High-frequency QRS Potentials Research Articles

High-frequency QRS potentials as a marker of myocardial dysfunction after cardiac surgery

Background High-frequency QRS potentials are sensitive to myocardial ischemia. The aim of this study was to evaluate the usefulness of high-frequency QRS potentials as a marker of myocardial dysfunction after cardiac surgery. Methods Seventy patients undergoing coronary artery bypass grafting or heart valve surgery were involved. High-frequency QRS potentials were measured by signal-averaged electrocardiogram, and calculated as the root-mean-square voltage of the total QRS duration (RMST). The postoperative RMST was expressed as a percentage of the preoperative RMST. The mean RMST at 1 to 2 hours after removing the aortic cross-clamp was compared with the cardiac index, inotropic agents, and aortic cross-clamping time. The occurrence of ventricular tachycardia within 24 hours and the RMST at 2 postoperative days were also evaluated. Patients were divided into quartile groups from highest to lowest at postoperative RMST (groups 1, 2, 3, and 4, respectively, from maximum to minimum). Results In postoperative states, cardiac index significantly decreased in accordance with the RMST decrease in a stepwise manner, although there were no differences in cardiac index among the four groups preoperatively. Inotropic agents and aortic cross-clamping time increased as RMST decreased. A high rate of ventricular tachycardia within 24 hours and delayed RMST recovery at 2 postoperative days were seen in group 4. The curve of sensitivity and specificity showed that severe reduction (threshold, 35%) of RMST indicated low-output syndrome. Conclusions The severe reduction of filtered high-frequency QRS potentials was related to myocardial dysfunction. Measurement of filtered high-frequency QRS potentials could become a useful, noninvasive, real-time monitor of myocardial dysfunction after surgery.

Recovery of high-frequency QRS potentials following cardioplegic arrest in pediatric cardiac surgery.

We examined the hypothesis that recovery of high-frequency QRS potentials at reperfusion is influenced by the duration of myocardial ischemia during cardioplegic arrest in pediatric cardiac surgery. Signal-averaged electrocardiograms were recorded after induction of anesthesia (baseline data) and every 1 to 5 minutes after aortic declamping in 14 patients aged 2 months to 6 years. The signals were processed with a band-pass filter between 80 Hz and 300 Hz to obtain high-frequency potentials in the QRS complex. The high-frequency QRS potentials (80-300 Hz) were expressed as the root mean square voltage over the filtered QRS complex. The high-frequency QRS potentials at baseline were 33.9 +/- 4.4 microV. They decreased to 13.7 +/- 9.6 microV 1 minute after aortic declamping (p = 0.005). Subsequently they gradually increased and then returned to the baseline level. The time that the potentials were over 90% of baseline value ranged from 10 to 35 minutes after aortic declamping. The recovery time of this reduction in the high-frequency QRS potentials correlated with the duration of aortic cross-clamping (r = 0.80, p = 0.0009) and the value of postoperative MB isozyme of the creatine kinase (r = 0.81, p = 0.0042). This study demonstrated that the high-frequency QRS potentials decreased at early reperfusion following cardioplegic arrest and then returned to preischemic levels. The recovery time of the high-frequency QRS potentials significantly correlated with cardioplegic arrest time and postoperative MB isozyme of the creatine kinase values. Our results raise the possibility that changes in high-frequency electrocardiographic signals in the QRS complex may reflect myocardial ischemia during cardioplegic arrest.

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 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.

The role of collateral circulation for ischemic preconditioning and the change of high-frequency QRS potentials during angioplasty

The role of collateral circulation for ischemic preconditioning and the change of high-frequency QRS potentials during angioplasty

Simulation of high-resolution QRS complex using a ventricular model with a fractal conduction system. Effects of ischemia on high-frequency QRS potentials.

Recent studies have analyzed the high-fidelity surface electrocardiographic signal, and efforts have been made to increase the diagnostic sensitivity of the electrocardiogram by observing its high-frequency components. It was found that the high-frequency (150-250-Hz) electrocardiogram appears to detect evidence of transient ischemia with greater sensitivity than visual inspection of the surface electrocardiogram. A finite-element three-dimensional model of the ventricles with a self-similar (fractal) conduction system has been introduced as a bridge to the understanding of electrocardiographic phenomena related to high-frequency potentials. The model was activated, and the dipole potential generated by adjacent activated and resting cells was calculated to obtain a high-resolution QRS complex. Normal and ischemic activation processes was stimulated by regional reduction in conduction velocity. It was found that although the resulted low-frequency QRS complex was not significantly altered from normal conditions, the high-frequency components exhibited morphological changes similar to the ones observed during animal experiments and human studies. Based on the results obtained from the model, it can be concluded that these morphological changes can be attributed to a slowing of conduction velocity in the region of ischemia and that the model is adequate for meeting the challenges imposed by the requirements of high-frequency methods applied in clinical cardiology.

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.

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).

Subtle alterations in the high-frequency QRS potentials during myocardial ischemia in dogs

The high-frequency components in the QRS complex were examined before and during the occlusion of the left anterior descending coronary artery. ECG waveforms from different stages of the ischemia state were averaged using cross-correlation technique and fast Fourier transform algorithm. The average waveforms were then filtered with nonrecursive digital filters (150–250 Hz) to obtain the high-frequency QRS complex. We tested our nonrecursive digital filter for ringing and the trigger jitter during the averaging process. We demonstrated that the high-frequency signal left after filtering is the result of a subtle lowamplitude constituent of the QRS complex and that the morphological change during ischemia (as zone of reduced amplitude) is a result of changes in these components of the original ECG signal.

Effect of exercise in healthy men on QRS power spectrum.

The effect of exercise on the QRS power spectrum has not been evaluated. We hypothesized that increased conduction velocity with exercise might selectively increase high-frequency QRS potentials. Using a digital electrocardiograph (ECG) cart, a single bipolar chest lead was recorded in 21 healthy adult males at rest and then immediately after treadmill exercise. Fast Fourier transform analysis of the ECGs was performed using a 128-ms sampling window, including the QRS but not the P wave. Step discontinuities between PR and ST segments were minimized using a linear correction function to obviate artifactual increases in high-frequency content after exercise. The power spectrum plots of rest and exercise data showed an increase in the amplitude of high frequencies that could not be accounted for on the basis of noise contamination. For the frequency band between 187.5 and 250 Hz, the root-mean-square (RSM) voltage of exercise QRS complexes (10.0 +/- 3.6 micro V) was significantly (P less than 0.02) greater than that of rest QRS complexes (7.8 +/- 1.2). However, base-line noise level (computed over a 32-ms interval during the ST segment) was not different between rest and exercise over this high-frequency band. The same exercise protocol was also applied in 11 normal male subjects using an analog ECG cart. For the 187.5- to 250-Hz band, the RMS voltage of the QRS after exercise (13.0 +/- 1.8 micro V) was also significantly (P less than 0.01) greater than at rest (10.2 +/- 2.8) without any difference in ST segment noise level over the same frequency range. These data indicate that exercise causes an increase in the amplitude of high-frequency QRS potentials in healthy men.

Peak-to-peak amplitude of the high-frequency QRS: A simple, quantitative index of high-frequency potentials

Previous attempts to measure high-frequency QRS potentials have been limited by methodologic difficulties in accurately quantitating these low-amplitude potentials. Therefore, we sought a simple, yet quantitative index of high-frequency ECG voltage. To make these high-frequency measurements, we adapted a commercially available microprocessor electrocardiograph with a signal-averaging program to reduce noise and an 80- to 300-Hz bandpass filter. The high-frequency output was then digitized and the rms value of the signal was computed in leads I, II, III, aVL, and aVF in both normal subjects and patients with organic heart disease. An excellent correlation ( r ≥ 0.92) was noted in all leads between the peak-to-peak amplitude of the high-frequency QRS and its rms value. Therefore, peak-to-peak amplitude can be used as an easily measured index of high-frequency potentials. Quantitative high-frequency electrocardiography may be helpful in increasing the diagnostic accuracy of the conventional ECG.

Effect of myocardial infarction on high-frequency QRS potentials.

Studies have shown that the number of high-frequency QRS notches increases after myocardial infarction (MI). To assess overall high-frequency (greater than 80 Hz) potentials more quantitatively, we adapted filtered and the root-mean-square (RMS) voltage of the residual (80-300 Hz) signal computed. High-frequency RMS values were significantly (p less than 0.01) greater in leads II, III and aVf in normal subjects (n = 12) than in patients with inferior infarction (n = 12). Similarly, high-frequency RMS values were higher (p less than 0.01) in leads V2 and V5 in normal subjects (n = 14) than in patients with prior anterior MI (n = 14). A reduction in high-frequency RMS values with inferior infarction was independently confirmed using Fourier analysis of the QRS in lead II. QRS notching in these subjects was also quantified by computing the number of baseline crossings of the first derivative (dV/dt). As predicted, notching was significantly greater (p less than 0.05) both with inferior MI (lead II) and anterior MI (lead V5). However, contrary to classic theory, the number of notches correlated negatively with direct measurements of high-frequency RMS voltage in lead II (r = -0.63) and lead V5 (r = -0.49). Positive correlations were obtained between high-frequency potentials and two new indexes that measure the amplitude of QRS dV/dt-peak-to-peak amplitude of dV/dt and RMS dV/dt. Using these indexes, absolute separation of inferior MI patients and normal subjects was obtained. We conclude that MI increases low-amplitude QRS notching but diminishes total high-frequency voltage, probably because of an overall decrease in electromotive potentials and slowing of ventricular conduction.

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.

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.

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.