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T R Engel

Publications and source records attributed to T R Engel.

At least 19 recordsLinked to original sources
PubMed1991

Reproducibility of the signal-averaged electrocardiogram.

Variation in measurements made from signal-averaged electrocardiograms was examined. Averaging 200 beats in 18 normal subjects, pairs of high-frequency QRS and low-amplitude signal durations correlated at immediate, short-term, and long-term intervals. The percent high-frequency (60 Hz to 120 Hz) voltages in the late potential region had modest correlations. However, 95% confidence intervals of differences in paired measurements were as much as 7% for high-frequency QRS, 20% for a low-amplitude signal, and 53% for percent high-frequency, similar at all time intervals. With electrocardiograms averaged to 0.3 microV noise, high-frequency QRS and low-amplitude signals prolonged, but variation was similar to that of 200 beat pairs. In contrast, low noise reduced percent high-frequency and lessened variation to 29%. Therefore variation in signal-averaged electrocardiographic measurements was considerable (high-frequency voltage greater than durations). Noise did not appreciably influence variation in durations but was critical to consistent voltage measurements in the frequency domain.

Adult↗
PubMed1989

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 less than 40 microV and the root mean square voltage of the last 40 ms. Late potentials were defined as terminal signals greater than 25 Hz that were less than 40 microV. 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 x [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 less than 0.0001) and longer high frequency terminal signals less than 40 microV (p less than 0.0004), but not significantly lower voltage in the last 40 ms. The most useful temporal domain measurement was high frequency QRS duration (if greater than or equal to 120 ms, odds ratio = 8.2). Patients with ventricular tachycardia had increased high frequency spectral areas (p less than 0.0002) in the late potential, and the percent high frequency was especially increased (p = 0.0000; if percent high frequency greater than 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 less than 0.03). All patients with ventricular tachycardia had a high frequency QRS complex greater than or equal to 107 ms or percent high frequency greater than or equal to 3.1% (sensitivity 100%). For a high frequency QRS complex greater than or equal to 107 ms and percent high frequency greater than or equal to 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.

Adult↗
PubMed1988

Signal-averaged electrocardiograms in patients with atrial fibrillation or flutter.

The signal-averaged QRS complex that is prolonged because of low amplitude late potentials predicts ventricular tachycardia. This study investigated if signal-averaged low amplitude atrial potentials predict atrial fibrillation or flutter (AFF). Low amplitude potentials were considered to be high-frequency, high amplitude P (HiFP) duration recorded between 50 and 250 Hz at 1.0 mm/microV amplitude minus unfiltered P (UnFP) duration at 0.1 mm/microV. In nine normals, HiFP averaged 115.6 msec +/- 9.8 SD. HiFP were wider in 26 control patients (133.5 msec +/- 15.7, p less than 0.005) but HiFP-UnFP (11.2 msec +/- 8.5) and signals less than 10 microV terminating HiFP inscription (21.7 msec +/- 23.4) were similar to normal values. Seventeen patients with paroxysmal or recently cardioverted AFF did not have significantly longer intervals than controls (HiFP averaged 138.8 msec +/- 23.0, HiFP-UnFP 13.2 msec +/- 9.3, and signals less than 10 microV 32.4 msec +/- 19.5). Therefore, signal-averaged P waves do not identify patients with AFF.

Adult↗
PubMed1987

Repolarization abnormalities in mitral valve prolapse.

Inferolateral ST depression, T wave inversion, and QT prolongation have been frequently described in reports of largely symptomatic mitral valve prolapse (MVP) patients, but not in a recent population-based survey of mainly asymptomatic subjects with MVP. To learn if there is a relationship between these ECG changes and symptoms, physical findings or hemodynamic sequelae, we reviewed ECGs from 119 patients, ages 18 to 60 years who had MVP diagnosed by echocardiography. Seventy-four percent had symptoms characteristic of MVP. ST-T changes were found as frequently in asymptomatic patients (29%) as in those symptomatic (27%), and did not identify those with hemodynamic sequelae of MVP (apical systolic murmurs, Doppler-defined mitral regurgitation, or left atrial enlargement). QT prolongation was found more frequently in the symptomatic group (25% vs 10%) but did not predict syncope. When compared to the expected 0.9% prevalence of ST abnormalities in a normal population, ST-T changes and QT prolongation are indeed frequent in MVP, but are not useful in identifying clinically important subsets.

Adolescent↗
PubMed1987

Ventricular fibrillation during coronary angiography: the precatheterization QT interval.

Ventricular fibrillation during coronary angiography is associated with contrast-induced changes in repolarization and thus pre-catheterization abnormalities could predispose to this event. We retrospectively examined angiograms, pre-catheterization electrocardiograms and records of 26 consecutive patients who had ventricular fibrillation during coronary angiography, and compared these patients to controls matched for age, sex, and left ventricular function. Diatrizoate meglumine was used as the angiographic contrast agent in all instances. Catheterization findings and the prevalence of prior myocardial infarction were similar in both groups. However, pre-catheterization QT intervals in the ventricular fibrillation group (0.43 +/- 0.05 sec) were significantly longer than in control patients (0.39 +/- 0.04 sec, P less than 0.005) as were their QT intervals corrected for heart rate (QTc) (0.47 +/- 0.04 vs 0.42 +/- 0.03 sec; P less than 0.001). Only seven of the 16 patients (44%) with ventricular fibrillation who had a precatheterization QTc greater than 0.44 sec had the arrhythmia during angiography of a critically stenosed (greater than 75%) coronary artery, whereas VF followed injection of critically stenosed vessels in eight of 10 (80%) of those with a normal QTc (p NS). After a follow-up period of 24 to 54 months (mean 39), two ventricular fibrillation patients have died (one suddenly), as compared to five in the control group (two suddenly) (p NS). Therefore, pre-catheterization QT prolongation was associated with ventricular fibrillation during coronary angiography, but ventricular fibrillation did not necessarily portend a worse long-term prognosis.

Angiography↗
PubMed1986

Pacing-induced angina pectoris and induction of ventricular arrhythmias in coronary artery disease.

Ischemia caused by rapid pacing during electrophysiologic study could facilitate induction of ventricular arrhythmias. The results of extrastimulation were retrospectively analyzed in 32 patients with coronary artery disease (CAD) without a history of symptomatic arrhythmia. These patients were studied at cardiac catheterization for angina pectoris refractory to medical therapy. Eleven patients (group I) had typical angina during trains of rapid right ventricular pacing (repeated trains of 8 stimuli [mean cycle length (CL) 473 +/- 47 ms]) but were asymptomatic during slower trains (CL 800 +/- 100 ms). Twenty-one patients (group II) had no symptoms with either rapid (CL 448 +/- 51 ms) or slow (CL 688 +/- 105 ms) trains, despite comparable left ventricular function, CAD severity and medication. Effective refractory periods (S1S2) after rapid drive were shorter in group I than in group II patients (225 +/- 9 vs 240 +/- 14 ms, p less than 0.002), but refractory periods during slow pacing were similar (251 +/- 12 vs 253 +/- 17 ms, difference not significant). No patient in either group had sustained arrhythmia (more than 15 beats) induced by single and double ventricular extrastimuli, decrementally applied at the right ventricular apex. The number of extra beats provoked in group I when rapid trains caused angina (4.3 +/- 3.6) was similar to that induced by extra-stimulation after slower pacing without angina (4.4 +/- 3.5) and to that obtained with rapid or slow pacing in group II (3.1 +/- 3.3 and 2.8 +/- 2.2).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1985

Effect of site of pacing on dispersion of refractoriness.

The variation in dispersion of ventricular refractoriness with different sites of pacing was measured in 11 patients not taking antiarrhythmic drugs. Dispersion of refractoriness between 3 right ventricular sites was determined at constant paced cycle lengths (S1S1). Refractoriness to ventricular extrastimulation (S2) using atrial pacing vs "clinical" pacing (drive or S1 at the right ventricular apex) vs the conventional measurement of dispersion (S1 at the site of S2) was compared. Effective and functional refractory periods (ERP and FRP) were measured from electrograms at the site of application of S2. Dispersion of ERP was always wider using clinical pacing (65.4 +/- 26 ms [+/- standard deviation]) than atrial pacing or traditional drive (20.4 +/- 14 and 19.1 +/- 10 ms, p less than 0.0001). Similarly, dispersion of FRP was greater with clinical pacing (45.0 +/- 35 vs 21.8 +/- 14 and 17.3 +/- 13, p less than 0.011). In 2 patients with left bundle branch block these differences were most striking. Clinical pacing foreshortened FRP relative to ERP (FRP shorter than ERP by an average 12.5 ms at nonapical sites) but this did not induce tachycardias, perhaps because FRP was still longer than the shortest V1V2 achieved conventionally (FRP was longer at nonapical sites than at the apex using clinical pacing, p less than 0.05). With atrial pacing there is less dispersion of refractoriness than with clinical ventricular pacing, although this difference is not appreciated when dispersion is measured in the conventional manner.

Arrhythmias, Cardiac↗
PubMed1985

Relationship of delayed depolarization to the QT interval after acute myocardial infarction.

The relationship between conduction delay, as manifested by a prolonged QRS or late potentials (LP) detected by signal averaging, and QT prolongation was analyzed in six patients who had QTc greater than or equal to 0.42 second within 48 hours of acute myocardial infarction (AMI). Total QRS, LP, QT, and QTc durations were measured on days 2 to 3, 4 to 5, 6 to 7, and 8-9. In each recording period, the QT interval and QTc interval did not correlate with the QRS duration and LP duration (r less than or equal to 0.52 for each comparison). In 19 out of 27 instances, a sequential change in QT or QTc intervals was discordant with changes in QRS duration and/or LP, i.e., temporal changes in QT intervals were not determined by conduction. Thus, QT prolongation after AMI is not primarily due to regional slowing of conduction that results in regional delays in termination of some action potentials. Global prolongation of repolarization would seem to result from dispersion of action potential duration, not onset.

Action Potentials↗
PubMed1985

Electrophysiologic studies of the ventricle.

Electrophysiologic assessment of ventricular tachyarrhythmias involves the application of paced ectopic beats at the discretion of the cardiologist and not by chance. Because this approach reproducibly induces the sort of symptomatic arrhythmias that are the major cause of death in our country, the procedure has attracted widespread interest. This methodology has accomplished two important alterations in the orientation of physicians to ventricular arrhythmias and sudden death. First, it has turned our focus away from innocent events such as ectopic beats and directed our attention to the architectural and electrophysiologic abnormalities that are the structural substrate for tachyarrhythmias. Second, it has taught us that malignant arrhythmias and sudden death can be treated empirically by repeatedly inducing VT under controlled conditions until a treatment is found. The physiologic and pharmacologic insight obtained with these early experiences will hopefully enable us to treat patients without the need for producing potentially lethal arrhythmias.

Anti-Arrhythmia Agents↗
PubMed1984

Sustained arrhythmias in hypertrophic obstructive cardiomyopathy.

Patients with hypertrophic obstructive cardiomyopathy are subject to syncope and sudden death. Ambulatory monitoring discloses frequent and complex ventricular ectopy in many of these patients, and the occurrence of ventricular tachycardia suggests an increased risk of sudden death. We prospectively evaluated whether induced sustained arrhythmia could explain episodes of cerebral dysfunction in hypertrophic cardiomyopathy. Seven consecutive symptomatic patients (six of whom had an intraventricular gradient of 40 to 130 mm Hg) were subjected to atrial and ventricular stimulation. An electrophysiologic abnormality that would explain the symptoms was identified in every patient: supraventricular tachycardia was present in two, sustained ventricular tachycardia in three, ventricular fibrillation in one, and a prolonged QT interval and dispersion of ventricular refractoriness in one. Antiarrhythmic drugs were selected on the basis of the response to electrophysiologic testing. There has been no recurrence of symptoms in 120 patient-months of follow-up. This experience suggests that arrhythmias are the principal cause of syncope or sudden death in obstructive cardiomyopathy and that electrophysiologic study may be useful in selecting prophylactic therapy.

Adult↗
PubMed1984

ST segment elevation with ventricular aneurysm: results of encircling endocardial ventriculotomy.

The ST segment elevation characteristic of ventricular aneurysm is thought to represent unmodified repolarization of the opposing wall or to arise from viable tissue at the border of the scar because of ischemia, traction or the non-uniform injury that is the architecture for ventricular tachycardia. Encircling endocardial ventriculotomy to prevent tachycardia interrupts coronary perfusion to the viable tissue bordering the scar, with noticeable loss of electrical and mechanical function. Five patients had anterior or apical aneurysms resected and encircled to treat recurrent ventricular tachycardia. ECGs were examined 49 days +/- 12 SEM post-operatively. Encircling did not eliminate their ST segment elevation. Only one patient had less ST elevation post-operatively. Thus ST elevation associated with aneurysms does not arise from viable tissue at the edge of the scar because it persists after this tissue is damaged by encircling endocardial ventriculotomy.

Aged↗
PubMed1984

Late induction of tachycardia in patients with ventricular fibrillation associated with acute myocardial infarction.

A prospective study was made of 57 asymptomatic patients, 1 to 24 months after acute myocardial infarction, 17 with (Group I) and 40 without (Group II) ventricular fibrillation during the acute event. None of the 57 patients had symptomatic arrhythmias, uncontrolled heart failure or unstable angina. There was no significant difference between the two patient groups in time from acute myocardial infarction, medication used or left ventricular ejection fraction. Repetitive forms of arrhythmia (Lown grade 4) were more prevalent (29 versus 16%, not significant) during 24 hour ambulatory monitoring in patients in Group I (ventricular fibrillation group). Programmed extrastimulation was performed using 1 to 3 twice-threshold, 2 ms decremental extrastimuli delivered during right ventricular drive. Of the 17 patients in Group I, 8 had no induced arrhythmia (less than or equal to 4 extra responses), 4 had nonsustained ventricular tachycardia and 5 had sustained ventricular tachycardia (degenerating into ventricular fibrillation requiring electrical reversion in 4). None of the 40 patients in Group II had induced sustained ventricular tachycardia (p less than 0.005), although 9 had nonsustained ventricular tachycardia. Patients with ventricular fibrillation during acute myocardial infarction may have an increased risk for ventricular tachycardia or ventricular fibrillation that may be exposed by programmed electrical stimulation even when not yet clinically manifest.

Adult↗
PubMed1983

Effect of procainamide on dispersion of ventricular refractoriness.

Ventricular arrhythmias after Q-T prolongation by drugs could result from a nonhomogeneous increase in refractoriness (dispersion). Dispersion of effective refractory periods (ERP) was measured before and after infusion of 1 g of procainamide using twice-threshold extrastimuli applied in sinus rhythm and with 500 ms ventricular drive cycle length at 3 right ventricular sites (2 patients) or 2 right and 1 left ventricular site (10 patients). Procainamide prolonged ERP. In drive, average ERP was 247 +/- 5 ms (standard error of the mean) before and 277 +/- 7 ms after procainamide (p less than 0.001). The Q-T interval was prolonged by 50 ms in drive (p less than 0.001), but Q-T prolongation did not reflect the increased ERP (r =-0.05). However, procainamide did not alter measured dispersion (54 +/- 16 to 44 +/- 14 ms in sinus, 48 +/- 14 to 47 +/- 13 ms in drive). Polymorphic ventricular tachycardia (VT) was induced in 6 patients in whom drive itself generally failed to reduce dispersion, and failure to induce tachycardia or shorter runs after procainamide was associated with narrowed dispersion. Polymorphic VT was not induced after procainamide in 2 patients with clinical episodes of torsades de pointes caused by type I agents. The mechanism of torsades de pointes was not explained by dispersion of refractoriness or by polymorphic VT initiated by premature beats after a type I drug.

Aged↗