Journal of Cardiovascular ElectrophysiologyVolume 8, Issue 2 p. 237-239 Explain the Change in PR Interval and Bundle Branch Block Pattern with Comparably Coupled Atrial Premature Beats BEHZAD B. PAVRI M.D., Corresponding Author BEHZAD B. PAVRI M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaAddress for correspondence: Behzad B. Pavri, M.D., 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104. Fax: 215-349-5894.Search for more papers by this authorKAR-LAI WONG M.D., KAR-LAI WONG M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaSearch for more papers by this authorDUSAN Z. KOCOVIC M.D., DUSAN Z. KOCOVIC M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaSearch for more papers by this authorMICHAEL B. SIMSON M.D., MICHAEL B. SIMSON M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaSearch for more papers by this author BEHZAD B. PAVRI M.D., Corresponding Author BEHZAD B. PAVRI M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaAddress for correspondence: Behzad B. Pavri, M.D., 3400 Spruce Street, 9 Founders, Philadelphia, PA 19104. Fax: 215-349-5894.Search for more papers by this authorKAR-LAI WONG M.D., KAR-LAI WONG M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaSearch for more papers by this authorDUSAN Z. KOCOVIC M.D., DUSAN Z. KOCOVIC M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaSearch for more papers by this authorMICHAEL B. SIMSON M.D., MICHAEL B. SIMSON M.D. Department of Medicine, Division of Cardiovascular Medicine, Hospital of the University of Pennsylvania, Philadelphia, PennsylvaniaSearch for more papers by this author First published: 20 April 2007 https://doi.org/10.1111/j.1540-8167.1997.tb00785.x Section Editor: Fred Morady, M.D. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Volume8, Issue2February 1997Pages 237-239 RelatedInformation

BACKGROUND:An abnormal signal-averaged ECG (SAECG) has predictive value for arrhythmic events in patients with coronary artery disease. The purpose of this study was to investigate whether an abnormal SAECG could provide prognostic information in patients with nonischemic dilated cardiomyopathy. METHODS AND RESULTS:We prospectively obtained SAECGs in 114 patients with dilated nonischemic cardiomyopathy. Twelve-lead ECGs, left ventricular ejection fractions, hemodynamic measurements, and peak exercise oxygen consumption (VO2) also were measured. An SAECG was defined as abnormal by any one of the three following criteria: filtered QRS duration > 120 msec, root-mean-square voltage in the last 40 msec < 20 microV, or duration < 40 microV > 38 msec at 40 Hz. Sixty-six patients had a normal SAECG, 20 patients had an abnormal SAECG, and 28 patients had bundle branch block (BBB). Mean follow-up was 10 +/- 5 months. Age, ejection fraction, peak VO2, pulmonary capillary wedge pressure, and cardiac index were not statistically different among the three groups. Use of antiarrhythmic drugs was similar among the three groups, although patients with BBB had more implantable defibrillators (p < 0.05). The incidence of previous atrial arrhythmias was similar for the three groups. Patients with abnormal SAECG or BBB had more past episodes of sustained ventricular tachycardia and/or sudden death episodes (n = 9) than patients with normal SAECG (n = 1) (p < 0.01). Prospectively, none of the 66 patients with normal SAECG died suddenly or had sustained ventricular arrhythmias. Two deaths occurred from progressive heart failure, and three patients required urgent transplant. In the 20 patients with an abnormal SAECG, four patients had sustained ventricular tachycardia, five patients died suddenly, two patients died from progressive heart failure, and one patient required urgent transplant. In the patients with BBB, four patients had sustained ventricular tachycardia, and four patients required urgent transplant. One-year event-free survival, i.e., absence of ventricular tachycardia and/or death, was 95% in patients with normal SAECG, 88% in patients with BBB, and only 39% in patients with an abnormal SAECG (p < 0.001). Multivariate analysis demonstrated that SAECG and New York Heart Association classification were independent predictors of survival. CONCLUSIONS:Patients with an abnormal SAECG had a statistically significant increase in sustained ventricular arrhythmias and/or death than did patients with a normal SAECG or BBB. This study demonstrates that an abnormal SAECG is a marker of past and future arrhythmic events in patients with nonischemic dilated cardiomyopathy. In contrast, patients with a dilated cardiomyopathy with a normal SAECG have an excellent prognosis with adverse outcome only from progressive heart failure.

Signal-averaged electrocardiography allows the detection of late potentials, which have been associated with delayed and disorganized ventricular activation. This article reviews the technique, describes the findings recorded from patients with ventricular tachyarrhythmias, and assesses the prognostic value of late potentials for ventricular tachyarrhythmias and sudden cardiac death in patients after an acute myocardial infarction. The role of signal-averaged electrocardiography in the evaluation of patients with syncope and cardiomyopathies is also briefly discussed.

The development of slow conduction during the first hours of acute transmural myocardial infarction (ATMI) was studied by signal-averaged electrocardiograms (SAE) in 19 adult anesthetized sheep. SAEs were recorded before and after intravenous infusions of lidocaine and bretylium were begun and 10, 30, and 60 min after ATMI produced by ligation of the left anterior descending and second diagonal coronary arteries. Four sheep died promptly of ventricular tachyarrhythmias; two others developed sustained ventricular arrhythmias, which precluded additional data. Biphasic changes in QRS duration, root mean square voltage of the terminal 40 ms of the QRS complex, and duration of terminal low-amplitude (less than 30 microV) signal were observed. Peak changes in conduction occurred 30 min after infarction and regressed toward baseline thereafter. At 30 min, all animals developed late potentials, which were defined as signals that exceeded both after-drug QRS duration and duration of terminal low-amplitude signal less than 30 microV by more than two standard deviations. At 60 min, only 3 of 13 (23%) animals had late potentials. Conduction is slowest 30 min after ATMI in sheep but may not be related to development of ventricular arrhythmias. In five of six sheep (83%), ventricular arrhythmias occurred within 15 min of infarction before peak slowing was observed by SAE.

Introduction Since 1978, investigators have recorded small high frequency waveforms that have heen recorded by signal averaged electrocardiography (SAECG) from patients with sustained ventricular tachycardia (VT) after myocardial infarction (MI).^"'' The microvolt level signals, commonly called "late potentials," are continuous with the QRS complex and last for tens of milliseconds into the ST segment. Late potentials appear to correspond to fragmented and delayed ventricular activation that has been observed on electrograms recorded from the myocardium in patients with VT.̂ ~^^ Late potentials are recorded frequently from patients with VT after MI, and recent studies have shown that patients with late potentials after an acute MI are at high risk for sudden cardiac death or sustained VT. This article briefly reviews SAECG as a noninvasive means to identify those patients at high risk for lethal arrhythmias.

This study was designed to examine 2 hypotheses: that acute myocardial infarction (AMI) alters early cardiac activation measured by signal-averaging; and that the magnitude of abnormality of early activation may be greater in patients with post-AMI ventricular tachycardia (VT). We examined the root-mean square voltage amplitude in 10-ms intervals over the first 80-ms of the signal-averaged QRS complex. Data from 42 healthy volunteers were compared with those from 52 patients with previous AMI (24 anterior) but no VT and 46 post-AMI patients (33 anterior AMI) with recurrent sustained VT. Patients with VT differed from other post-AMI patients because of lower left ventricular ejection fraction, more frequent aneurysm formation and higher levels of ventricular ectopic activity. A significant decrease in initial voltage amplitude occurred at 30 to 40 ms after the beginning of the QRS in both anterior and inferior AMI patients compared with the normal group. A further significant decrease in initial amplitude occurred in VT patients both after anterior and inferior AMI. These differences persisted for the remainder of the 80-ms interval. These changes were weakly related to QRS duration (r = 0.45), ejection fraction (r = 0.50) and poorly correlated with the presence of Q waves On 12-lead electrocardiogram (r = 0.21). Direct endocardial catheter recordings performed in VT patients confirmed abnormalities of local septal activation after anterior and inferior AMI. An amplitude at 40 ms of <50 μV was significantly related to the presence of VT in anterior AMI patiente (28 of 33 with VT vs 10 of 24 without VT, p < 0.001, chisquare analysis). A similar trend existed for inferior AMI patiente but was not statistically significant (p = 0.07). We conclude that MI alters early activation measured by signal-averaging. The presence and extent of septal abnormalities may be important in the development of VT.

The mechanism of cycle length oscillation and its role in spontaneous termination of reentry was studied in an in vitro preparation of canine atrial tissue surrounding the tricuspid orifice. Reentry occurred around a fixed path with incomplete recovery of excitability. Among 18 experiments, there was complete concordance between the occurrence of spontaneous cycle length oscillation and spontaneous terminations; both were observed in 10 experiments and neither in the other eight (p less than 0.001). Local changes in conduction during oscillations resulted from the dependence of both conduction velocity and action potential duration on the preceding local diastolic interval. Interval-dependent changes in action potential duration contributed to the oscillation by altering the next diastolic interval. Because of changes in action potential duration, changes in cycle length were poorly correlated with changes in diastolic interval and, therefore, with local conduction velocity. Complex oscillations resulted from variations in conduction time at multiple sites in the circuit. Oscillations caused most spontaneous terminations. The critical event was an exceptionally long diastolic interval preceding the next-to-last cycle that accelerated local conduction (which tended to shorten the last cycle) and prolonged action potential duration and refractoriness at the site of block. Ninety-two of 99 recordings of spontaneous termination showed evidence of oscillation of conduction and refractoriness causing block.

A computer model of the AV node was developed in order to study mechanisms of conduction delay in the AV node. Three cells were used corresponding to the AN, N, and NH region. The basic mechanisms for delay were a high intercellular resistance and a delayed, time dependent recovery of excitability in the center cell. The action potentials for all cells were held constant. The model reproduces antegrade conduction characteristics of the AV node and the waveform of the center cell resemble the two component action potentials of N cells. The model suggests that the conduction properties of the AV node may be due to subthreshold phenomenon.

Fractionated electrograms are frequently recorded during mapping studies in patients with coronary artery disease and ventricular tachycardia. The authors developed a computer model of electrogram generation based on the biophysics of volume conductor fields. They show that fractionated electrograms can be produced as otherwise uniform wavefronts of activation encounter regions of increased cellular coupling resistance. Because of this, local activation may not correspond to the largest or most rapid deflection in a polyphasic, fractionated electrogram.

Programmed stimulation and signal-averaged electrocardiography were performed in 43 consecutive patients with nonsustained ventricular tachycardia (VT) after healing of inferior (29 patients) or anterior wall (14 patients) acute myocardial infarction. Twenty-two patients had inducible sustained VT. Patients with inferior infarction and inducible sustained VT had significantly longer filtered QRS durations (125 +/- 19 vs 112 +/- 15 ms, p less than 0.01) and significantly lower voltage in the last 40 ms of the filtered QRS complex (19 +/- 5 vs 30 +/- 14 microV, p less than 0.05) than those without inducible sustained VT. In contrast, the signal-averaged electrocardiographic measurements in patients with anterior infarction and inducible sustained VT did not differ significantly from those without inducible sustained VT. The results of these studies were compared with those of 2 control groups: 45 patients without ventricular arrhythmias after myocardial infarction and 95 patients with spontaneous and inducible sustained VT after myocardial infarction. The signal-averaged electrocardiographic measurements in patients with spontaneous nonsustained VT after inferior infarction were intermediate between the control group without arrhythmias and the control group with sustained VT. The signal-averaged electrocardiograms in patients with nonsustained VT after anterior infarction were not significantly different from those in patients without ventricular arrhythmias. The study shows that the site of infarction influences the signal-averaged electrocardiogram in patients with VT after myocardial infarction. The signal-averaged electrocardiogram may be useful in identifying patients with nonsustained VT after a remote inferior myocardial infarction who have inducible sustained VT.

THE APPLICATION of signal averaging to electrocardiography allows the detection of microvolt level waveforms that are masked by noise when recorded with conventional techniques. This article briefly reviews signal-averaging methods and discusses the HisPurkinje potential and late potentials as examples of new information available from the body surface with the technique. Method. The purpose of signal averaging is to reduce the level of noise that contaminates the electrocardiogram (ECG)."2 The primary sources of noise are skeletal muscle activity, electrodes, powerline interference, and amplifiers. The noise amplitude is typically 5 to 20 ,uV under optimal conditions before averaging. There are two types of signal averaging. In ensemble averaging sequential samples of a repetitive waveform are averaged. Random noise, not synchronized with the waveform of interest, cancels and is reduced in proportion to the square root of the number of beats processed.2 The noise level in most studies is under 1 ,uV after averaging 100 to 500 cycles, the equivalent of 1/100 of a millimeter at standard electrocardiographic display scale. Ensemble averaging requires that the waveform of interest must repeat precisely and be linked in time with a fiducial point, usually a portion of the QRS, which is used to align the beats before averaging. If the waveform of interest lacks a fixed temporal relationship with the fiducial point, then the averaged waveform will be smoothed and the highfrequency details will be lost.2 A second form of signal averaging is spatial averaging.3'4 Potentials from four to 16 independent electrodes are summed, yielding a theoretical noise reduction of two to four times. The advantage of spatial averaging is that transient events can be analyzed. There is a practical limit, however, to the number of electrodes if all are to record the same electrocardiographic vector and, moreover, the closely spaced electrodes may record a common noise source that would not effectively cancel. Flowers et al.3 developed a vari-

Im letzten Jahrzehnt wurde von mehreren Arbeitsgruppen beschrieben, daß Patienten und Tiere mit ventrikulären Tachykardien einen charakteristischen Befund im EKG während Sinusrhythmus aufweisen: hochfrequente Signale im Mikrovolt-Bereich, die im QRS- Komplex beginnen und sich eine variable Zeit in die ST-Strecke ausdehnen (1–9). Diese Signale, die im allgemeinen nur im signalgemittelten EKG zu erfassen sind, scheinen in langsam leitenden Gebieten des Myokards zu entstehen (2, 10). Elektrogramme mit verzögerter und desorganisierter Erregung konnten in infarziertem Myokard nachgewiesen werden, und es gibt viele Hinweise, daß langsame Leitung durch geschädigtes Gewebe kreisende ventrikuläre Rhythmusstörungen durch Kreiserregung begünstigt (11–14). Diese Arbeit gibt einen Überblick über die Techniken der Signalmittelung des EKG und über die Befunde bei Patienten mit ventrikulären Tachykardien (VT).