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Introduction The electrophysiologic basis for characteristic rate-dependent, constant-late-coupled (390+54 msec) premature ventricular beats (PVBs) present 4–5 days following coronary artery occlusion were examined in 108 anesthetized dogs. Methods and results Fractionated/double potentials were observed in injured zone bipolar and composite electrograms at prolonged sinus cycle lengths (1296 ± 396 msec). At shorter cycle lengths, conduction of the delayed potential decremented, separating from the initial electrogram by a progressively prolonged isoelectric interval. With sufficient delay of the second potential following an isoelectric interval, a PVB was initiated. Both metastable and stable constant-coupled PVBs were associated with Wenckebach-like patterns of delayed activation following an isoelectric interval. Signal-averaging from the infarct border confirmed the presence of an isoelectric interval preceding the PVBs (N = 15). Pacing from the site of double potential formation accurately reproduced the surface ECG morphology (N = 15) of spontaneous PVBs. Closely-spaced epicardial mapping demonstrated delayed activation across an isoelectric interval representing “an arc of conduction block”. Rate-dependent very slow antegrade conduction through a zone of apparent conduction block (N = 8) produced decremental activation delays until the delay was sufficient to excite epicardium distal to the original “arc of conduction block”, resulting in PVB formation. Conclusion The present experiments demonstrate double potential formation and rate-dependent constant-coupled late PVB formation in infarcted dog hearts. Electrode recordings demonstrate a prolonged isoelectric period preceding PVB formation consistent with very slow conduction (

The electrophysiologic basis for characteristic rate-dependent, constant-late-coupled (390 + 54 milliseconds) premature ventricular beats (PVBs) present 4-5 days following coronary artery occlusion were examined in 108 anesthetized dogs.Fractionated/double potentials were observed in injured zone bipolar and composite electrograms at prolonged sinus cycle lengths (1,296 ± 396 milliseconds). At shorter cycle lengths, conduction of the delayed potential decremented, separating from the initial electrogram by a progressively prolonged isoelectric interval. With sufficient delay of the second potential following an isoelectric interval, a PVB was initiated. Both metastable and stable constant-coupled PVBs were associated with Wenckebach-like patterns of delayed activation following an isoelectric interval. Signal-averaging from the infarct border confirmed the presence of an isoelectric interval preceding the PVBs (N = 15). Pacing from the site of double potential formation accurately reproduced the surface ECG morphology (N = 15) of spontaneous PVBs. Closely-spaced epicardial mapping demonstrated delayed activation across an isoelectric interval representing "an arc of conduction block." Rate-dependent very slow antegrade conduction through a zone of apparent conduction block (N = 8) produced decremental activation delays until the delay was sufficient to excite epicardium distal to the original "arc of conduction block," resulting in PVB formation.The present experiments demonstrate double potential formation and rate-dependent constant-coupled late PVB formation in infarcted dog hearts. Electrode recordings demonstrate a prolonged isoelectric period preceding PVB formation consistent with very slow conduction (70 mm/s) across a line of apparent conduction block and may represent a new mechanism of PVB formation following myocardial infarction.

Bi-ventricular (BiV) pacing is an effective therapy for the treatment of cardiac electromechanical (EM) dysfunction. The reason(s), however, for therapy non-response in approximately one-third of the subjects remains unclear, especially as it relates to myocardial perfusion and pacing location. In this study, we examined how acute BiV pacing response may be related to underlying myocardial perfusion coupled with pacing near or distant to the area of perfusion. In 10 open-chest anesthetized canines, coronary blood flow to the left ventricular (LV) anterior wall (AW: n = 5) and lateral wall (LW: n = 5) was controlled during four pacing conditions: right atrial, right ventricular (pseudo-left bundle branch block; [pseudo-LBBB]), BiV-LW and BiV-AW. Local EM function (piezo-electrical crystals and electrodes), along with global hemodynamic parameters, were measured during all pacing conditions at three coronary perfusion rates (≥0.40 mL/min/g, 0.20–0.40 mL/min/g and

A safe, easy, and quick access into the pericardial space may provide a window for diagnostics and therapeutics to the heart. The objective of this study was to provide proof of concept for an engagement and access catheter that allows access to the pericardial space percutaneously. A multilumen catheter was developed to allow navigation and suction fixation to the right atrial appendage/wall in a normal swine model. Advancement through the multilumen catheter using a second catheter with a distal needle tip allows access to the pericardial space without pericardial puncture and advancement of a standard guide wire into the space. Navigation into the pericardial space was undertaken by fluoroscopy alone and was accomplished in 10 swine (5 acute and 5 chronic). As a specific application of this pericardial access method, a pacing lead was implanted on the epicardial surface. Five chronic swine experiments were conducted with successful pacing engagement verified by lead impedance and pacing threshold and sensing. Lead impedance exceeded 1,000 Omega preengagement and dropped by an average of 200 Omega upon implant (769 +/- 498 Omega). Pacing thresholds at 0.4 ms ranged from approximately 0.5 to 2.1 V acutely (1.03 +/- 0.92 V). No cardiac effusion or tamponade was observed in any of the acute or chronic studies. The ability to engage, maintain, and retract the right atrial appendage/wall and to engage an epicardial lead was successfully demonstrated. These findings support the feasibility of safe access into the pericardial space in a normal swine model and warrant further investigations for clinical translation.

Previous studies have speculated, based on indirect evidence, that the action potential at the transverse (t)-tubules is longer than at the surface membrane in mammalian ventricular cardiomyocytes. To date, no technique has enabled recording of electrical activity selectively at the t-tubules to directly examine this hypothesis. We used confocal line-scan imaging in conjunction with the fast response voltage-sensitive dyes ANNINE-6 and ANNINE-6plus to resolve action potential-related changes in fractional dye fluorescence (DeltaF/F) at the t-tubule and surface membranes of in situ mouse ventricular cardiomyocytes. Peak DeltaF/F during action potential phase 0 depolarization averaged -21% for both dyes. The shape and time course of optical action potentials measured with the water-soluble ANNINE-6plus were indistinguishable from those of action potentials recorded with intracellular microelectrodes in the absence of the dye. In contrast, optical action potentials measured with the water-insoluble ANNINE-6 were significantly prolonged compared to the electrical recordings obtained from dye-free hearts, suggesting electrophysiological effects of ANNINE-6 and/or its solvents. With either dye, the kinetics of action potential-dependent changes in DeltaF/F during repolarization were found to be similar at the t-tubular and surface membranes. This study provides what to our knowledge are the first direct measurements of t-tubule electrical activity in ventricular cardiomyocytes, which support the concept that action potential duration is uniform throughout the sarcolemma of individual cells.

For generations of electrocardiogram (ECG) analysis, the presence of premature ventricular beats (PVBs) has been characterized as a common event in the ECG without regard to the mechanism which has caused the PVB in the first place. At best, the coupling interval with the preceding sinus beat may be noted. This viewpoint persisted throughout the era of automated ECG analysis, as well as influencing the treatment of more life threatening events by PVB suppression strategies alone. This study proposed three hypotheses which would link the PVB to a specific mechanism or milieu. Each of these hypotheses requires significant signal processing of the continuously recorded high resolution ECG. Data are presented which demonstrate that abnormal intra-QRS potentials may be linked to a reentrant mechanism for the PVBs and that many patients have significant changes in these potentials in the sinus beats preceding the PVB. Changes in the characteristics of the repolarization as measured in the T/U wave period were also observed and could be linked to triggered activity mechanism for some PVBs. Finally, the role of subclinical ST segment changes also indicates that low grade ischemia may play a role in modulating either PVB mechanism. The data generated by this study suggest that a new view toward PVB mechanism as measured by ECG characteristics may warrant a more rational approach to renewed interest identifying the malignant PVBs and their eventual clinical management.

Maps of AF After Ablation. Introduction: The purpose of this study was to investigate the mechanisms by which atrial linear ablation lesions eliminate atrial fibrillation (AF). Methods and Results: With an array of 112 unipole, epicordial maps of electrically induced AF in 6 dogs (acute group), self-sustained AF in 6 dogs (chronic group), and sinus rhythm and atrial pacing in 3 dogs (control group) were analyzed before and after creating linear radiofrequency ablation lesions in both atria that eliminated the AF. In the acute and chronic groups, activation maps showed multiple wavelets with complex patterns of activation and reentry during AF. Conduction velocity and the number, size, and complexity of wavelets did not change, whereas median fibrillatory cycle length increased with the number of linear lesions. In the control group, refractoriness and conduction velocity were unaffected by the number of lesions. Conclusions: In these models of AF, linear lesions that eliminate AF increase the cycle length of AF without changing conduction velocity, number or size of wavelets, or complexity of activation patterns.

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 microV (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.

This study considers the problem of representing high-resolution ECG (HRECG) signals in the time-frequency plane using spectrotemporal mapping (STM). High-resolution ECG signal components overlap in both time and frequency. The central issue with STM techniques is whether sufficient time-frequency resolution exists to discriminate normal and abnormal QRS signals. The trade-off between signal resolution in time and in frequency must be made without a priori knowledge of the HRECG's time-frequency structure. A simulation experiment was performed to examine the time-frequency distribution of normal, abnormal low-level (late potentials), and bundle branch block components of the QRS. Results suggest that discrimination of these signals with STM is problematic. Signals and noise within the HRECG ensemble can, however, be easily distinguished. This observation forms the basis of a new optimally filtered ensemble averaging technique for signal-to-noise ratio enhancement.

Most studies of cardiac late potentials (LPs) recorded from the body surface use signal processing definitions to characterize these abnormal ventricular potentials. For many years, the focus of the clinical studies have been on those signals that outlast the QRS complex; however, cardiac mapping studies have clearly identified that the such abnormal activation occurs during the QRS complex as well and can be distinguished from normal QRS potentials using advanced signal processing tools. Thus, both the abnormal intra-QRS potentials and the LP represent a continuum of the same signal sources. The electrogram recordings of these signals are often characterized as multiphasic with ambiguous/multiple depolarization times spanning tens of milliseconds within very short distances (30 milliseconds) and decremental conduction. Hence, the role of this passive cell coupling in the generation of abnormal patterns of conduction as well as arrhythmogenesis has yet to be fully determined but may in fact define another mechanism of cardiac conduction.

T HIS ARTICLE presents an overview of the signal processing methods used to estimate and subsequently analyze late potentials in the high-resolution electrocardiogram (ECG). The high-resolution ECG is universally acquired using signal averaging techniques. The goal in acquisition is to improve the signal-tonoise ratio of the ECG: Resolution of signals on the order of 0.5 uV is required to detect late potentials accurately. The essential elements of signal averaging include computerized data acquisition, QRS detection and alignment, averaging, and noise measurement, and each is discussed in detail. Analysis of the signal average in the time domain is presented with discussions of filtering, vector magnitude transformation, and measurement techniques. Frequency domain analysis is introduced, with a discussion of spectral analysis techniques. Application to the high-resolution ECG is presented. Arguments for time-varying spectral representations and advanced time-frequency distributions are then considered. A summary of applications of other signal processing techniques to the high-resolution ECG follows. Several classes of Wiener filtering methods that have the potential to improve the signal-to-noise ratio significantly, compared with conventional signal averaging, are introduced. The review concludes with a description of techniques of high-resolution ECG analysis from Holter recordings and possible time-varying late potential activity.

Models of cardiac electrical activation have been proposed for over 100 years. While the major components of the cardiac source and volume conductor models have not changed over the years, they have become increasingly complex and more robust. Although modeling of body surface potentials (forward model) and cardiac potentials (inverse model) has been a major topic of research, the clinical utility has yet to be fully realized. Integrated cardiac models with electrical, mechanical, neural, metabolic, circulatory, and genetic inputs are currently being developed. These integrated models are likely to provide new insights into cardiac electrical activation during heart failure and generate new hypotheses about multi-system coupling in the heart. The objective of this chapter is to provide an overview of the history, theory, and clinical use of electrical heart models with applications to heart failure.

Although high voltage direct current (DC) shock is a standard technique to terminate ventricular fibrillation (VF), it can cause severe pain and tissue damage. The exact effect of the DC electric fi eld, which can depolarize the heart during VF is still unknown. We hypothesized that lo w-energy DC field in combination with pacing (pacing+DC) could terminate VF by affecting the ventricular propagation pattern. In six Langendorff-perfused isolated rabbit hearts with the ablated sinoatrial (SA) node, the DC field was delivered to the left ventricle (cathode) and right ventricle (anode). We designed a timed protocol using LabVIEW programming that delivers pacing, DC and pacing+DC stimuli for two seconds time intervals each. The pacing pulse (with varying pacing cycle length: 300ms-30ms) was delivered to the apex. Transmembrane voltage was reco rded with optical mapping technique for 16 seconds at a sampling rate of 2ms/frame. We crushed the sinoatrial node to reduce the heart rate. The baseline activation appeared to have endocardial origins with a mean escape ventricular ra te of 60 ± 5bpm at baseline. The DC field (30mA-60mA) alone increased the mean heart rate to 120±5bpm. Although DC alone terminated VF in a few cases, the rate of termination was very low (6.2%). However, when pacing+DC was app lied, it was possible to terminate VF in 34 of 130 episodes in six rabbits. The rate of successful defibrillation of VF with pacing+DC was significantly higher than that with DC alone (20% vs 6.2%, p

Bandwidth of Late PotentialsIntroduction: Limited bandwidth systems such as Holter recorders are being used to record cardiac late potentials. Standard late potential systems have a low-pass frequency of 300 Hz. This suggests that Holter tape systems may significantly distort the late potential measurements, when compared to standard late potential systems. Methods and Results: Signal-averaged recordings were obtained with an analog bandwidth of 0.05-300 Hz. Digital filters were then used to do high-pass filtering and low-pass filtering. All XYZ signal-averaged recordings were low-pass filtered at frequencies of 250, 150, 100, 75, 50, and 25 Hz using a second order Butterworth filter. A fourth order 40 Hz bidirectional high-pass filter was then applied to each set of recordings. The QRS duration (QRSd) was measured in the filtered vector magnitude. Thirty-eight syncope patients who had negative electrophysiologic studies for ventricular tachycardia, no prior infarction, normal ejection fractions (> 50%), and a QRSd 120 msec served as the positive late potential group. Conclusions: A statistically significant lengthening of the QRSd (P

Ectopic conduction is defined as the premature exit of the cardiac impulse from the specialized conduction system across a damaged Purkinje-ventricular muscle interface. This anomalous form of atrioventricular (AV) conduction was induced in the dog heart by lidocaine injection of the His bundle-interventricular septum interface and by ischemic damage of the AV junction subsequent to anterior septal artery ligation in the dog heart. The electrocardiogram (ECG) manifestation of ectopic conduction is the loss of initial forces and replacement of the Q waves with delta waves. In order to verify these effects, the authors devised a multi-electrode, malleable plaque (63 electrode sites) that could be secured at the AV junction during venous occlusion in the open-chest, anesthetized dog. Preliminary maps indicated a dramatic change in activation that proceeded from apex to base of the heart in the control state and reversed after ischemic damage to the His bundle. In vitro, it was possible to induce ectopic conduction by lidocaine injection at the interface of the right bundle branch and septal muscle. Microelectrode studies demonstrated that foot potentials, for example, electrotonic, or subthreshold potentials mediated the connection from Purkinje to muscle in the damaged zone. In a recent set of experiments in vivo, subthreshold stimulation (STS) was delivered to simulate electrotonic potentials to the His bundle region, and right ventricular apex, using multipolar electrode catheters. In the normal heart, STS delivered as DC constant current or pulse trains (1000 Hz, 50 ms pulse duration) induced shortened P-R intervals and delta waves with or without bundle branch block patterns.(ABSTRACT TRUNCATED AT 250 WORDS)

Multielectrode cardiac mapping has at least a 50-year history in cardiac research, and the development of this methodology has closely followed the technological advances in instrumentation and computing. The methodology has proven to be quite effective in characterizing potential distributions on both the body surface and the epicardial surface of the heart. However, the more challenging problem for multielectrode systems is the identification and display of cardiac activation or isochronal maps. In the earlier era of cardiac mapping, hardware limitations, particularly the speed of computer processing and digital data acquisition, were the major challenges for obtaining continuous data from a high number of recording channels. For the current generation of digital electronics and computers this is no longer a significant challenge. The analysis and interpretation of the data still pose a number of challenges, since in many cases, such as diseased myocardium or during complex tachyarrhythmias, the biophysical basis of conduction is not fully developed. For example, the use of contour-generation software often does not consider the actual nature of the underlying pathophysiology. Many standard interpolation algorithms will indeed create contours overlying scar tissue within infarcted regions. This is an inherent error. A number of newer mapping approaches rely on mathematical models to create images based on data at some distance from the actual sources. In some cases these systems are proprietary and may have indeed conquered some long-standing problems. In other cases, because the systems produce “good looking” images that fit a preconceived model of activation, their underlying models are not challenged. This chapter focuses on the issues surrounding direct contact, multielectrode mapping approaches and will concentrate on the problems associated with producing activation maps, especially from regions surrounding and within infarct regions.

Modeling abnormal depolarization of the ventricles may provide a means to localize sites of arrhythmia foci from the body surface recordings. In this paper, we present a single moving dipole (SMD) model of the ventricular depolarization. The model can reproduce characteristic QRS patterns comparable to the clinical recordings when it is located in an inhomogeneous torso model. Our approach involves estimating a series of dipole moments based on vectocardiograms and estimating trajectories based on the three-dimensional isochrone of the ventricular activation. The patterns of body surface potential isochrones are consistent with those from previous studies. The SMD model was also used to simulate posterior wall infarction, which matched the criteria for this diagnosis. In conclusion, our SMD model provided a base for further ventricular depolarization studies and this equivalent dipole approach might be useful in investigating ventricular arrhythmias and their site of origin.

The high resolution ECG (HRECG) is a method used for identifying patients at high risk of sudden cardiac death. This project focuses on globally distributed student teams working in the development of several contextual methods of HRECG analysis. Each team has worked on various elements of the overall project, e.g., data collection, algorithm development, data analysis, which allows the development effort to proceed in parallel. The specific educational objectives of the project are: (a) to give students experience of working collaboratively in globally distributed teams; (b) to obtain staff experience of operating distributed, collaborative projects; (c) to develop team oriented working and communications skills that take advantage of today's electronic connectivity. The project is addressed in three stages: (1) collecting of HRECGs; (2) establishing a database; and (3) development of software tools. Besides of the scientific impact, we expect to invigorate our labs with new ideas, strengthen the understanding among students and faculty, and provide every participant an opportunity to engage in an international research project

Since the advent of computer-based electrocardiographic systems, it was recognized that these devices could add many features to analyze the electrocardiogram (ECG) that were beyond an individual's ability in making standard measurements from the paper version of the 12-lead ECG. These features have included the development of noise reduction techniques, such as signal averaging, and spectral measurements of frequency content using Fourier analysis. Both of these methods reveal electrocardiographic features that cannot be normally visualized or hand measured. Thus the field of high-resolution electrocardiography is defined as recording cardiac signals from the body surface that are not visible or apparent from the standard ECG. It most often implies a computer-based approach for processing the ECG. The signal-averaged ECG (SAECG) is the most common form of the high-resolution ECG but should be considered as only one approach for producing a high-resolution ECG.

Holter 24-h ECG tape recordings have been used to identify patients susceptible to ventricular arrhythmias. The authors record ventricular late potentials from an ambulatory ECG using the technique of signal averaging. To commence signal averaging, a trigger template and a time interval, relative to the fiducial point, from which to measure noise are visually selected. The trigger template is used to define the shaping filter, and the ECG data file is continuously deconvolved with the shaping filter. As beats are accepted into the signal average they are graphically displayed, and a record of individual beat noise estimates is made. The results demonstrate that with an enhanced signal-averaging technique it is technically feasible to obtain high-resolution ambulatory ECG recordings. >

Selective beat signal averaging and spectral analysis were implemented to identify whether reentry, triggered activity or parasystole is the mechanism of the isolated premature ventricular contraction (PVC). 2-hour, high resolution ECG recordings were digitally obtained from 9 patients with frequent PVCs (>250/hr). For reentry, in 7/9 patients with a positive average for late potentials (LP) there were no changes of LP in sinus beats before and after PVCs. However, changes in the T/U waves in the difference waveform between the pre-PVC beat and its precedent beat (in 2/9 patients), and their T/U wave amplitudes (in 9/9 patients, mean amplitude difference of 0.0269 mV) implied a triggered activity, mechanism. Also, significant periodicities in PVC interval series and low correlation between sinus and PVC intervals (in 9/9 patients), suggested a parasystolic mechanism. Based on the limited data set, triggered activity and parasystole may be significant PVC mechanisms while reentry may not. >

Epicardial electrograms from infarct regions have multiple deflections due to the superposition of different activation wavefronts. This study aims to separate local and distant wavefronts by two-dimensional spatial highpass filtering. For that purpose, extracellular electrograms were recorded from thin ( >

The aim of this study was to develop an ECG based method to identify changes in repolarization which may presage the appearance of premature ventricular beats (PVBs). Our hypothesis is that these surface repolarization changes may be the manifestation of cellular after depolarizations (ADs). ADs have been shown to be the mechanism of PVBs in the form of triggered automaticity in several settings. Data were collected from 14 patients using XYZ leads, and a digital ambulatory ECG monitor. Beat sequences of 5 sinus beats and a PVB of a single morphology were selected for analysis. A window from the end of the QRS to the next 4 wave or the PVB was chosen for analysis. The pre-PVB T/U wave was compared with all the prior T/U waves using three methods: (1) statistical analysis of 4 T/U wave measurements; (2) residual analysis of signal averaged T/U waves; and (3) power spectrum analysis of a time series of the vector magnitude of the integral of the T/U wave. The statistical analysis was not significant for any of the T/U wave parameters. The power spectrum analysis and residual analysis produced concordant results for 3 of 14 patients showing significant changes in the comparisons of the pre-PVB T/U wave and the prior T/U waves. This study suggests that, in some patients, changes occur in repolarization prior to a PVB. These changes may be evidence of the body surface manifestation of ADs which are large enough to initiate the mechanism of triggered automaticity for the induction of a PVB.

Atrial fibrillation (AF) has been described as a "random" or "chaotic" rhythm. Evidence suggests that AF may have transient episodes of temporal and spatial organization. The authors introduce a new algorithm that quantifies AF organization by the mean-squared error (MSE) in the linear prediction between two cardiac electrograms. This algorithm calculates organization at a finer temporal resolution (/spl sim/300 ms) than previously published algorithms. Using canine atrial epicardial mapping data, the authors verified that the MSE algorithm showed nonfibrillatory rhythms to be significantly more organized than fibrillatory rhythms (p

Background Using the signal-averaged ECG (SAECG), this study developed a new electrical index for predicting arrhythmic events: abnormal intra-QRS potentials (AIQP). Methods and Results We studied 173 patients followed after myocardial infarction for a mean duration of 14±7 months. Sixteen arrhythmic events occurred, defined as sudden cardiac death, documented sustained ventricular tachycardia, or nonfatal cardiac arrest. Noninvasive indices of arrhythmia risk were measured, including AIQP, conventional SAECG, Holter, and left ventricular ejection fraction (LVEF). Abnormal intra-QRS potentials were defined as abnormal signals occurring anywhere within the QRS period. They were estimated with a lead-specific, parametric modeling method that removed the smooth, predictable part of the QRS. AIQPs are characterized by the remaining transient, unpredictable component of the QRS and manifest as low-amplitude notches and slurs. A combined XYZ-lead AIQP index exhibited higher specificity (95%) and predictive value (PV) (+PV, 47%; −PV, 94%) than the conventional SAECG in combination with Holter and LVEF (specificity, 89%; +PV, 25%; −PV, 93%). Conclusions AIQP improved specificity and predictive value, compared with conventional tests, for prediction of arrhythmic events. AIQP emerged as the best noninvasive univariate predictor of arrhythmic events after myocardial infarction in this study. A review of several other reports shows that AIQP in the present study outperformed the conventional predictive indices reported in those other data sets.

The signal-averaged electrocardiogram (SAECG) facilitates noninvasive recording of low-amplitude cardiac signals such as ventricular late potentials. The SAECG has been used to accurately predict life-threatening ventricular tachyarrhythmias in patients after acute myocardial infarction and with nonischemic dilated cardiomyopathy, and to screen for inducible ventricular tachycardia in patients with unexplained syncope and with nonsustained ventricular tachycardia. This review focuses on currently accepted methodology and clinical and research applications of the SAECG.

The low predictive value of the signal averaged ECG (SAECG) at rest may be due to the absence of any physiological perturbation. This study assessed changes of late potentials (LP) in the SAECG due to acute ischemia in five susceptible (S) and five resistant (R) dogs for sudden cardiac death. SAECGs were measured at rest prior to and during the last 3 min of 4 min transient occlusion of the left circumflex artery (CAO). At rest no significant differences were seen in the QRS duration (QRSD), the low amplitude signal duration (LAS40) and the root mean square voltage (RMS20) between S and R dogs. However, acute ischemia caused significant increases in QRSD and LAS40, but only in the S dogs. These results indicate differences in the ischemic modulation of the arrhythmogenic substrate in S and R group. Analysis of LP during acute ischemia may provide an important increase in the positive predictive value of the SAECG.

TWIDALE, N., ET AL.: Late Potentials Are Unaffected by Radiofrequenc y Catheter Ablation in Patients with Ventricular Tachycardia. Reentrant ventricular tachycardia is dependent on an area of myofibers, embedded in scar tissue, which exhibit slow conduction. Late potentials recorded by signal-averag ed electrocardiography appear to correspond to these zones of slow conduction and frequently are present in patients with VT. We hypothesized that elimination of inducible VT by catheter-mediated ablation of critical areas of slow conduction would alter late potentials. Four patients underwent catheter ablation in which radiofrequency current was delivered to zones of slow conduction exhibiting isolated mid-diastoUc potentials that could not be dissociated from the tachycardia. The four patients had developed VT (cycle length 382 ± 50 msec; mean ± SEM) 13-180 months after inferior myocardial infarction. Late potentials were present in each patient before catheter ablation was attempted. Although VT was not inducible in anv patient immediately after ablation, late potentials were still present in all four patients and there was no significant difference in the QRS duration (136.5 ±4.0 msec postablation; 135.7 ±4.5 msecpreablation), root mean square voltage in the terminal 40 msec of the QRS (10.0 ± 1.0 fxV postablation; 5.9 ± 0.4 ^V preablation). or in the duration of the low amplitude signal (69.2 ± 2.0 msec postablation; 62.7 ± 3.4 msec preablation). At follow-up eiectrophysioiogy study performed 14 ± 7 days after ablation, one of the four patients had inducible VT. In conclusion, late potentials persist even after successful radiofrequency catheter ablation and do not appear to be useful for predicting results of follow-up eiectrophysioiogy study. (PACE, Vol. 17, February 1994)

Late Potentials: Epicardial and Body Surface. Introduction: Identification of the end of the QRS is perhaps the single most important feature obtained from the high resolution signal-averaged electrocardiogram (SAECG). This point relies on computer algorithms to select a point ahove the noise levels. Prior studies to suhstantiate this approach using eleetrograms for comparison have demonstrated many examples of the hody surface recordings failing to detect the full extent of the late potentials. Methods and Results: An animal model that generates late potentials was used in conjunction with epicardial cardiac mapping system to systematically examine the rea.sons for these failures. In I I of 13 dogs we found a concordance hetween the signal-averaged recordings and Ihe epicardial recordings within 5 msec. The two discordant studies were attrihuted to a failure of epicardial mapping to record all late potential sources. Also, a means of accurately comparing measurements from the two recording technologies was required in this study as well as a new definition for identifying the end of activation currents in epicardial eleetrograms. Conclusion: To achieve these results required approaches different from those used in the clinical setting to record the SAECG. These include: (1) the analysis of individual XYZ leads as opposed to the vector magnitude derived from these leads; (2) visual identification of very low level signals, as automatic algorithms often fail to detect low level signals: and (3) the use of finite impulse response digital filters instead of the bidirectional Butterworth filter.

Signal averaging is the most common computer method for improving the signal-to-noise ratio of the ECG in order to record low level cardiac signals which are not identifiable with standard ECG techniques. The process of signal averaging assumes that the interfering noise is random and that the signal of interest repeats with every beat included in the average. The process uses the computer to detect each beat and to time align each beat. The average is performed for each moment in time, for a specified number of beats, and over a selected period of the cardiac cycle. Typically the signal averaged ECG is performed while the patient is connected to the system and stored on computer disk for later processing. Quality assurance of the SAECG should be part of the data acquisition phase because of the statistical nature of signal averaging. There is a significant literature on ECG based signal averaging and several in-depth technical reviews have been published1,2.

BACKGROUND This study performed a critical analysis of signal-averaging methods. The objective was to optimize detection of late potentials. METHODS AND RESULTS We studied two patient populations: a low-arrhythmia-risk group with no evidence of heart disease and a group with clinically documented ventricular tachycardia (VT). Filtered QRS duration (QRSD) and terminal QRS amplitude (RMS40) were measured from the vector magnitude. A QRS duration based on the latest detectable ventricular activity in any of the three individual XYZ leads was also measured. Because of improved signal-to-noise ratio, both individual lead analysis and extended (600-versus 200-beat) averaging yielded significant changes in signal-averaged ECG parameters. Both approaches gave an increased sensitivity for VT identification. Sensitivity, specificity, and accuracy were evaluated as functions of critical values of QRSD and RMS40. RMS measurements in the terminal QRS, ranging from 20 to 100 msec and including RMS40, did not contribute to maximizing sensitivity and were highly correlated with QRSD. Our results from the low-arrhythmia-risk group suggest that age and sex should be considered in the definition of late potentials. CONCLUSIONS We propose a VT risk stratification scheme using signal-averaged ECG parameters obtained from both individual lead and vector magnitude analysis. This allows definition of four categories of VT risk derived statistically from the study data. This definition is based on combined measures of sensitivity, specificity, and negative and positive predictive value.

The high resolution ECG is now commonly used in the clinical setting. It is the most advanced ECG signal processing methodology commercially available to the physician. The methodology is reviewed with comments about its limitations and future applications.