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This investigation was performed to evaluate the feasibility of detecting repolarization alternans with the heart rate elevated with a bicycle exercise protocol. Sensitive spectral signal-processing techniques are able to detect beat-to-beat alternation of the amplitude of the T wave, which is not visible on standard electrocardiogram. Previous animal and human investigations using atrial or ventricular pacing have demonstrated that T-wave alternans is a marker of vulnerability to ventricular arrhythmias. Using a spectral analysis technique incorporating noise reduction signal-processing software, we evaluated electrical alternans at rest and with the heart rate elevated during a bicycle exercise protocol. In this study we defined optimal criteria for electrical alternans to separate patients from those without inducible arrhythmias. Alternans and signal-averaged electrocardiographic results were compared with the results of vulnerability to ventricular arrhythmias as defined by induction of sustained ventricular tachycardia or fibrillation at electrophysiologic evaluation. In 27 patients alternans recorded at rest and with exercise had a sensitivity of 89%, specificity of 75%, and overall clinical accuracy of 80% (p <0.003). In this patient population the signal-averaged electrocardiogram was not a significant predictor of arrhythmia vulnerability. This is the first study to report that repolarization alternans can be detected with heart rate elevated with a bicycle exercise protocol. Alternans measured using this technique is an accurate predictor of arrhythmia inducibility. [ABSTRACT FROM AUTHOR]

We report 2 cases of exudative left pleural effusion following radiofrequency catheter ablation of cardiac arrhythmias complicated by cardiac perforation. We suggest that radiofrequency ablation may be a previously unsuspected cause of postcardiac injury syndrome. [ABSTRACT FROM AUTHOR]

Thrombolytic therapy and angioplasty during the early phase of an acute myocardial infarction (AMI) have been shown to improve prognosis. Time-domain analysis of the signal-averaged electrocardiogram (SAECG) provides strong, independent prediction of arrhythmic events (arrhythmic death/resuscitated cardiac arrest) after AMI. To determine whether the prognostic significance of an abnormal SAECG (QRS duration > or = 120 ms) measured after AMI is influenced by thrombolytic therapy/angioplasty given in the AMI period, the predictive value of SAECG was compared in patients with and without prior thrombolysis/angioplasty in a substudy of the Cardiac Arrhythmia Suppression Trial. Information was available in 787 patients. The average follow-up was 10 +/- 3 months and arrhythmic events occurred in 33 patients (4.2%). The prevalence of abnormal SAECG in patients with and without thrombolytic therapy/angioplasty was 9.4% (34 of 363 patients) and 14.9% (63 of 424 patients), respectively (p < 0.02). The arrhythmic event rate for patients with abnormal SAECG with and without thrombolytic therapy/angioplasty was 20.6% (7 of 34 patients) and 20.6% (13 of 63 patients), respectively. The arrhythmic event rate for patients with normal SAECG with and without thrombolytic therapy/angioplasty was 0.9% (3 of 329 patients) and 2.8% (10 of 361 patients), respectively. It is concluded that in patients with an AMI (1) the use of thrombolytic therapy/angioplasty is associated with a significantly decreased prevalence of abnormal SAECG, (2) thrombolytic therapy/angioplasty associated with a normal SAECG portends an excellent prognosis, and (3) an abnormal SAECG is predictive of an increased incidence of arrhythmic events in all patients regardless of prior thrombolytic therapy/angioplasty.(ABSTRACT TRUNCATED AT 250 WORDS)

The value of time-domain and spectral turbulence analyses of the signal-averaged electrocardiogram (SAECG) for predicting induction of sustained monomorphic ventricular tachycardia (VT) was prospectively investigated in 70 patients with idiopathic dilated cardiomyopathy. Sustained VT was induced in 9 patients (13%). The prevalence of abnormal time-domain and spectral analyses was 16 and 37%, respectively. The total predictive accuracy of time-domain and spectral analyses for VT induction was 86 and 67%, respectively (p < 0.01). The predictive accuracy of time-domain and spectral analysis was similar in patients without an intraventricular conduction defect (94 and 84%, respectively). However, the predictive accuracy of time-domain was higher than that of spectral analysis in patients with an intraventricular conduction defect (65 vs 25%; p < 0.05). The poor concordance between spectral analysis and programmed stimulation results was mainly due to the high number of false-positive recordings in the presence of an intraventricular conduction defect (9 of 20 cases). With the use of stepwise discriminant function analysis, an abnormal time-domain SAECG was the only variable predicting the induction of sustained VT (p < 0.0003). In dilated cardiomyopathy, an abnormal time-domain SAECG and induced sustained VT are rare, both time-domain signal-averaged electrocardiography and spectral analysis have a high predictive accuracy for VT induction in patients without an intraventricular conduction defect, and spectral analysis does not improve VT prediction in those with a conduction defect.

Programmed premature stimulation and burst pacing were compared for initiation of ventricular tachycardia (VT) in 16 patients with inducible sustained monomorphic VT. In all patients VT could be induced by programmed stimulation with 2 or 3 extrastimuli. On the other hand, initiation of VT by burst pacing was dependent on the length of the train; only 2 to 4 of the 11 trains tested could induce VT in any single patient. Recordings obtained from the slow zone of reentry showed that programmed premature stimulation that induced VT resulted in a critical degree of conduction delay as revealed by lengthening of local fractionated electrograms spanning 70 to 100% of the diastolic interval. Similarly, the last beat of a burst pacing train that induced VT was always followed by a similar degree of local conduction delay, whereas trains that failed to induce VT were followed by a lesser delay. It is concluded that although programmed stimulation with up to 3 extrastimuli was consistently successful in inducing VT, burst pacing succeeded in only 26% of the trials and was dependent on the length of the train, which varied from one patient to the other. Similar to what was shown previously in the experimental model of reentrant VT, burst pacing could initiate, conceal, terminate, and reinitiate reentry depending on the length of the train.

This study was designed to assess the accuracy of a new noninvasive frequency analysis method for predicting patients with inducible sustained monomorphic ventricular tachycardia (VT) at electrophysiologic study and hence the risk of spontaneous ventricular tachyarrhythmias. Signal-averaged electrocardiograms from 3 orthogonal bipolar surface leads were evaluated using a microcomputer-based frequency analysis system that performs analysis of conventional time-domain late potentials as well as incorporating a new technique for spectral analysis of relatively short, overlapping signal segments spanning the whole QRS complex. The spectral analysis technique measured abnormalities anywhere in the entire QRS complex and did so without dependence on any arbitrarily defined frequency, duration or amplitude cutoffs. The hallmark of arrhythmogenic abnormality was hypothesized to be frequent and abrupt changes in the frequency signature of the QRS wave front velocity as it propagates throughout the ventricle around areas of abnormal conduction, resulting in a high degree of spectral turbulence. One-hundred forty-two subjects were studied, including 71 totally normal control subjects ("true negatives"), 33 with both late potentials by time-domain analysis and inducible sustained monomorphic VT ("true positives"), 28 with late potentials but no evidence of spontaneous or inducible sustained monomorphic VT ("false positives") and 10 with inducible sustained monomorphic VT but absence of time-domain late potentials ("false negatives"). The frequency analysis technique correctly classified 100% of the true negatives, 97% of the true positives, 86% of the late potentials false positives and 60% of the late potentials false negatives. The total predictive accuracy of frequency analysis for all groups was 94%, compared with 73% for time-domain late potential analysis. The results suggest that a high degree of spectral turbulence of the overall QRS signal during sinus rhythm may provide a more accurate marker for the anatomic-electrophysiologic substrate of reentrant tachyarrhythmias than detection of late potentials in the terminal QRS region by either time- or frequency-domain analysis. Spectral turbulence analysis is applicable to patients irrespective of the QRS duration and the presence or absence of bundle branch block.

The effects of transient myocardial ischemia on the signal-averaged electrocardiogram were investigated in 13 patients with coronary artery disease and spontaneous angina undergoing 3-channel ambulatory electrocardiography. Ischemia was seen as ST elevation in 2 patients or ST depression in 11; it was anterior in 5 patients, inferior in 4 and undefined in 4. Signal-averaged electrocardiograms with noise levels less than or equal to 1 microV were obtained from Holter tapes during 54 of 61 ischemic attacks recorded in the study group (88%), and compared with 54 tracings recorded within 60 minutes of the index attacks. Baseline tracings were normal in 8 patients (62%), showed a long QRS duration in 2 (15%), and both a long QRS duration and a late potential in the remaining 3 (23%). Comparison of recordings at baseline and during ischemic attacks revealed no significant changes in signal-averaged electrocardiographic parameters. Absence of significant differences was also noted when analysis was performed according to the type of ischemic attacks (associated with ST elevation [n = 14] or ST depression [n = 40]), their location (anterior [n = 21] or inferior [n = 23]), their duration (greater than 10 minutes [n = 29] or less than or equal to 10 minutes [n = 25]), and their magnitude (greater than 2 mm [n = 18] or less than or equal to 2 mm [n = 36]). It is concluded that spontaneous transient myocardial ischemia, independent of its type, location, duration and magnitude, does not generate a substrate for late potentials on the signal-averaged electrocardiogram.

The effects of exercise on the signal-averaged electrocardiogram (SAECG) were investigated in 52 patients with stable coronary artery disease. The SAECG was recorded before and immediately after the exercise test and analyzed at 25 to 250 Hz and 40 to 250 Hz. All patients had SAECG with noise level less than or equal 0.8 microV at 25 Hz and less than or equal to 0.6 microV at 40 Hz and with the difference in noise level between control SAECGs and SAECGs after exercise less than or equal to 0.2 to 0.3 microV. Twenty-eight patients developed ST changes consistent with transient subendocardial ischemia that persisted during the SAECG recording after exercise. There was no significant difference between control SAECGs and SAECGs after exercise in patients with or without a positive exercise test. The absence of significant change on the SAECG was not related to the presence or absence of prior myocardial infarction, site of infarction, development of exercise-induced ventricular arrhythmias or presence of an abnormal recording at baseline. These data suggest that exercise-induced electrophysiologic changes and ventricular arrhythmias may not be related to the anatomic-electrophysiologic substrate that underlies late potentials on the SAECG.

To study the effects of digitalis on the sinus node and the mechanisms involved, 16 patients with the sick sinus syndrome had electrophysiologic assessment of sinus nodal function during (1) control study, (2) after pharmacologic autonomic blockade with propranolol (0.2 mg/kg body weight and atropine sulfate 0.04 mg/kg intravenously), and (3) 10 minutes after 0.01 mg/kg of intravenous ouabain. The study was completed within 30 minutes of pharmacologic autonomic blockade. During the control study 50 percent of patients had an abnormal corrected sinus nodal recovery time or abnormal sinoatrial conduction time, or both. The effects of ouabain on sinus nodal function were compared with those after pharmacologic autonomic blockade. Ouabain significantly increased both intrinsic sinus cycle length (ouabain 975 +/- 194 ms [mean +/- standard deviation]; autonomic blockade 1,025 +/- 218 ms, probability [p] less than 0.001) and corrected sinus nodal recovery time (ouabain 615 +/- 503 ms; autonomic blockade 575 +/- 536 ms, p less than 0.05). In contrast there was no significant change in sinoatrial conduction time after ouabain (ouabain 141 +/- 56 ms; autonomic blockade 132 +/- 45 ms; difference not significant). The effects of ouabain were similar in patients with both normal and abnormal sinus nodal function. These findings suggest that (1) digitalis in therapeutic doses has a depressant effect on intrinsic sinus nodal automaticity in patients with normal as well as abnormal sinus nodal function; (2) digitalis has no significant effects on sinoatrial conduction; and (3) the effects of digitalis on sinus nodal automaticity are primary and independent of its vagal and antiadrenergic effects.

The electrophysiologic effects of propafenone were studied by conventional microelectrode techniques in ischemic myocardial and Purkinje fibers from 1-day-old myocardial infarction in the dog. Propafenone reduced the amplitude and rate of rise of normal myocardial and Purkinje action potentials and had little effect on the resting potential. In the control state, both ischemic myocardial and Purkinje fibers had reduced resting potential, action potential amplitude and upstroke velocity. These fibers were more susceptible to the depressant effects of propafenone than normal fibers. Ischemic myocardial fibers were particularly sensitive to the actions of propafenone that resulted in marked depression of action potential characteristics, with little effect on resting potential. These changes resulted in cycle length-dependent conduction disorders in ischemic epicardial preparations. However, in ischemic endocardial preparations in which triggered activity could be initiated, propafenone reversibly suppressed the triggered activity. Termination of the triggered activity was preceded by slowing of the rate, which was attributed to a decrease in the rate of rise of the delayed afterdepolarizations. This activity terminated when the delayed afterdepolarization failed to attain threshold potential. This study suggests that propafenone has a membrane-anesthetic effect, with the abnormal fast channel in ischemic cells being more sensitive; propafenone depresses delayed afterdepolarizations in ischemic Purkinje fibers; and the actions of propafenone could result in an antiarrhythmic effect in vivo on both reentrant ventricular rhythms in ischemic myocardium and triggered rhythms in ischemic Purkinje fibers.

Triggered activity arising from a delayed afterdepolarization occurs in canine subendocardial Purkinje fibers 1 day after myocardial infarction (MI). Standard microelectrode techniques were used to study small preparations (20 to 48 mm2) in vitro. Nifedipine, 1 mg/liter, reversibly suppressed triggered activity by reducing maximum diastolic potential, action potential amplitude and the rate of depolarization of the delayed afterdepolarization. Complete quiescence or exit block resulted. The effects of nifedipine were antagonized by elevating extracellular calcium ion concentration. These results suggest that spontaneous ectopic rhythms 1 day after MI that are the result of triggered activity are dependent on transmembrane calcium ion movement, which nifedipine can directly antagonize.

Studies were conducted in 45 patients to determine whether the reliability of the measurement of the His bundle potential from the body surface was increased by signal averaging of three simultaneously recorded electrocardiographic potentials from horizontal (X), frontal (Y) and sagittial (Z) axes as opposed to recording of any of these. Potentials from the X, Y and Z leads were amplified by 250,000, filtered between 80 hertz (12 dB/octave) and 200 hertz (24 dB/octave) and signal averaging of 1,000 beats was performed. The His bundle potential could be clearly defined in 25 of the 45 patients in the X, Y, or Z lead. His bundle potentials were evident in the X lead in 17 (68 percent) of these 25 patients, in the Y lead in 19 (77 percent) and in the Z lead in 11 (44 percent). No single lead gave satisfactory His bundle electrographic potentials in all patients. In 20 patients the His bundle electrogram could not be recorded because terminal atrial activity overlapped activity of the His bundle potential. The three lead system defined the His bundle potential in a significantly greater number of patients than did the best single lead because it (1) displayed the vectorial lead with the largest His bundle potential, (2) permitted validation of the His bundle potential in more than one lead, and (3) displayed the vectorial lead with the most isoelectric terminal P wave. It is concluded that reliable His bundle potential measurements are obtained in a significantly greater number of patients with use of the simultaneous three lead system than with use of any single lead.

A microcomputer-based system capable of performing time- and frequency-domain analysis on the same set of acquired and signal-averaged raw data was used to correlate late potentials detected in the time domain with the results of frequency-domain analysis. Ten patients with spontaneous or inducible sustained ventricular tachycardia (VT) known to have abnormal late potentials in the time-domain signal-averaged electrocardiogram and 10 normal subjects without late potentials were studied. Fast Fourier transform analysis was performed on a segment that comprised the last 40 ms of the QRS and the ST segment up to the onset of the T wave as identified visually. The high-frequency signal content, expressed as the area ratio or the peak magnitude, was found to be markedly dependent on the length of the analyzed QRS-ST segment. A change of as little as 3 ms in the duration of the estimated QRS-ST segment changed the results of the frequency analysis across proposed boundaries of normalcy in normal subjects and in patients with VT. This resulted in both false-negative and false-positive conclusions. Similar results were obtained when the effects of varying analyzed signal length or phase were studied using a pure synthesized sine wave signal. For frequency analysis to be clinically useful and reproducible, standards of normalcy must be established for a signal region of fixed duration or the technique must be modified so as to be insensitive to duration of signal sample.

Twenty dogs were studied 3 to 9 days after myocardial infarction. None had ventricular arrhythmias during sinus rhythm, and ventricular automaticity (as revealed by sinus nodal crush procedure or vagal stimulation, or both) was within the normal range. With regular atrial pacing or pacing with long-short cycle sequences it was possible to induce ventricular arrhythmias in all animals. Quadrigeminal and pentageminal rhythms (19 of 20 dogs) and trigeminal (17 of 20) and bigeminal ventricular rhythms (8 of 20) were observed. These rhythms which were manifest or partially or entirely concealed were always associated with delayed and fractionated electrical activity within the "infarcted" subepicardium. Continuous electrical activity (electrical activity that bridged the interval between two or more successive beats) was recorded from the infarct zone. Such activity either was manifest as ventricular arrhythmia during atrial pacing or remained concealed until atrial pacing was stopped and then was manifest as ventricular tachycardia.

An in vivo and in vitro correlative study of second degree atrioventricular (A-V) block in the canine proximal His-Purkinje system after ligation of the anterior septal artery is reported. Evidence is presented to suggest that Mobitz type II and the Wenckebach ypte of conduction represent different degrees of the same disorder rather than two distinct electrophysiologic processes. The in vivo study showed that an increment of conduction delay almost always preceded the blocked impulse in second degree A-V block. The increment, as 1 or 2 msec at the early stage of block, often increased gradually up to 180 msec. The in vitro study consistently showed an increment of conduction delay preceding the blocked impulse. The same experiments revealed a greater increment in conduction delay early after excision that, on recovery during superfusion, gradually decreased to a few milliseconds (the reverse order of the in vivo observation). Characteristic changes in duration and configuration of action potentials in the ischemic proximal His-Purkinje system were observed depending on the state of transmission and the temporal relation of the impaled cell to areas of slow propagation and block. The study revealed a remarkable similarity between characteristics of conduction in the ischemic His-Purkinje system and conduction in both the normal A-V doe and Purkinje fibers subjected to various pathophysiologic interventions. It is suggested that in the pathologic situation--exemplified in this study by acute myocardial ischemia--the normal His-Purkinje system may gradually lose the characteristics of the fast response and start showing properties of the slow response. At an early stage of departure from normal, the proximal His-Purkinje system may show second degree A-V block with no perceptible to a few milliseconds' increment of conduction delay (the equivalent of Mobitz type II block). On further departure from normal, the His-Purkinje system resembles the A-V node in showing a significant increment of conduction delay prior to the blocked impulse (the equivalent of Wenckebach periodicity). Both the in vivo and in vitro observations demonstrated a clear propensity of the ischemic proximal His-Purkinje system to develop paroxysmal A-V block during the stage of second degree A-V block when there is no perceptible to a few milliseconds' increment of conduction delay. A new classification of second degree A-V block is presented based on the suggested electrophysiologic mechanism.

A prospective assessment of several clinical variables, left ventricular function indexes, Holter recording characteristics and signal-averaged electrocardiogram (ECG) for their value in predicting the inducibility of sustained ventricular tachyarrhythmias was carried out in a consecutive series of 105 patients with nonsustained ventricular tachycardia (VT). The patients were divided into 3 groups based on the results of programmed electrical stimulation: group 1, 22 patients with induced sustained monomorphic VT; group 2, 14 patients with induced ventricular fibrillation (VF) and group 3, 69 patients with no induced sustained VT/VF. Left ventricular ejection fraction less than 0.40, history of syncope/presyncope and abnormal signal-averaged ECG were significantly more common in group 1 than in group 3. No significant difference was found between groups 2 and 3. The sensitivity, specificity and predictive accuracy of the signal-averaged ECG for the induction of sustained monomorphic VT were 64, 89 and 84%, respectively. Using stepwise discriminant function analysis, the signal-averaged ECG was found to be the single most accurate screening test to predict the inducibility of sustained VT in patients with nonsustained VT and its value was independent of the etiology of heart disease and the length of spontaneous runs. Because of the very high specificity and negative predictive accuracy, patients with normal signal-averaged ECGs may not require invasive evaluation.

To evaluate the effects of isoproterenol and atropine on patients with poor ventriculoatrial (VA) conduction, 17 patients were studied who did not have 1-to-1 VA conduction during ventricular pacing at a rate slightly faster than sinus rate (group I) and 11 patients were studied who had 1-to-1 VA conduction, but only at constant ventricular pacing cycle lengths longer than 600 ms (group II). Isoproterenol infusion at a rate causing a 20 to 30% increase in sinus rate or up to 4 micrograms/min shortened the ventricular pacing cycle lengths that induced VA block in all group II patients. Atropine administration at a dose causing a 20 to 30% increase in sinus rate or up to a total dose of 2 mg also shortened the ventricular pacing cycle lengths that induced VA block in all group II patients. At similar pacing cycle lengths, isoproterenol and atropine induced shorter VA intervals than control. Nine of 17 group I patients had demonstrable 1-to-1 VA conduction either during isoproterenol infusion or after atropine administration. Of these 9 patients, 1-to-1 VA conduction could be found only during isoproterenol infusion in 3 patients and only after atropine administration in 4 patients. The improvement of VA conduction by these drugs was related to their effects on the atrioventricular node. The change in VA conduction mediated by autonomic changes induced by these drugs may explain why some patients without demonstrable VA conduction during rest may have, under certain circumstances, "endless-loop" tachycardia or paroxysmal supraventricular tachycardia using atrioventricular nodal conduction as the retrograde limb.(ABSTRACT TRUNCATED AT 250 WORDS)

Normal values for the signal-averaged electrocardiogram (SAECG) at 11 different high-pass filter settings were obtained from 100 normal subjects (group I). The filtered QRS duration and the duration of low amplitude signals less than 40 microV, but not the root mean square voltage of the last 40 ms (RMS40), showed normal distribution. A normal distribution for RMS40 could be obtained by transforming each value to its natural logarithm. The normal values were used in a systematic approach to optimize the accuracy of the SAECG to predict the results of programmed stimulation in 80 patients with spontaneous nonsustained ventricular tachycardia (VT). Fifty-two patients with no inducible VT (group II) and 28 patients with inducible sustained monomorphic VT (group III) were investigated. The 3 SAECG parameters at each high-pass filter in groups II and III were categorized as normal or abnormal and were evaluated singly or in combinations of 2 or 3. There was no combination that provided a sensitivity greater than 82% that could also be obtained by single determinations of low amplitude signals less than 40 microV at 25 to 40 Hz or RMS40 at 40 Hz. On the other hand, there were 267 different combinations that provided a maximal specificity of 98%. The best total predictive accuracy of a single parameter was 85%, provided by RMS40 at 40 or 60 Hz. The total predictive accuracy could be improved to 89% by 1 of 32 different combinations. The top combinations were mostly in triplets and included SAECG parameters recorded at different high-pass filter settings. The only 2 paired combinations with the best total predictive accuracy were RMS40 at 20 or 25 Hz paired with RMS40 at 40 Hz. Frequencies at both ends of the analyzed high-pass filter settings (less than 20 Hz and greater than 60 Hz) were not represented in the top predictive combinations. The SAECG parameters analyzed at 40 Hz were most frequently represented in the top predictive combinations, suggesting that the SAECG may have the best predictive accuracy at this filter setting. In summary, the combination of SAECG parameters analyzed at different filter settings can enhance the accuracy of the technique as a screening test for the results of programmed stimulation in patients with spontaneous nonsustained VT.

Unlabelled: Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anteriograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway., In Conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, oine for anterograde and the other for retrograde conduction.