Independent value of signal-averaged electrocardiography and left ventricular function in identifying patients with sustained ventricular tachycardia with coronary artery disease

To determine if the signal-averaged electrocardiographic detection of late potentials is an independent marker of sustained ventricular tachycardia (VT) in patients with documented chronic coronary artery disease (CAD), 57 patients underwent signal-averaged electrocardiography. Mean ejection fraction was 47 +/- 13% in the 14 patients with sustained VT and 56 +/- 19% in the 43 patients without VT (difference not significant). The sensitivity, specificity and accuracy of late potentials for detecting patients with VT were 64% (9 of 14), 79% (34 of 43), and 75% (43 of 57), respectively. Univariate analysis and stepwise logistic regression of angiographic and electrocardiographic variables identified late potentials as an independent marker of the patient with sustained VT. The odds ratio for late potentials to detect patients with prior sustained VT was 2.6. Six-month follow-up revealed a cardiac mortality rate of 11% and an arrhythmia event rate of 22% in patients with late potentials vs a cardiac mortality rate of 3% and an arrhythmia event rate of 13% in patients without late potentials. Thus, signal-averaged electrocardiographic detection of late potentials is useful in identifying patients with prior sustained VT independent of left ventricular function.     

Nonsustained ventricular tachycardia in patients with coronary artery disease: role of electrophysiologic study

Sixty-two consecutive patients with chronic coronary artery disease referred for evaluation of nonsustained ventricular tachycardia (VT) underwent electrophysiologic studies. Sustained VT was induced by one to three ventricular extrastimuli in 28 patients (45%). Therapy was guided by the results of electrophysiologic testing in 44 patients: 19 patients without inducible sustained VT received no antiarrhythmic therapy, and 25 patients with inducible sustained or symptomatic nonsustained VT received therapy guided by the results of electrophysiologic studies. The results of electrophysiologic studies were ignored by physicians for a second group of 18 patients: four had inducible sustained VT but received no antiarrhythmic therapy, and 14 had inducible sustained or nonsustained VT and received antiarrhythmic therapy not guided by results of electrophysiologic testing. After a mean follow-up period of 28 months, 11 patients had died suddenly. Seven of the 11 patients who died suddenly had inducible sustained VT. Three of 44 patients in the group receiving therapy guided by electrophysiologic studies died suddenly versus eight of 18 in the group receiving therapy not guided by electrophysiologic studies (p = .001). Only one of 19 patients without inducible sustained VT who were not treated experienced sudden death. Two of four patients with inducible sustained VT who did not receive antiarrhythmic therapy died suddenly. Multivariate analysis of the relationship of induced arrhythmias, left ventricular ejection fraction, site of myocardial infarction, history of syncope, or type of antiarrhythmic therapy to outcome revealed a greater than twofold increased risk for sudden cardiac death in patients whose therapy was not guided by results of electrophysiologic study.(ABSTRACT TRUNCATED AT 250 WORDS)     

冠心病持续性室性心动过速患者的Q—T离散度

为评价Q-T_d对冠心病患者发生室性心动过速的预测价值,观察18例冠心病持续性室性心动过速患者和20例对照组的Q-T_d。结果显示持续型室性心动过速组Q_(Td)(104±28ms)明显大于对照组(61±19ms,P<0.01)。表明Q-T_d的增加可作为预测室性心动过速发生的重要指标。     

Efficacy and electrophysiologic effects of oral sotalol in patients with sustained ventricular tachycardia caused by coronary artery disease.

The efficacy of oral sotalol in preventing sustained ventricular tachycardia induction by invasive electrophysiological testing was assessed in 22 patients (60 +/- 9 years) with prior myocardial infarction. Programmed stimulation consisted of two basic drives followed by up to three extrastimuli at two right ventricular sites. At baseline, sustained monomorphic ventricular tachycardia was inducible in all patients. With sotalol (360 +/- 172 mg/day), it was no longer inducible in 10 patients; in 12 others, it remained inducible and its cycle length was only minimally prolonged (322 +/- 42 to 345 +/- 44 msec, p less than 0.05). Sotalol markedly prolonged sinus cycle length, uncorrected QT interval, and right ventricular effective and functional refractory periods, but had little effect on ventricular conduction time either in sinus rhythm or with right ventricular pacing. There was no significant difference in drug dose or in electrophysiologic effect of drug that related to efficacy, nor was there any correlation between drug-induced prolongation of ventricular tachycardia cycle length and its effects. Six patients received oral sotalol over the long term without spontaneous recurrence of ventricular tachycardia (follow-up: 23 +/- 18 months). These results demonstrate that sotalol is effective (45%) against sustained ventricular tachycardia induction at moderate doses and is well tolerated over a long term in the setting of remote myocardial infarction. However, its electrophysiologic effects as measured at invasive testing are not predictive of efficacy against ventricular tachycardia induction.     

Predictors of sustained ventricular tachycardia inducibility in patients with nonsustained ventricular tachycardia and chronic coronary artery disease

To assess the likelihood of inducing sustained ventricular tachycardia, we analyzed a cohort of 58 retrospective and 18 prospective patients with chronic coronary artery disease who underwent electrophysiologic study because of spontaneous nonsustained ventricular tachycardia (three or more beats, lasting less than 30 seconds, at a rate greater than 100/min). In 24 of the 58 retrospective patients (41%) sustained ventricular tachycardia was inducible. Stepwise logistic regression identified two "major" variables--left ventricular aneurysm/dyskinesis/akinesis (p = 0.0001; relative risk = 11.88) and ejection fraction less than 40% (p = 0.0002; relative risk = 9.69)--and one "minor" variable--nonsustained ventricular tachycardia longer than 10 beats (p = 0.0151; relative risk = 4.21)--as significant predictors of inducibility. Nineteen patients with both major variables had a high probability of inducibility (greater than 90%). Nineteen patients with neither major variable had a low probability of inducibility (less than 5%). The remaining 20 patients with only one of the major variables had an intermediate probability of inducibility (14% to 75%). The significance of the third minor factor, nonsustained ventricular tachycardia longer than 10 beats, was confined to this intermediate group, in which it could be used to segregate relatively high (65% to 75%) and relatively low (14% to 20%) probability of inducibility. Prospective application of the predictor function stratified 18 additional patients into three groups with high (six patients), intermediate (seven patients), and low (five patients) probability of inducibility. The observed rate of inducibility in each group was 5 of 6 (83%), 2 of 7 (29%), and 0 of 5 (0%), respectively. These data suggest that patients with nonsustained ventricular tachycardia and chronic coronary artery disease can be stratified into subgroups with high, intermediate, and low probability of inducibility of sustained ventricular tachycardia on the basis of ejection fraction and regional ventricular wall motion defects alone.     

Spectral mapping of the electrocardiogram with Fourier transform for identification of patients with sustained ventricular tachycardia and coronary artery disease

In time domain analysis, detection of late potentials is limited by high pass filtering, noise interference and the necessity to exclude patients with bundle branch block. We therefore used frequency analysis with Fourier transform of multiple segments of the surface electrocardiogram (25 segments, size 80 ms, time shift 3 ms) during sinus rhythm after signal averaging. Thirty-two post-myocardial infarction patients with sustained ventricular tachycardia (VT), 19 post-myocardial infarction patients without VT and 17 healthy subjects were studied. A total of 18 patients had bundle branch block. In 24 out of 32 patients with VT, three-dimensional spectral plots were characterized by spectral peaks greater than 10 dB in the range of 40-200 Hz in segments only at the end of QRS and the early ST wave, but not far outside the QRS. In only 2 out of 19 patients without VT and in 1 out of 17 healthy subjects could such peaks be observed. Noise caused spectral peaks throughout all segments. Sixteen out of 18 patients with bundle branch block were correctly classified with spectral mapping. With the Simson method, patients with bundle branch block had to be excluded, abnormal results were found in 10 out of 19 patients with VT, but also in 5 out of 15 patients without VT and in 3 out of 16 healthy subjects. Thus, spectral mapping of the electrocardiogram offers promise for better identification of patients prone to sustained VT in the presence of coronary artery disease.     

Clinical and electrophysiologic findings in patients with repetitive monomorphic ventricular tachycardia and otherwise normal electrocardiogram

Natural history, structural substrate, electrocardiographic and electrophysiologic characteristics and therapy were evaluated in 18 patients who demonstrated repetitive ventricular tachycardia, defined as repeated episodes of ventricular tachycardia that had a uniform QRS configuration and normal sinus-conducted QRS complexes between the episodes of tachycardia. The patients were young (mean age 37 years) and frequently had a long history of arrhythmia before this evaluation; only two patients had a history of syncope and six were completely asymptomatic. Fourteen patients had no evidence of underlying structural heart disease, three had mitral valve prolapse and one had congestive cardiomyopathy. Episodes of ventricular tachycardia tended to occur in clusters over a 24 hour electrocardiographic recording period.Repetitive ventricular tachycardia was induced in two of nine patients by programmed electrical stimulation, and in seven patients incremental atrial and ventricular pacing suppressed spontaneous arrhythmia. In the one patient whose tachycardia was induced by incremental ventricular pacing there was an inverse relation between pacing cycle length and the interval from the last paced complex to the first complex of ventricular tachycardia, indicating there was overdrive suppression.At a follow-up time of 0.5 to 8 years no patient had died or had worsening of symptoms. Encainide completely eliminated episodes of ventricular tachycardia during acute treatment in five of six patients tested. Seven patients received no antiarrhythmic therapy and the arrhythmia appeared to have spontaneously resolved in four of these patients. Repetitive ventricular tachycardia appears to have distinct clinical and electrophysiologic characteristics. In this series the arrhythmia had a good prognosis and often required no treatment. The electrophysiologic features are consistent with a mechanism of automaticity.     

Prospective comparison of Holter monitoring and electrophysiologic study in patients with coronary artery disease and sustained ventricular tachyarrhythmias

Baseline 24-hour Holter monitoring (HM) and electrophysiologic study (EPS) were compared in 43 consecutive patients with coronary artery disease who had sustained ventricular tachyarrhythmias to determine the fraction of patients in whom each could be performed and the fraction in whom each could be used to guide therapy. Patients were excluded from HM if sustained ventricular tachycardia (VT) requiring termination occurred and from EPS if heart failure was sufficiently severe to cause excessive risk. More patients completed EPS than HM (90% vs 71%), but this difference was not statistically significant (p = 0.12). Overall, HM detected arrhythmias suitable for antiarrhythmic drug assessment in 50% of patients: 30 or more ventricular premature complexes (VPCs) per hour in 50%, 10 or more VPC pairs in 44%, 5 or more runs in 19%, and 10 or more pairs and runs in 44%. Sustained monomorphic VT suitable for electropharmacologic testing was induced at EPS in 82% (p = 0.003 vs HM). Drug efficacy could be assessed in 70% of patients evaluated by HM, compared with 96% evaluated by EPS (p = 0.02). Thus, in consecutive coronary patients with sustained ventricular tachyarrhythmias, EPS could be used to guide therapy more frequently than HM.     

The signal-averaged electrocardiogram in predicting coronary artery disease

The ability to noninvasively detect coronary artery disease (CAD) in patients undergoing diagnostic cardiac catheterization was studied using a signal-averaged electrocardiogram. An initial study of 13 patients revealed that a QRS duration greater than or equal to 100 msec, a root mean square voltage in the terminal 40 msec of the QRS less than 50 microV, and a low amplitude signal (LAS) duration greater than 28 msec were suggestive of CAD. These parameters were then used prospectively to examine 40 consecutive patients with chest pain of undetermined etiology referred for cardiac catheterization. Patients with CAD had significantly longer filtered QRS and LAS durations and lower root mean square voltages compared with patients without CAD. The sensitivity, specificity, and positive predictive value of a single parameter ranged from 62% to 76%, 74% to 89%, and 75% to 87%, respectively. Thus the signal-averaged electrocardiogram may be a useful tool in evaluating patients for the presence of CAD.     

Noise in the signal-averaged electrocardiogram and accuracy for identification of patients with sustained monomorphic ventricular tachycardia after myocardial infarction

Late potentials are detected at various noise levels in clinicalstudies. The aim of this study was, in a case-control design,to assess the effect of residual noise level on the identificationof patients with sustained monomorphic ventncular tachycardiaafter myocardial infarction. Electrocardiograms from 16 patientswith prior myocardial infarction and documented sustained monomorphicventricular tachycardia and 41 patients with prior myocardialinfarction and without ventncular tachycardia, were analysedby two signal averaging procedures to noise level 0·2and 0·4 µV Standard time domain parameters weremeasured. Two definitions of late potential were analysed: (1)if any two of the following criteria were present (signal-averagedQRS duration >120 ms, late potential duration >40 ms,and root-mean-square voltage of the terminal 40 ms of the filteredQRS <25µV); or (2) if the signal-averaged QRS duration120 ms. Overall the signal-averaged electrocardiogram performedbetter at noise level 0·4µV compared to noise level0·2µV with respect to identification of patientswith or without ventricular tachycardia after myocordial infarction.Reducing noise level from 0·4 to 0·2 µVincreased the sensitivity, but the consequence was a substantialdecrease in specificity. Our data indicate that when a highsensitivity is the goal, the definition based only on signal-averagedQRS duration 120 ms should be applied; sensitivity was 88% andspecificity 59% at noise level 0·4 µV. If a highspecificity is the goal, the definition should be based on thedefinition with two abnormal parameters; sensitivity was 69%and specificity 68% at noise level 0·4µV.     

Frequency analysis of signal-averaged electrocardiogram in patients with right ventricular tachycardia.

OBJECTIVES. The purpose of this study was to analyze the frequency content of signal-averaged electrocardiograms (ECGs) in patients with idiopathic ventricular tachycardia of right ventricular origin and in patients with arrhythmogenic right ventricular dysplasia. BACKGROUND. The late potentials in the time domains are usually found in patients with arrhythmogenic right ventricular dysplasia. They are not usually found in patients with idiopathic ventricular tachycardia of right ventricular origin. METHODS. Fast Fourier transform analysis of signal-averaged ECGs was performed with the use of a Blackman-Harris window in 43 subjects: 20 normal volunteers (group I), 12 patients with idiopathic ventricular tachycardia of right ventricular origin (group II) and 11 patients with arrhythmogenic right ventricular dysplasia (group III), and the frequency spectrum was displayed in a three-dimensional graph. Area ratio (ratio of the area under the spectral plot from 40 to 120 Hz to the area from 0 to 120 Hz) was calculated in all subjects. RESULTS. Area ratio was significantly higher in group II than in group I (243 +/- 45 vs. 196 +/- 15, p < 0.01) and significantly higher in group III (396 +/- 51) than in group I or II (p < 0.001). The high frequency components in group II were confined within the QRS complex in the three-dimensional graph, whereas those in group III extended outside the QRS complex. CONCLUSIONS. Frequency analysis of the signal-averaged ECG with fast Fourier transform analysis can detect the high frequency components in patients with right ventricular tachycardia, including idiopathic ventricular tachycardia and arrhythmogenic right ventricular dysplasia.     

Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease

Previous studies in patients with sustained ventricular tachycardia (VT) have demonstrated the efficacy of surgical and catheter-mediated ablative procedures based on activation mapping during VT. Since extensive preoperative or intraoperative mapping may be impractical due to time constraints or patient intolerance, we sought to define characteristics of the 12-lead electrocardiogram (ECG) during VT that could suggest a particular endocardial region of origin and thus facilitate mapping studies. Endocardial mapping was performed during 182 VTs in 108 patients with prior myocardial infarction of either the anterior or inferior wall. Endocardial sites of origin (sites from which greater than or equal to 40 msec of presystolic electrical activity was consistently recorded) were identified with use of catheter (154 VTs) or intraoperative (85 VTs) activation mapping (both methods used in 57 Vts). Twelve-lead ECGs obtained during these VTs were characterized by four features: location of infarction, bundle branch block type configuration, quadrant of QRS axis, and precordial R wave progression pattern. A specific combination of these four features was associated with a particular endocardial region containing the mapped site of origin in 87 VTs (48% of total). An association (greater than or equal to 70% positive predictive accuracy) was more likely to be found in the presence of left, as opposed to right, bundle branch block type patterns (53/73 [73%] vs 34/109 [31%]; p less than .001) and in the presence of VT related to inferior, as opposed to anterior, infarction (40/54 [74%] vs 47/128 [37%]; p less than .001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Flecainide-related alterations in the signal-averaged electrocardiogram: similarity between patients with or without ventricular tachycardia.

The signal-averaged electrocardiogram (SAECG) identifies patients at risk of sustained ventricular tachycardia (VT), but the influence of anti-arrhythmic agents on the SAECG is not yet established. We have evaluated the effects of flecainide on the SAECG (XYZ leads, high-pass filters 25 Hz and 40 Hz, noise level 0.2 microV-0.4 microV, Model 1200 EPX, ART) in 25 patients: 15 (VT group) had documented sustained VT (nine post-MI, two dilated cardiomyopathy, four normal hearts) and 10 (control group) had supraventricular arrhythmias and structurally normal hearts. The SAECG was recorded in all patients prior to, and 5 min following a flecainide infusion (2 mg.kg-1 over 10 min). Before flecainide administration an abnormal SAECG was recorded in six patients from the VT group and in no control patient. Following flecainide, 13 patients from the VT group and eight control subjects demonstrated abnormal SAECG. Flecainide produced similar significant percentage changes in all SAECG indices in both the VT and control groups: total QRS duration was prolonged by 26.0 +/- 10.4% vs 26.7 +/- 15.7%, late potential duration under 40 microV was prolonged by 55.5 +/- 62.0% vs 106.1 +/- 61.4%, and the root mean square voltage of the last 40 ms of the QRS was reduced by 42.1 +/- 34.9% vs 55.3 +/- 24.4%, respectively. We conclude that flecainide significantly changes the SAECG parameters in patients with and without a history of VT, irrespective of the underlying disease.     

信号平均心电图预测冠心病患者心律失常事件的前瞻性研究

目的：评价心室晚电位（ＶＬＰ）预测心律失常事件（ＡＥ）的价值。方法：对２６１例冠心病患者进行２４小时Ｈｏｌｔｅｒ和信号平均心电图（ＳＡ－ＥＣＧ）检测，其中ＡＭＩ患者于发病后２～４周行ＳＡ－ＥＣＧ检测。所有患者均进行临床随访。结果：２６１例冠心病患者中ＶＬＰ阳性率１４９％，随访１３６±６９（４～３６）月，发生ＡＥ１８例。ＶＬＰ阳性组ＡＥ发生率２９７％，明显高于ＶＬＰ阴性组ＡＥ发生率３６％（Ｐ＜００００１）。发生ＡＥ组ＶＬＰ阳性率６１１％，明显高于未发生ＡＥ组ＶＬＰ阳性率１２３％（Ｐ＜０００１）。ＶＬＰ时域分析预测冠心病患者发生ＡＥ的敏感性６１１％、特异性８７７％、阳性预测值２９７％、阴性预测值９６４％、准确性８５６％。结论：ＶＬＰ预测ＡＥ有较高的敏感性、特异性和准确性。ＶＬＰ有助于冠心病（尤其心肌梗死）患者的危险性分层。     

Comparison of frequency and time domain analysis of the signal-averaged electrocardiogram in patients with ventricular tachycardia and coronary artery disease: methodologic validation and clinical relevance

Frequency analysis with fast Fourier transform and time domain analysis after signal averaging of the electrocardiogram (ECG) have given contradictory results in patients with sustained ventricular tachycardia after myocardial infarction. Therefore, the same orthogonal ECGs were analyzed in the frequency domain (Blackman-Harris window) and the time domain after signal averaging and high gain, low noise amplification (0 to 300 Hz) in 30 patients with sustained ventricular tachycardia after myocardial infarction, 15 patients without ventricular tachycardia after infarction and 15 healthy subjects. Patients with bundle branch block were not excluded. Twenty-one of the 30 patients with ventricular tachycardia had late potentials in the time domain and abnormal Fourier transform of the ST segment (defined as increased spectral area of 60 to 120 Hz and spectral peaks greater than 10 dB). Among the remaining nine patients with ventricular tachycardia all had no late potentials in the time domain and one manifested abnormal frequency spectra. In contrast, of the 15 patients without ventricular tachycardia after infarction, 2 had late potentials in the time domain and only 1 demonstrated abnormal frequency spectra; none of the healthy subjects manifested either phenomenon. Patients with bundle branch block were correctly classified by Fourier analysis, but were frequently missed by time domain analysis. Normalization of the spectra and area ratio proved potential pitfalls, and the choice of an appropriate ST segment was crucial: if the segment was long with respect to the duration of the late potentials and if it extended too far into the QRS complex, fast Fourier transform yielded random results.(ABSTRACT TRUNCATED AT 250 WORDS)     

Periodicity of global ventricular activation of sinus beats in patients with coronary artery disease and sustained ventricular tachycardia

Despite increasing clinical reliance on signal-averaged electrocardiograms for determining risk for development of sustained ventricular tachycardia (VT), the periodicity of global ventricular activation during sinus rhythm has not been defined. Accordingly, epicardial and transmural ventricular electrograms during 6 consecutive sinus beats were evaluated in 10 patients with abnormal signal-averaged electrocardiograms who were undergoing surgery for VT. Bipolar electrograms were recorded with sock and needle electrodes from up to 96 epicardial and 156 transmural sites. Electrogram morphology, duration and activation were compared on a beat-to-beat basis. In all, 9,816 electrograms were analyzed. Mean durations of epicardial and transmural electrograms were 33 +/- 16 ms (range 6 to 199) and 23 +/- 10 ms (range 6 to 72), respectively, with a beat-to-beat variation of 1.9 +/- 1.4 ms per site. Similarly, local activation times did not vary significantly during the 6 cardiac cycles analyzed (mean variation 1.7 +/- 2.0 ms). Local conduction failure was not observed. Although electrograms during the terminal 40 ms of the QRS were significantly longer (36 +/- 20 vs 26 +/- 12 ms, p less than 0.001) when compared with those recorded earlier during the QRS complex, beat-to-beat variation in duration (2.1 +/- 1.6 ms) and activation (1.7 +/- 2.3 ms) was not significant. Results demonstrate that epicardial and transmural electrograms recorded during sinus rhythm in patients with sustained VT are periodic signals and thus establish a physiologic basis for signal averaging of electrocardiographic waveforms in these patients.     

Correlation between signal-averaged electrocardiogram and programmed stimulation in patients with and without spontaneous ventricular tachyarrhythmias

This study examined the incidence of delayed ventricular activation on signal-averaged electrocardiograms and the incidence of inducible sustained ventricular tachycardia (VT) at programmed stimulation (1 or 2 extrastimuli) in patients with and patients without spontaneous ventricular tachyarrhythmias. The correlation between delayed ventricular activation and inducible VT was investigated in 371 patients with acute myocardial infarction (AMI). In 32 patients with no ventricular disease and no spontaneous arrhythmias (group I), ventricular activation time averaged 115 +/- 2 ms, compared with 166 +/- 3 ms (p less than 0.001) for 65 patients with spontaneous ventricular tachyarrhythmias late after AMI (group II). In AMI patients with no spontaneous arrhythmias, ventricular activation time averaged 133 +/- 2 ms for 306 patients studied 1 to 4 weeks after AMI (group III) and 130 +/- 2 ms for 67 patients studied 3 to 12 months after AMI (group IV). The values for group III and group IV patients were each significantly higher than for group I (p less than 0.001), but lower than that for group II (p less than 0.001). The incidence of delayed ventricular activation was 89% for group II, 26% for group III and 18% for group IV. Sustained VT was not inducible in group I patients, but was inducible in 78% of group II (p less than 0.001 vs group I) and 20% of group III (p less than 0.05 vs group I; p less than 0.001 vs group II) (group IV was not studied).(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of atrial pacing on the signal-averaged electrocardiogram in patients with coronary artery disease

The effects of atrial pacing on the signal-averaged electrocardiogram were studied in 14 patients with remote myocardial infarction and a history of cardiac arrest or sustained ventricular tachycardia (group I) and in 13 patients with coronary artery disease and no history of sustained ventricular tachyarrhythmia (group II). Recordings of the signal-averaged electrocardiogram were obtained at control and during atrial pacing at rates of 80, 100, and 120 beats/min. All patients had recordings analyzed from at least two paced rates. At control, the mean high frequency total duration of the QRS complex (HFTD) was significantly longer in group I versus group II patients (123 +/- 5.6 versus 111 +/- 3.5 msec, p less than 0.05). Although the duration of the QRS signal under 40 microV (D40) was higher in group I versus group II patients (42 +/- 4.7 versus 32.4 +/- 3.5 msec) and the root mean square amplitude of the terminal 40 msec QRS (RMSA) was lower in the group I patients (27 +/- 7.5 versus 38.1 +/- 8.8 microV), these differences did not achieve statistical significance. There was no effect of atrial pacing on the measured signal-averaged parameters of HFTD, D40, and RMSA. Although there was a difference between group I and group II at each paced rate analyzed, atrial pacing did not help to further stratify the groups. In patients with coronary artery disease, atrial pacing is not a useful method of stratifying high-risk patients. Changes in serial signal-averaged electrocardiograms from the same patient are not due to heart rate variability.     

Effects of exercise on the signal-averaged electrocardiogram in coronary artery disease

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.     

Cryoablation of refractory sustained ventricular tachycardia due to coronary artery disease

Thirty-nine patients with medically refractory sustained monomorphic ventricular tachycardia (VT) due to coronary artery disease underwent map-guided cryosurgery. Locations of prior myocardial infarctions had been inferior in 22, anterior in 16 and combined in 1. Mean age was 61 +/- 9 years and the mean number of drug trials per patient before surgery was 3.8 +/- 1.4. Intraoperative endocardial mapping induced 67 tachycardias in 35 patients. Each patient received 6 to 18 (11 +/- 3) endocardial cryothermic applications (15 mm, -60 degrees C, 2 minutes) at areas of earliest activation during VT. Encircling endocardial cryoablation was performed in 4 patients who had unsuccessful mapping. In addition, 11 patients had subendocardial resection of their well-demarcated septal scars as well as cryosurgery. There were 2 in-hospital deaths. At postoperative programmed ventricular stimulation, 28 of the 37 patients (76%) had no inducible or spontaneous VT before hospital discharge. Six patients (16%) with spontaneous or inducible VT had a single morphology and were controlled with antiarrhythmic drugs that had previously failed. Therefore, surgery alone or in combination with drugs was efficacious in 92% of the population surviving surgery. The remaining 3 patients (8%) received automatic implantable cardioverter defibrillators. No significant difference in surgical outcome was seen between patients who had cryosurgery alone and those who had subendocardial resection together with cryoablation. Mean left ventricular ejection fractions before and after surgery were 33 and 39%, respectively (p less than 0.01). Clinical follow-up ranged from 2 to 36 months (18 +/- 12). One patient died of heart failure and another underwent heart transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)