Determinants of the Natural Course of Ventricular Late Potentials After Thrombolytic Therapy for Acute Myocardial Infarction

The intraindividual changes of ventricular late potentials and their possible determinants were examined prospectively in 88 consecutive patients (male: 75; mean age: 58 ± 9 years) after thrombolytic therapy for acute myocardial infarction. Late potential analysis was performed 4 weeks and 12 months after acute myocardial infarction. At the same time, a left heart catheterization was performed to assess the extent of coronary heart disease and left ventricular ejection fraction. The incidence of late potential 4 weeks after acute myocardial infarction was 15% (13/88 patients). Eighteen percent (16/88) of the patients revealed changing results of late potential analysis: 9 patients lost late potential (late potential pos./neg.) 1 year after acute myocardial infarction and 7 patients presented new formation of late potential (late potential neg./pos.). Preserved late potentials were found in four patients (late potential pos./pos.). Late potential analysis remained negative in 68 patients (late potential neg./neg.). There was no influence of age, gender, site of infarction, clinical course, and medical treatment on the natural course of late potential. Changing results of late potential analysis seemed to be correlated with the evolution of left ventricular ejection fraction and the dynamics of coronary heart disease. In the group late potential pos./pos., comparable values for left ventricular ejection fraction were measured at both examinations, whereas late potential neg./neg. had a significant increase in ejection fraction. In the group late potential pos./neg., a significant improvement in left ventricular function was also measured. In contrast, the late potential neg./pos. group tended to have lower left ventricular ejection fractions 1 year after infarction. In the late potential neg./pos. and late potential pos./pos. groups, the extent of coronary artery disease returned to conditions comparable to baseline despite an initial reduction after coronary revascularization performed 4 weeks after infarction. Late potential neg./neg. and late potential pos./neg. revealed a stable benefit gained from coronary revascularization with a persistent reduction in the number of diseased vessels. Dynamic changes in the results of the signal-averaged ECG 1 year after thrombolytic therapy for acute myocardial infarction were observed in 18% of the patients. These changes seem to be correlated with the evolution of left ventricular function and the dynamics of coronary artery disease.     

A Critical Appraisal of Quantitative Spectro-Temporal Analysis of the Signal-Averaged ECG: Predicting Arrhythmic Events After Myocardial Infarction

The objective of this study was to determine if spectra-temporal analysis of the signal-averaged ECG (SAECG) predicts spontaneous sustained ventricular tachyarrhythmias and sudden death in patients prospectively followed after myocardial infarction (MI). A SAECG was recorded in 177 patients 9 ± 5 days after MI. Spectro-temporal analysis of the SAECG involved incrementing a Hanning window every 3 ms beginning 20 ms before the end of the QRS complex and extending into the ST segment. Quantitative analysis was performed using a cross-correlation function to create a normality factor. A normality factor < 0.3 was deemed abnormal. The SAECG was abnormal in 41 % of patients using time-domain analysis and 44% of patients using spectra-temporal analysis. There was no correlation between an abnormal SAECG in the time domain and the frequency domain. Patients with inferior wall MI were more likely to have an abnormal spectra-temporal map (odds ratio 2.26, P < 0.05). Time-domain analysis of the SAECG (relative risk (RE) 2.6) was a statistically significant univariate predictor of arrhythmic events. Spectra-temporal analysis of the SAECG was only weakly (RR 1.8) and not significantly (P = 0.15) associated with the spontaneous occurrence of these arrhythmias. When both time-domain analysis and spectra-temporal analysis of the SAECG were abnormal, the relative risk for an arrhythmic event was increased by 3.3-fold. Quantitative spectra-temporal analysis of high frequency signals within the SAECG cannot by itself predict the occurrence of spontaneous ventricular arrhythmias in patients after MI.     

Prognostic Implications of Loss of Late Potentials Following Acute Myocardial Infarction

The prognosis of patients following myocardial infarction is adversely affected by the finding of late potentials at the time of hospital discharge. Loss of late potentials has been previously reported during seriai testing during the first year after infarction, but it is not known whether such patients remain at risk of arrhythmic events. This study prospectively followed 243 patients after myocardial infarction. Late potentials were observed in 92 patients (group 1) at the time of hospital discharge. Of these patients, 23 no longer had late potentials at G-week follow-up and 8 had had an arrhythmic event (sudden death or ventricular tachycardia). In patients with loss of late potentials, overall QRS duration had decreased from 109 ± 11 msec at discharge to 104 ± 11 msec (P < 0.01), terminal QRS voltage rose from 15 ± 4 μV to 31 ± 9 μV (P = 0.001), and late potential duration fell from 42 ± 6 msec to 28 ± 6 msec (P = 0.001) at the 6-week study. Predictors of loss of late potentials were: initial duration of the QRS duration (P < 0.001) and terminal voltage (P < 0.005); non-Q wave infarction (P < 0.001); and being a male (P < 0.05). After the 6-week assessment, 11 additional arrhythmic events occurred during median follow-up of31 months. The risk of arrhythmic events was similar in patients with loss of late potentials and those who retained late potentials in group I (9% vs 11%, P - NS) but significantly greater than palients with no late potentials at discharge (group II, 2%). Of those patients with events beyond 6 weeks, a normal signal-averaged ECG (either lost late potentials or group II) was observed in 6/11 (55%) patients on at least one occasion prior to the occurrence of the event. Hence, a significant number of arrhythmic events occurring ≥ 6 weeks after myocardial infarction occur in palients with a normal signal-averaged ECG even when late potentials are initially present. “Loss’ of late potentials does not necessarily confer an improved prognosis in terms of risk of arrhythmic events.     

Electrophysiological Basis of Ventricular Late Potentials

EL-SHERIF, N., ET AL.: Electrophysiological Basis of Ventricular Late Potentials. The presence of late potentials on the body surface recording was correlated with ventricular activation maps of reentrant circuits in the postinfarction canine model of reentrant excitation. Late potentials were found to correlate with delayed myocardial activation. However, during a reentrant rhythm complete diastolic activity on the body surface could not be detected if the mass of electrically active cells was too small and/or if very slow conduction in part of the reentrant circuit generated low amplitude extracellular potentials. Myocardial zones responsible for late potentials during a basic rhythm (e.g., sinus rhythm) may not necessarily be part of the critical zone of slow conduction during reentrant activation. Dynamic changes in late potentials are not amenable to temporal signal averaging techniques but could be detected by a high resolution beat-to-beat recording. A thorough understanding of the electrophysiological limitations of late potentials in the signal-averaged ECG could result in better utilization of the technique in clinical practice as well as in the development of new approaches for the detection of the arrhythmogenic substrate.     

Arrhythmic risk stratification after myocardial infarction using ambulatory electrocardiography signal averaging

Ambulatory ECG had been proposed to examine the amplified high resolution signal-averaged electrocardiogram (SAECG). Clinical investigations are required to confirm the predictive value of such a high resolution technique in arrhythmic risk stratification. The prognostic value of ambulatory Holter SAECG was evaluated in 108 postinfarction patients for the purpose of predicting the occurrence of serious arrhythmic (SARR) events (sudden cardiac death [SCD], VT, or VF) in comparison with classical real-time SAECG. During the 42+/-8 months of follow-up, the sudden cardiac death mortality was 4.6% (five deaths), six (5.6%) patients had VT, and one (0.9%) VF. QRSd was found to be the most predictive parameter using ROC curves analysis for SAAR + outcome (W = 0.833 and W = 0.803 for 25-250 Hz and 40-250 Hz filters, respectively) followed by RMS (W = 0.766 and W = 0.721) and LAS (W = 0.759, W = 0.709) (all P < 0.01). Abnormal Holter SAECG for 25 and 40-Hz LP filter were significant predictors of SARR+ by log-rank test (P < 0.01, P < 0.05, respectively). This study confirms that valuable prognostic information can be obtained from the ambulatory high resolution ECG technique and that Holter SAECG may predict arrhythmic risk in a postinfarction population.     

"Peudo" Late Potentials Unmasked by Spectrocardiography

We present a patient with chronic obstructive pulmonary disease and sustained ventricular tachycardia in the setting of unstable coronary artery disease. Signal-averaged ECG (SAECG), inadvertently performed during an atrial tachycardia with 2:1 atrioventricular (AV) block, was abnormal by time-domain analysis, but was normal by a relatively new frequency analysis technique of the entire QRS (spectocardiography). The patient was noninducible for sustained ventricular arrhythmias. Following cardioversion to sinus rhythm. SAECG was normal by time-domain analysis and Spectrocardiography. This technique may show promise in the management of patients who are at risk for sustained ventricular arrhythmias, particularly those who cannot be evaluated by time-domain analysis.     

Which Factors Determine the Development of Late Potentials After First Myocardial Infarction? A Multifactorial Analysis

A multifactorial analysis was performed to study the factors that contributed to the occurrence of late potentials on the signal-averaged electrocardiogram in 106 consecutive patients with a first myocardial infarction. Ninety-three (88%) patients received intravenous thrombolytic therapy within 6 hours of symptom onset. Thirty-two (30%) patients had a late potential on the signal-averaged electrocardiogram on day 6, including 17 of 31 (55%) in whom the infarct-related artery was occluded and 15 of 75 (20%) in whom it was patent (P = 0.0004). Twenty-three variables were analyzed by a multifactorial stepwise regression analysis. Predictors of a late potential were (1) an occluded infarct-related coronary artery (t = -3.653, P = 0.0004) and (2) the extent of myocardial necrosis as indicated by the peak serum lactate dehydrogenase level (t = 3.094, P = 0.0025). The lower incidence of late potentials when the infarct-related coronary artery was patent was independent of left ventricular election fraction and peak enzyme levels after infarction.     

Prediction of Arrhythmia Risk Based on Signal-Averaged ECG in Postinfarction Patients

In patients surviving acute MI, identification of those at high risk for life-threatening ventricular tachyarrhythmias and/or sudden death is of great importance. Numerous strategies based on indices such as the degree of left ventricular dysfunction, complex ventricular arrhythmias, or parameters of autonomic dysfunction have not yet led to an effective identification of the individual patient at risk. During the past decade, many investigators have recorded low amplitude, high frequency components in the terminal QRS complex (so-called late potentials) from patients prone to sustained ventricular tachycardia. The SAECG has been used to predict life-threatening tachyarrhythmias in patients after acute MI and to screen for inducible ventricular tachycardia in patients with unexplained syncope or sustained ventricular tachycardia. This review article describes the most frequently applied methodology and clinical applications of the SAECG in post-MI patients and discusses the usefulness of noninvasive recordings in various other clinical settings.     

Spectrotemporal Mapping of High-Resolution ECGs in Experimental Myocardial Infarction: Comparison with Time-Domain Analysis and Epicardial Electrograms

The study was undertaken to evaluate the relationship of signal-averaged ECG (SA-ECG) readings in the frequency domain (STM) and epicardial electrograms (EE) recorded before and after acute myocardial infarction (AMI) in pigs and to compare the changes with findings in time-domain analysis (TDA). In 20 pigs the left anterior descending artery (LAD) was ligated. Prior to ligation, a SA-ECG was recorded (method of Simson) and bipolar electrodes were used to register EE in the areas supplied by the LAD and the circumflex artery (CIRC). Five minutes after LAD ligation, all measurements were repeated. Time-domain parameters were QRS duration (QRS D) and the duration of the signal below 30 microV (LAS 30). Beginning at a point of 20 ms before the QRS end, the frequency spectra (0-200 Hz) of 25 segments of 80-ms duration at the QRS end were analyzed. The volumes below the 25 curves were analyzed separately for 0-50 Hz, 51-100 Hz, 101-150 Hz, and 151-200 Hz. After AMI, five pigs died within 7 minutes. In 15 pigs, QRS D as well as LAS 30 lengthened significantly (P<0.05; P<0.001). Spectrotemporal mapping (STM) showed a significant decrease of the frequencies above 50 Hz (51-200 Hz) in the entire group and in the animals with late potentials (P<0.05). EE of the LAD area were significantly prolonged (P<0.01); this did not correlate with the changes in STM parameters. In pigs acute myocardial infarction causes a shift towards lower frequencies in the STM which most likely reflects the slowed depolarisation in the ischemic area.     

Evolution of Late Potentials During the First 8 Hours of Myocardial Infarction Treated with Thrombolysis

It has been demonstrated that successful thrombolytic therapy is associated with a reduction of late potentials in the signal-averaged electrocardiogram (SAECG) recorded within 48 hours after hospital admission. This study extends these observations, using for the first time a longitudinal design investigating whether ischemia and its potential reversal by thrombolytic therapy are associated with dynamic changes in SAECG recordings obtained continuously for 8 hours after the start of therapy in patients with acute myocardial infarction (MI). SAECGs were obtained from 12 patients (2 women and 10 men; ages 63 ± 13 years) with acute MI. The SAECG (X²+ Y²+ Z²)^1/2 was generated with a high pass filter of 40 Hz, noise ≤ 0.3 μV. Comparing the SAECG recordings during the first and eighth hours, there was a significant decrease in filtered QRS duration (fQRS; 119.5 ± 17.1 vs 106.3 ± 15.3 ms) and duration of the low amplitude signals ≤ 40 μV of the terminal QRS (LAS40; 48.8 ± 18 vs 34.2 ± 14.2 ms), and increase of root mean square voltage of the last 40 ms of the QRS (t-RMS; 14.8 ± 9.3 vs 37.8 ± 34.4 μV) (rank test, P ≤ 0.05). In this patient series, there was a significant improvement of fQRS, t-RMS, and LAS40 during the first 8 hours of acute MI, perhaps indicating reversal of ischemia with thrombolysis. Even during acute MI, these markers of delayed conduction allow investigation of intervention induced changes in myocardial conduction and possibly prediction of the patency of the infarct related artery using signal-averaging techniques.     

Signal-Averaged ECG Prior to and Serially After Thrombolytic Therapy for Acute Myocardial Infarction

Signal averaging has been performed to evaluate late potentials following infarction and the administration of thrombolytic therapy. Most studies have recorded signal-averaged electrocardiograms (SAECGs) at least 12 hours after the onset of the infarction. In this study, SAECGs were recorded before thrombolytic therapy and serially over 7–10 days following infarction in 21 patients. The high frequency QRS duration was significantly shortened at 1 and 24 hours compared to presentation (96.8 ± 11.3 ms and 93.4 ± 8.0 ms vs 103.3 ± 14.3 ms, respectively, P < 0.05) and there was an increase in the terminal voltage over time, significant at 1 hour and 3 days (57.3 ± 29.1 μV and 58.6 ± 44.7 μV vs 44.4 ± 35.5 μV, respectively, P < 0.01). Five patients met criteria for ventricular late potentials on at least one SAECG. The prevalence of late potentials was higher in patients with Q wave infarctions, or with occluded infarct related arteries. These changes in myocardial activation may be related to ischemia and reperfusion, and may not correlate with the development of a fixed substrate for reentry.     

Frequency and Significance of Left and Right Ventricular Late Potentials after Myocardial Infarction in Man

Left and right heart catheterization was conducted on 45 patients with a history of myocardial infarction in order to detect so-called ventricular late potentials by means of endocardiac mapping. The endocardiac signals were amplified 100 to 10,000 times at a low noise level using bipolar electrode catheters. The signals were stored unfiltered and visualized directly on an oscilloscope. Consistently recurring late potentials were recorded after QHS complexes in 32 patients (71%). They ranged in amplitude from 50 to 780 μV, while the coupling intervals were measured in the range of 80 to 620 ms from the beginning of the QRS complex to the beginning of the late potential. In some patients, the intracardially registered and/or Holter-monitored ventricular ectopic beats occurred with a delay, corresponding to the delayed occurrence of the ventricular late potentials.     

The Effect of Age on the Electrophysiological and Autonomic Correlates of Sudden Death After Acute Myocardial Infarction

To examine the influence of age on the autonomic and electrophysiological correlates of sudden death after myocardial infarction, 223 patients aged <60 and 195 patients aged ≥60 were followed up for a mean of 790 days. The patients had Holter monitoring and a signal-averaged EGG 5–11 days after infarction. A mean ventricular ectopic beat frequency >10 beats/ hour (VE10) was present in 17.0% of young versus 28.2% of old patients (P < 0.01); a low heart heart variability index in 17.9% of young but in 32.3% of old patients (P < 0.001) and late potentials in 17.5% but 32% of young and old patients, respectively (P < 0.01). There was no difference in the incidence of sudden death between young and old patients (3.6% vs 3.1%). However, sudden death accounted for 50%, compared with 24% of all deaths in the young and old groups, respectively (P < 0.01). Sudden death was more closely associated with low heart rate variability and VE10 in the young than in the older group. The predictive values of a heart rate variability index <20 units with VE10 in younger patients were a sensitivity of 50%, a positive predictive accuracy (PPA) of 33% and risk ratio (RR) of 18 (P < 0.001); these values did not reach significance in older patients (16.7%, 4.3% and 1.4%, respectively.) Late potentials had a sensitivity of 50%, a PPA of 12.1%, and an RR of 4.7 in young patients (P < 0.05): the corresponding values in the older group were 80%, 8.9, and 8.4 (P < 0.02). It is concluded that sudden death is a more predominant mode of death and is more strongly associated with lower heart rate variability and with the VE10 incidence in young than in older postinfarction patients. Age should be taken into account when assessing the risk of sudden death after myocardial infarction.     

急性心肌梗死首诊误诊26例临床分析

目的:探讨基层医院急性心肌梗死(AMI)误诊原因及防范对策,以提高对AMI的认识和诊治水平。方法:回顾性分析2010年6月-2014年6月我院门急诊首诊误诊的26例AMI患者的临床资料。结果:误诊为呼吸系统疾病9例,其他心血管疾病8例,消化道疾病6例,泌尿系结石肾绞痛、颈椎病、肩周炎各1例;5例在门急诊发生猝死。结论:AMI的临床表现复杂多样,容易误诊,加强对AMI的认识,规范诊疗过程,可提高其诊治水平,降低误诊率及死亡率。     

ST Reelevation at Reperfusion is Associated with the Occurrence of Late Potentials in Patients with Acute Anterior Infarction

The relationship between ST reelevation at reperfusion and the occurrence of late potentials (LPS) in 35 patients with a first anterior infarction who had single vessel disease was investigated. All patients underwent a successful primary angioplastv and had a patent infarct related artery confirmed angiographically 4 weeks later. Patients were classified into groups based on changes in the ST level at reperfusion: patients with ST reelevation (group A, n = 22) and patients without ST reelevation (group B, n = 13). Signal-averaged ECG was performed 4 weeks after primary angioplasty to detect LPS. Cineventriculography was performed to measure left ventricular ejection fraction (LVEF) and evaluate regional wall motion of the infarct area (SD/chords). LPS were present in eight of the 22 group A patients (36%) and in none of the 13 group B patients (P < 0.05). Left ventricular function was impaired in patients in group A compared with patients in group B (LVEF: 51 ± 12 vs 63 ± 10, P < 0.01; SD/chords: −2.7 ± 0.9 vs −1.9 ± 1.1, P < 0.05). These data suggest that ST reelevation and myocardial damage at reperfusion are associated with the occurrence of LPS in patients with successfully recanalized infarct related arteries after acute anterior infarction.     

Prolonged QRS duration increases QT dispersion but does not relate to arrhythmias in survivors of acute myocardial infarction

QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2-3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%-15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 +/- 7 vs 78 +/- 1 ms, JT disp 80 +/- 6 vs 79 +/- 2 ms, mean +/- SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction.     

Late Potentials in a Porcine Model of Anterior Wall Myocardial Infarction and Their Relation to Inducible Ventricular Tachycardia

In this study, normal values for signal averaged electrocardiographic parameters were assessed in healthy pigs (n = 100) and the development of late potentials after myocardial infarction (n - 41) in relation to inducible ventricular tachycardia was investigated. Normal values are: filtered QHS duration (QRS) ± 78 msec; root mean square voltage of the averaged QRS complex (V_tot) ± 51 μV, and duration of terminal activity below 30 μV (D₃₀) ± 37 msec. The distribution of the root mean square voitage in the last 30 msec (V₃₀) was biphasic. Two weeks after myocardial infarction, QRS was prolonged from 55 ± 10 to 66 ± 19 msec (P < 0.002), D₃₀ was prolonged from 19 ± 6 msec to 28 ± 13 (P < 0.002). V₃₀ was decreased from 107 ± 135 μV to 45 ± 77 (P < 0.02). The total voltage (V_tot) was decreased from 195 ± 78 to 123 ± 61 μV (P < 0.002). In four pigs (19%) late potentials developed. Sustained ventricular tachycardia was inducible in 11 pigs (52%), ventricular fibrillation in two pigs (10%) and eight pigs (38%) were noninducible. Three of 11 inducible pigs and one of the noninducible pigs had a late potential. The incidence of late potentials and their relation to inducibie sustained ventricular tachycardia is comparable to the situation in man. Therefore, this pig model is an attractive alternative to the commonly used dog models.     

Heart Rate Variability Used as an Arrhythmia Risk Stratifier After Myocardial Infarction

Heart rate variability (HRV) is considered to represent a noninvasive tool to assess cardiac autonomic tone at the level of the sinus node. It has been shown to have predictive power for risk assessment in patients surviving acute myocardial infarction. For this purpose, HRV should be assessed from 24-hour Holter recordings obtained 7–10 days following the infarction. Although there is some recovery of HRV during the first 3 months after infarction, HRV remains reduced in postinfarction patients compared to values obtained in healthy individuals. Compared to assessment of left ventricular function as a risk marker, HRV is superior with respect to prediction of arrhythmic events and sudden death whereas both parameters yield comparative power for prediction of total cardiac mortality. Since the predictive power of HRV analysis alone is relatively low, the combined use of HRV measurements together with traditional risk markers (such as ventricular ectopic beats, signal-averaged ECG, or left ventricular function) results in improved risk prediction with positive predictive accuracy in the range of 30%–50%.     

QT离散度及心室晚电位对心肌梗塞急性期室性心律失常的预测价值

目的：研究QT离菜度（QTd)及心室晚电位（VLP）对心肌梗塞急性期室性心律失常的预测价值。方法：计算48例急性心肌梗塞患QTd,其中34例行VLP检测。结果：12例严重室性心律失常组QTd,校正的QT离散度（QTcd)明显延长,VLP阳性率明显高于无室性心律失常组（P＜0．01）,结论：QTd和VLP检测对心肌梗塞急性期发生室性心律失常有较高预测价值。