocardial infarction (AMI) and fails to occur when thrombolysis fails was tested. Clinical markers for successful or failed reperfusion following thrombolytic therapy for AMI are notoriously insensitive. The amplitude of the high-frequency components of the QRS complex decreases during ischemia and returns to normal with resolution of ischemia, but neither the variability in measurement of these potentials nor their patterns of change during the course of AMI have been described. In 32 control subjects, the average coefficient of variation for the amplitude of the high-frequency QRS complex was 10% or 0.3 uV. Based on these data, for the acute infarction population a significant change in this measurement was therefore defined as a change in amplitude > 20% or 0.6 uV on two consecutive recordings. In 30 patients with AMI treated with a thrombolytic agent, either cardiac catheterization, serial serum myoglobin, or complete resolution of ST-segment elevation were used to define successful or failed reperfusion. High-frequency QRS electrocardiograms were obtained at the start of treatment with a thrombolytic agent and for 3 h thereafter using a signal-averaging technique and digital filtering. Standard 12-lead electrocardiograms were obtained at the same time. In patients who reperfused successfully, the high-frequency QRS amplitude increased significantly (1.2 +/- 0.9 uV above its nadir at 83 +/- 36 min after initiation of thrombolytic therapy) in 23 of 25 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of high frequency QRS potentials observed during acute myocardial infarction

The value of high frequency QRS potentials (HFQRS) during acute myocardial infarction (AMI) was assessed to define infarct size and prognosis. HFQRS were recorded by signal-averaged ECG with 150–250 Hz frequency ranges, using X, Y, Z orthogonal leads. Recordings were obtained in surviving AMI patients ( n = 33, 12 inferior, 11 anterior, 10 anterior-inferior) on the first and tenth days, but in non-survived patients ( n = 5, 2 inferior, 1 anterior, 2 anterior-inferior) only on the first day. Additionally, the frequency of ventricular tachycardia (VT) was evaluated by 24-h Holter monitoring in all patients at the same days. The control group consisted of 11 healthy people. In surviving AMI patients, RMS voltage of vector magnitude reduced in anterior and anterior-inferior MI but filtered QRS duration was longer in inferior MI than normals ( P < 0.05, < 0.05, < 0.01, respectively). In nonsurvived patients, RMS voltages of leads X, Y, Z and vector magnitude were lower than normals ( P < 0.01, < 0.05, < 0.01, < 0.01, respectively) and surviving AMI patients ( P < 0.01, < 0.05, < 0.05, < 0.05, respectively), the filtered QRS duration was found to be longer than normals and survived patients ( P < 0.01, < 0.01). In patients who had VT on Holter monitoring, filtered QRS duration was significantly longer than in patients without VT ( P < 0.05). As a result, HFQRS was important for defining infarct size but not malignant ventricular arrythmias. VT was related to filtered QRS duration. HFQRS may offer significant prognostic information and contribute to early risk stratification of AMI patients.

A spectral analysis of the high frequency QRS potentials observed during acute myocardial ischemia in dogs

Electrocardiographic manifestations of transient myocardial ischemia were studied in 10 dogs undergoing occlusion of the left anterior descending coronary artery, using frequency domain analysis of the high frequency QRS potentials. Ischemia was induced via a balloon occluding cuff placed around the coronary artery. Electrocardiographic waveforms recorded before and during the ischemic state were averaged together and then filtered between 150 and 250 Hz to obtain the high frequency QRS complex. The spectral curve in the power spectrum of the high frequency QRS components was calculated using an algorithm for fast Fourier transformation. Balloon inflation was accompanied by morphological changes in the spectral curve in 7 of 10 experiments. Morphological changes, seen as zones of reduced amplitude in the time domain, appear as two separate peaks in the frequency domain. These changes were seen early in ischemia and were not accompanied by significant changes in the QRS complex or ST segment of the conventional surface electrocardiogram. The power spectrum of the high-frequency QRS potentials appears to detect evidence of transient ischemia and may provide useful information regarding the presence of myocardial ischemia.

Fast fourier transformation of the entire low amplitude late QRS potential to predict ventricular tachycardia

Signal-averaged electrocardiograms (X, Y and Z leads) were acquired from 24 patients with coronary artery disease and recurrent ventricular tachycardia, 24 control patients with coronary artery disease and 23 normal subjects to assess the discriminant value of fast Fourier transformation of the entire late potential period of the QRS complex. Analysis of the vector magnitude in the temporal domain (25 to 250 Hz bandpass filters) measured high frequency QRS duration, the duration of terminal signals < 40 μV and the root mean square voltage of the last 40 ms. Late potentials were defined as terminal signals >25 Hz that were <40 μV. Analysis in the frequency domain used a 120 ms window that encompassed (had onset with) all of the late potential, but the mean value was first subtracted to eliminate a direct current component. High frequency spectral areas (60 to 120 Hz) and the percent high frequency (100 × [60 to 120 Hz/0 to 120 Hz]) were calculated.Results in both temporal and frequency domains were similar in control patients with coronary artery disease and normal subjects. Patients with ventricular tachycardia had a longer high frequency QRS complex (p < 0.0001) and longer high frequency terminal signals <40 μV (p < 0.0004), but not significantly lower voltage in the last 40 ms. The most useful temporal domain measurement was high frequency QRS duration (if ≥ 120 ms, odds ratio = 8.2). Patients with ventricular tachycardia had increased high frequency spectral areas (p < 0.0002) in the late potential, and the percent high frequency was especially increased (p = 0.0000; if percent high frequency ≥3.1%, odds ratio = 18.4).The odds ratio and the area under the receiver operating characteristic curve were both greater for percent high frequency than for high frequency QRS duration (p < 0.03. All patients with ventricular tachycardia had a high frequency QRS complex ≥107 ms or percent high frequency ≥3.1% (sensitivity 100%). For a high frequency QRS complex ≥107 ms and percent high frequency ≥3.1%, specificity was 96%. Therefore, high frequencies in late potentials, not their duration or reduced voltage, most usefully identify patients with coronary artery disease who are prone to ventricular tachycardia.

High Frequency Electrocardiography of Three Orthogonal Leads in Dogs During a Coronary Artery Occlusion

The ability to detect cardiac ischemia in dogs was studied using high frequency electrocardiography and signal averaging technique. Ischemia was induced via a balloon occluding cuff placed around the left anterior descending coronary artery. Three surface orthogonal bipolar leads (X, Y, and Z) were recorded prior to inflation of the occluding cuff. The cuff was then inflated, causing a complete occlusion of the coronary artery. The surface electrocardiogram was recorded before and during ligation and during reperfusion. The recorded waveforms were divided into sequential 10-15 second segments representing different stages of the ischemic state and were aligned using cross-correlation scheme, averaged and band pass filtered between 150-250 Hz. Analysis of the filtered high frequency QRS complexes revealed that coronary ligation was accompanied by changes in waveform morphology including the appearance of zones of reduced amplitude. In seven out of ten experiments reduced amplitude zones were absent before the ligation, present during the occlusion and absent following reperfusion. In two experiments, reduced amplitude zones that were present prior to ligation became wider during occlusion. In one experiment no reduced amplitude zone was present during any stage of the experiment. Such zones may represent slow conduction in regions of the heart rendered ischemia during coronary ligation. Therefore, the morphology of the high frequency QRS complex, as determined by analysis of the signal averaged electrocardiogram, may provide useful information regarding the presence of myocardial ischemia.

Clinical significance of high frequency QRS potentials in myocardial infarction: analysis based on power spectrum of lead III

Power spectrum analysis of ECG lead III QRS potentials using the Fast Fourier Transform technique was performed in 10 normal subjects and nine patients with inferior wall myocardial infarction (IWMI). A relative lowering in both low and high frequency QRS potentials was observed in the infarct group, in agreement with previous studies on power spectrum of lead II. However, contrary to earlier conclusions, the lowering was independent of a general attenuation in QRS voltages. Discriminant analysis of the frequency components showed that the high frequency components (190-310 Hz) were able to discriminate better between the two groups than the low frequency components (10-120 Hz).

Correlation between the signal-averaged electrocardiogram and electrophysiologic study findings in patients with coronary artery disease and sustained ventricular tachycardia

Ventricular late potentials at the end of the surface QRS, detected on the signal-averaged electrocardiogram (SAECG) have been shown to be markers for spontaneous end/or inducible ventricular tachycardia (VT) in patients with coronary artery disease (CAD). We examined the correlations between electrophysiologic study (EPS) findings and SAECG indexes in 50 patients with chronic CAD with documented spontaneous VT/ventricular fibrillation (VF), who had either syncope (24 patients) or aborted sudden cardiac death (SCD). The prevalence of late potentials was significantly higher in the syncope patients (75%) compared with the SCD group (46%) ( p < 0.05), No correlation was found between the ventricular refractoriness and the SAECG indexes. There was a significant difference in quantitative SAECG indexes comparing the induction mode of the sustained VT/VF by single and double versus triple extrastimuli; the types of the induced VT (sustained monomorphic, sustained pleomorphic or VF, noninducible); and the cycle length of the induced sustained monomorphic VT with the high frequency QRS duration (QRSD). In conclusion, differences in prevalence and characteristics of ventricular late potentials were found between patients with syncope and with SCD. The degree of abnormality of SAECG indexes correlated with the type and the mode of induction of sustained VT. The magnitude of QRSD of the SAECG correlated, with the cycle length of monomorphic VT. The above findings suggest that in patients with CAD and sustained VT/VF the SAECG variables are related to the area of reentry.

Effect of localized surface cooling of the heart muscle on the high-frequency content of ECG waveforms in dogs.

Hypothermia is known to affect the electrophysiology of the myocardium in various ways. A marked increase in action potential duration, combined with a decrease in rate of depolarization and conduction velocity, has been observed. We studied the effect of localized hypothermia of the ventricular myocardium on the high-frequency (HF) components of the ECG waveform. Signals were obtained from 6 anesthetized dogs using simultaneous recording of three orthogonal body surface leads before, during, and following surface cooling of different areas of the epicardium. Computer analysis included digital averaging and filtering in a frequency range of 150-250 Hz. For each intervention in each animal, the variance of the average nonfiltered QRS complex was used for a quantitative estimate of the total power, whereas the variance of the derived filtered wave (HF QRS complex) expressed the power content in the HF range. The total power increased during localized cooling of the anterior as well as the inferior epicardial surface, while a clear reduction of power was observed in the HF range. This reduction was shown to be lead dependent and nonuniformly distributed during the course of the QRS. In all cases, hypothermia of either anterior or inferior ventricular epicardium produced a zone of reduced amplitude in the HF QRS complex of at least one lead. Thus, typical changes in the morphology of the HF QRS complex are reliable markers for cooling-induced localized electrophysiological (EP) variations. Therefore, the HF analysis of the body surface ECG may provide noninvasive insight into the EP properties of the myocardium.

High frequency electrocardiography using an advanced method of signal averaging for non-invasive detection of coronary artery disease in patients with normal conventional electrocardiogram

The ability to detect coronary artery disease (CAD) in patients with normal, conventional electrocardiograms (ECG) was studied using high frequency electrocardiography and an advanced method of signal averaging in three groups of subjects. Group A consisted of ten healthy subjects under the age of 30; Group B of 15 patients with chest pains and normal coronary arteries; and Group C of 20 patients with chest pains and CAD. Four hundred ECG waveforms from leads V3, V4 and V5 were recorded, and the recorded analog data were digitized. The digitized waveforms were averaged using a cross-correlation function which operates in the frequency domain (fast-Fourier transform algorithm). The signals were filtered with a digital band pass filter with 150 and 250 Hz low and high cut-off frequencies, respectively. Zones of reduced amplitude in the envelope of the filtered QRS complex of at least two precordial leads were found more significantly in patients with CAD (75%) than in patients without CAD (12% for Groups A and B, p less than 0.00003). However, no significant difference was found between the voltage over the high frequency QRS complex and that of its envelope between the three groups. It is concluded that the morphology of the high frequency QRS complex as determined by this advanced method of analysis of the signal averaged ECG may be a useful indicator for the presence of CAD in patients with normal conventional ECG's.

QRS duration measurement using high-frequency electrocardiography: Applications and limitations of a new technique

Accurate, objective measurement of QRS duration is of central importance in clinical electrocardiography. The applicability of a new computer technique based on the observation that the QRS, unlike other ECG waveforms, contains significant frequencies >50 Hz was studied. Accordingly, a microprocessor-based ECG system was adapted with a signalaveraging program to reduce noise and a 50- to 300-Hz phaseless digital filter which permitted direct “extraction” of the QRS complex from surrounding low-frequency PR and ST segments. The hypothesis first tested was that, owing to greater cardiac mass, QRS duration in men should be slightly greater than in women. High-frequency QRS duration measurements were performed in 30 healthy adult men and 28 healthy adult women from simultaneously acquired orthogonal leads I and a VF. QRS duration in men (85.5 ± 12.3 msec, X ± SD ) was significantly ( p < 0.05) greater than in women (78.7 ± 11.0 msec). Furthermore, after pooling these two groups of healthy subjects ( n = 58), modest but significant ( p < 0.001) correlations were noted between QRS duration and height ( r = 0.51), weight ( r = 0.46), and body surface area ( r = 0.48). The question then addressed was whether QRS duration in patients with myocardial infarction (after excluding those with apparent conduction delays, hypertension, or axis deviation) is greater than normal due to myocardial scarring or conduction system involvement. QRS duration in 25 men with prior transmural infarction (90.6 ± 14.2 msec) was slightly greater than normal; however, this difference was not statistically significant. Furthermore, in 7 of the 25 cases (28%) QRS duration was <86 msec, the mean for normal men. These results indicate that (1) high-frequency electrocardiography provides a useful new technique capable of detecting subtle (<10 msec) differences in QRS duration between men and women; (2) body size and therefore cardiac mass is one determinant of QRS duration; and (3) QRS duration in patients with infarction overlaps with normals. Therefore, QRS duration criteria cannot be used to exclude previous infarction.

Temporal stability of the high frequency QRS waveform in normal subjects

Previous attempts to assess high frequency QRS components relied primarily on counts of QRS notches and slurs. In order to measure high frequency potentials in a more quantitative manner, we adapted a commercially-available microprocessor ECG system equipped with a signal-averaging program to reduce noise and an 80-300 Hz digital band-pass filter. The high frequency QRS output was digitized for measurement of its root-mean-square (RMS) value. Serial high frequency recordings were then obtained in ten normal subjects approximately 100 days apart. Both the morphology and RMS voltage of the high frequency signal were stable over this time period. Furthermore, comparison of inter- and intra- observer variability in making these computer assisted RMS measurements revealed a high degree of reproducibility. This new technique offers a reliable way of quantitatively measuring high frequency QRS potentials and should be useful in assessing serial changes in various pathologic states.

Myocardial infarction diminishes both low and high frequency QRS potentials: Power spectrum analysis of lead II

Previous studies based primarily on counts of QRS notches and slurs have suggested that myocardial infarction (MI) increases high frequency QRS components. However, this technique does not quantitatively measure total high frequency voltage. To further study this problem, a microprocessor ECG system was employed capable of averaging multiple QRS complexes to reduce noise. Power spectrum analysis of the QRS using a Fast Fourier Transform was then performed in lead II in ten normal subjects and ten patients with prior inferior MI. The infarct group showed a decrease in QRS potentials over a broad frequency range (7.81-304.7 Hz). Therefore, contrary to previous estimates, MI may attenuate high as well as low frequency QRS potentials as part of a general decrease in electromotive force.

Effect of myocardial infarction on the peak amplitude of high frequency QRS potentials

Studies based on analysis of QRS notching and slurring have suggested an increase in high frequency QRS potentials following myocardial infarction (MI). We investigated the sensitivity and specificity of an indirect, but easily quantitated index of high frequency potentials--the peak-to-peak amplitude of the high frequency signal. A commercially-available micro-processor ECG system was employed with a QRS-averaging program to reduce random noise and an 80-300 Hz filter to selectively record higher frequency potentials. High frequency ECGs were recorded in leads II, III and aVF in 40 normal men and 41 patients with prior inferior MI. Peak-to-peak amplitude of the high frequency signal was less than or equal to 35 micro V in one or more of these leads in 18 of 41 MI patients (44%) compared with only 1 of 40 normals (2.5%) (P < 0.001). In the infarct group, reduced peak amplitude of the high frequency signal was also noted in some leads where the standard ECG did not show pathologic Q waves. This diminution in peak amplitude probably reflects a reduction in high frequency voltage. Therefore, contrary to previous theory, MI may actually cause a decrease in high frequency potentials as part of an overall loss of electromotive force or a slowing of conduction associated with myocardial necrosis. Quantitative high frequency QRS measurements may be of critical value in selected cases.