Abnormal signal-averaged electrocardiograms in patients with incomplete right bundle-branch block

Background and hypothesis: A hypothesis was formulated that regional delayed activation of the right ventricle, as seen in incomplete right bundle-branch (IRBBB) aberrancy, may simulate late potential activity and may be responsible for abnormal signal-averaged electrocardiograms (SAECGs). No previous studies have specifically addressed this issue in this particular group of patients (with IRBBB). Therefore, the aim of the present study was to investigate the incidence of abnormal SAECGs in patients with IRBBB. If this were confirmed, our purpose would further be to investigate ways of reducing the false positive results. Methods: The study group included 53 patients (28 men and 25 women), aged 53 ± 13 years, with no history of previous myocardial infarction or ventricular tachycardia and who had an electrocardiogram (ECG) showing IRBBB. An SAECG was also performed in a control group of 19 age-matched individuals with a normal ECG. Time domain analysis was performed using a band pass filter of 40–250 Hz. The following parameters were considered normal: filtered QRS duration (QRSD) < 114 ms, root mean square of the voltage of the last 40 ms of the QRS complex (RMS) > 20 μV, and the duration of the low amplitude signal (< 40 μV) at the terminal portion of the QRS (LAS) < 38 ms. An SAECG was considered abnormal if any two of these criteria were abnormal. Results: The mean values of the SAECG parameters were: QRSD 101 ± 11 ms, RMS 32 ± 20 μV, LAS 32 ± 12 ms, and noise 0.29 ± 0.13 μV. Abnormal SAECGs with at least two criteria satisfied were present in 16 of 53 (30%) patients compared with 0 (0%) of 19 individuals in the control group (p = 0.02). Abnormal values included the combination of RMS and LAS in 12 patients and all three parameters in 4 patients. However, if the definition of late potentials were limited to the combination of abnormal QRSD and either RMS or LAS values, the incidence of false positive results (4 patients) (7.5%) would be significantly decreased (p = 0.007). At 21 months of follow-up, no arrhythmic events occurred. Conclusions: Delayed terminal conduction observed in IRBBB may cause a high incidence of false positive late potentials on SAECGs. Based on this study, we propose that this can be largely remedied if the optimal criteria for the presence of late potentials in patients with IRBBB always include the combination of QRSD and either RMS or LAS.     

Effects of early captopril therapy after myocardial infarction on the incidence of late potentials

Background: Late potentials (LP) on signal‐averaged electrocardiography (SAECG), recorded 6 to 30 days after an acute myocardial infarction (AMI), identify patients at risk for late arrhythmic events. Angiotensin‐converting enzyme (ACE) inhibitors have been shown to reduce ventricular remodeling and cardiovascular mortality after AMI. Hypothesis: The aim of this study was to investigate the effect of early (< 24 h) administration of captopril on the presence of LP on Days 6–30 after AMI. Methods: The study included 117 patients with a first AMI; 63 patients (53 men and 10 women, aged 59±12 years), 35 with an anterior and 28 with an inferior AMI (44 thrombolyzed), received early captopril therapy. The control group consisted of 54 age‐matched patients (39 men and 15 women, aged 60 ± 12 years), 19 with an anterior and 35 with an inferior AMI (31 thrombolyzed, p = NS), who did not receive early therapy with an ACE inhibitor. The mean left ventricular ejection fraction was similar in both groups (48 vs. 46%). Time domain analysis of SAECG was performed using a band‐pass filter of 40–250 Hz. Late potentials were considered present if any two of three criteria were met: (1) Filtered QRS duration (QRSD) > 114 ms, (2) root‐mean‐square voltage of the last 40 ms of the QRS complex (RMS) > 20 m?V, and (3) duration of low amplitude (< 40 m?V) signal of the terminal portion of the QRS (LAS) > 38 ms. Results: In the two groups of patients there were no differences in mean values of SAECG parameters. No patient was receiving any antiarrhythmic drugs. In the captopril group LPs were present in 9 of 63 patients (14%) and in the control group in 17 of 54 patients (31 %) (p =0.046). There was no difference in the number of patients with a patent infarct‐related artery in the two groups (76 vs. 59%). Conclusion: Captopril treatment early after an AMI reduces the incidence of LPs recorded on Days 6–30 and may thus favorably affect the arrhythmogenic substrate.     

Initial depolarizing potentials in wolff-parkinson-white syndrome using signal-averaged electrocardiograms: Correlation with reciprocating tachycardia

Initial depolarizing potentials were examined in patients with Wolff-Parkinson-White (WPW) syndrome using signal-averaging techniques. In all, 25 WPW patients and 21 agematched healthy children were studied. Ten of the patients were symptomatic and 15 were asymptomatic. Symptomatic patients with supraventricular tachycardias had longer durations of lowamplitude signals (LAS) < 40 μ V in the initial portion of the QRS complex (initial LAS, 49 ± 7 ms vs. 37 ± 9 ms, p < 0.01) and lower root-mean-square (RMS) voltage in the initial 40 ms of the QRS complex (initial RMS, 12 ± 4 μ V vs. 23 ± 8 μ V, p < 0.01) compared with asymptomatic patients. When a symptomatic patient was defined as having an initial LAS of > 46 ms or an initial RMS of < 15 μ V, the sensitivity and specificity for predicting documented supraventricular tachycardia were 100 and 67%, respectively. These SA-ECG findings may reflect instability of conduction in symptomatic patients through an accessory pathway and may identify those at high risk for supraventricular tachycardia.     

Prevalence of Spectral Turbulence and Late Potentials in a Random Population Sample

Background: Late potentials (LP) and spectral turbulence (STU) in the signal‐averaged ECG (SAECG) in patients with heart disease mark a risk of malignant ventricular arrhythmias. The prevalence and cause of STU in otherwise healthy subjects have not been established. Methods: The SAECGs of a randomly selected population sample without known heart disease, 55 men and 66 women aged 50 ± 10 years, were analyzed for LP and STU. An STU score > 1 qualified for an echocardiographic examination (echo) and a 24‐hour Holter ECG (Holter). Results: The QRS duration in lead V₂ in men was 99.5 ± 8.5 ms (mean ± SD) vs 94.2 ± 8.5 in women, P = 0.0008. The QT end was 406.7 ± 27.0 ms in women and 394 ± 24 in men, P = 0.01. The FQRSD (40 Hz) was 98.0 ± 8.6 ms in men vs 90.2 ± 9.0 in women, P = 0.0001. Subjects > 50 years of age had a lower RMS40 (33.0 ± 16.3 μV) than subjects < 50 years (40.2 ± 18.3 μV, P = 0.02). Nine (7%) subjects were LP‐positive. The STU score variables LSCR, ISCM, ISCSD and SE were positive in 12 (10%), 13 (11 %), 41 (34%) and 17 (14%) of the subjects, respectively. The mean spectral score was 0.69 ± 0.98. Eight (7%) subjects had a score of 3 or 4, considered STU‐positive. No correlation between score and gender, age or 12‐lead QRS duration was found. In score > 1, 27 (84%) had a completely normal ECHO and 31 (86%) a normal Holter. Cardiac dimensions measured by ECHO correlated with SAECG variables. Conclusions: Men had a longer mean QRS duration than women. Women had longer mean QT and JT intervals than men, which might imply an increased risk during antiarrhythmic therapy. The STU variables were not gender‐ or age‐dependent. The variable ISCSD was positive in as many as 41 (34%) presumably healthy subjects and did not seem to be a useful variable. Seven percent of the subjects were spectral turbulence‐positive and 7% were LP‐positive. A.N.E. 2000;5(1):30–38     

New sex dependent normal limits of the signal averaged electrocardiogram.

BACKGROUND--An earlier study of 1555 normal 12 lead electrocardiograms has shown that the mean QRS duration in men is 8 ms longer than in women. OBJECTIVE--To establish the sex related normal limits of the signal averaged electrocardiogram. PEOPLE--195 people (160 men and 35 women aged 40 to 69) with normal clinical history, physical examination, 12 lead electrocardiogram, and echocardiogram were recruited for this study. METHODS--Signal averaged electrocardiograms were recorded by the Arrhythmia Research Technology 1200 EPX machine and analysed twice with bidirectional Butterworth filters with frequency ranges of 25-250 Hz and 40-250 Hz. Three time domain parameters of the QRS vector magnitude, namely filtered total QRS duration, duration of low amplitude signals under 40 microV (LAS40), and root mean square voltage of the last 40 ms (RMS40), were evaluated. RESULTS--There were significant differences between the two sexes in QRS duration (mean (95% confidence interval (95% CI) (8.0 (3.1 to 13.0) ms, t = 3.29, degrees of freedom = 41, p = 0.0021 with the 25-250Hz filter; mean (95% CI) 10.2 (6.9 to 13.5) ms, t = 6.26, degrees of freedom = 53, p < 0.0001 with the 40-250Hz filter)) and in body surface area (mean (95% CI) 0.26 (0.21 to 0.31) m2, t = 10.63, degrees of freedom = 57). There was no significant correlation between age and QRS duration, LAS40, or RMS40, but there was a highly significant correlation between body surface area and QRS duration (correlation coefficient = 0.396, p < 0.0005) and RMS40 (correlation coefficient = -0.159, p < 0.025). Current sex independent criteria defining ventricular late potentials as the presence of any two of QRS duration > 114 ms, LAS40 > 38 ms, RMS40 < 20 microV, give a specificity of 85% for men and 91% for women in this normal population. RECOMMENDATIONS--Ventricular late potentials should be regarded as present when (a) QRS duration exceeds 114 ms in men or 104 ms in women and (b) either LAS40 > 38 ms or RMS40 < 20 microV. This gives a specificity of 97% in men and 100% in women in the population studied.     

Spectral and bidirectional filters give different results for signal-averaged ECG analysis in patients with postmyocardial infarction. GISSI-3 Arrhythmias Substudy Investigators

This study aims at assessing the specific effects of bidirectional filters (BF) and spectral filters (SF) on signal-averaged ECG (SAECG) analysis. The GISSI-3 Arrhythmias Substudy collected SAECGs of 598 patients 10 +/- 4 days after myocardial infarction (MI) from 20 Italian coronary care units. BF and SF were applied on 340 and 258 patients, respectively. QRS duration (QRSD), low amplitude signal duration (LAS40), and root mean-square-voltage (RMS40) were measured with filters set at 40 to 250 Hz. For ventricular late potentials (VLP) detection filter-specific criteria were adopted: QRSD > 114 ms, LAS40 > 38 ms, RMS40 < 20 microV for BF and QRSD > 120 ms, LAS40 > 38 ms, RMS40 < 20 microV for SF. VLP were considered present if any 2 of the criteria were met. The QRSD obtained by BF (100.6 +/- 13 ms) was shorter (P < .0001) than that obtained by SF (109.1 +/- 12 ms). Nevertheless, a higher prevalence of VLP for patients with BF than for patients with SF was found (23.8% vs 16.7%; P < .04). Indeed, filter-specific criteria were able to avoid any differences in the prevalence of abnormal QRSD and LAS40, but not of RMS40 (25.6% vs 17.1%, P < .02). Finally, the difference of VLP prevalence was mainly owing to the higher number of abnormal pairs of RMS40 + LAS40 (58% vs 44%) for BF than for SF. This multicentric study suggests that after MI, BF and SF produce discordant results on low-amplitude signals of filtered QRS that are not avoided by adopting filter-specific criteria. On the contrary, specific criteria seem to be suitable for comparison of QRSD between different SAECG devices in post-MI patients.     

Effect of pre-infarction angina on ventricular late potentials in patients with acute myocardial infarction and successful thrombolysis

OBJECTIVE: Pre-infarction angina is considered as a good clinical model of ischaemic preconditioning which facilitates myocardial protection. Late potentials (LP) have prognostic significance following acute myocardial infarction (AMI). It is also well established that thrombolytic therapy reduces the incidence of LP. Our aim was to evaluate the relationship between pre-infarction angina and LP in patients receiving successful thrombolytic therapy. METHODS AND RESULTS: We prospectively studied 55 patients presenting with AMI (<6 hours). All patients received thrombolytic therapy and were evaluated with coronary angiography at predischarge. Signal-averaged recordings (SAECG) were obtained serially prior to thrombolysis, 48 hours after and 10 days later. Pre-infarction angina was present in 14 (25%) patients. There were no significant differences between the clinical characteristics and angiographic findings of the groups. Baseline SAECG parameters of the groups were also similar. After thrombolysis, the 48th hour values of LAS (the duration of the terminal low amplitude signals), and both the 10th day values of LAS and RMS (root mean square voltage of the last 40 ms of the QRS) were significantly better in the pre-infarction angina group. The mean filtered QRS duration and RMS 40 values changed significantly at the 10th day recordings of patients with pre-infarction angina [QRS duration, 110+/-34 ms before to 91+/-11 ms after (p = 0.039); RMS 40, 40+/-17 microV before to 50+/-14 microV after (p = 0.02)]. The incidence of LP significantly decreased after thrombolytic therapy in the pre-infarction angina group, however, this change was not observed in patients without angina. CONCLUSION: Presence of pre-infarction angina reduces the incidence of LP following thrombolysis in AMI. This might be explained by the possible beneficial effect of ischaemic preconditioning on the arrhythmogenic substrate.     

Prediction of the Recurrence of Atrial Fibrillation After Successful Cardioversion with P Wave Signal‐Averaged ECG

Background: The recurrence of atrial fibrillation (AF) was often observed after cardioversion. Methods: In our study, a P wave triggered P wave signal‐averaged ECG (P‐SAECG) was performed on 118 consecutive patients 1 day after successful electrical cardioversion in order to evaluate the utility of this method to predict AF after cardioversion. We measured the filtered P wave duration (FPD) and the root mean square voltage of the last 20 ms of the P wave (RMS 20). Results: During a 1‐year follow‐up, a recurrence was observed in 57 patients (48%). Patients with recurrence of AF had a larger left atrial size (41.9 ± 4.0 vs 39.3 ± 3.1 mm, P < 0.0003), a longer FPD (139.6 ± 16.0 vs 118.2 ± 14.1 ms, P < 0.0001), and a lower RMS 20 (2.57 ± 0.77 vs 3.90 ± 0.99 μV, P < 0.0001). A cutoff point (COP) of FPD ≥126 ms and RMS 20 ≤3.1 μV could predict AF with a specificity of 77%, a sensitivity of 72%, a positive value of 75%, a negative predictive value of 75%, and an accuracy of 75%. A stepwise logistic regression analysis of variables identified COP (odds ratio 9.97; 95% CI, 4.10–24.24, P < 0.0001) as an independent predictor for recurrence. Conclusions: We conclude that the probability of recurrence of AF after cardioversion could be predicted by P‐SAECG. This method seems to be appropriate to demonstrate a delayed atrial conduction that might be a possible risk factor of reinitiation of AF.     

Absence of change of signal-averaged electrocardiogram identifies patients with ventricular arrhythmias who are non-responders to amiodarone

OBJECTIVES: The aim of this study was to assess the ability of a non-invasive study, the signal-averaged ECG (SAECG), to predict the effect of amiodarone at ventricular level. BACKGROUND: Amiodarone is the main drug drug used in the treatment of ventricular arrhythmias. Standard ECG does not detect any change in QRS complex resulting from amiodarone therapy. SAECG is more sensitive than ECG for detecting changes in QRS complex. METHODS: The study examined the effects of amiodarone on SAECG in relation to the results of programmed ventricular stimulation in 68 patients with old myocardial infarction, spontaneous and inducible sustained ventricular tachycardia (VT). RESULTS: Amiodarone prolonged the total QRS duration (dur) (129+/-28 vs. 140+/-30 ms, P<0.05) and low amplitude signal (LAS) dur (45+/-20 vs. 51+/-20 ms, P<0.1), whereas the root-mean-square voltage of the last 40 ms of QRS complex (RMS 40) was significantly reduced (20+/-16 vs. 14+/-9 microV, P<0.05). Changes in SAECG parameters did not differ significantly in patients in whom amiodarone prevented the inducibility of VT (n=15) and those in whom VT remained inducible with amiodarone (n=53), but in baseline QRS duration was significantly shorter in patients in whom amiodarone prevented the VT induction (118+/-26 vs. 133+/-28 ms, P<0.05). In patients in whom amiodarone did not prolong the cycle length of VT (n=15), SAECG did not change significantly (QRS dur 131+/-29 vs. 132+/-27 ms, LAS 42+/-20 vs. 42+/-19 ms, RMS 40 22+/-14 vs. 19+/-11 microV). Comparison of the SAECG data in patients with no inducible VT and those with slowed VT differed significantly (P<0.05) between the control state and the recording with amiodarone. CONCLUSIONS: The effects of amiodarone on VT inducibility are predicted by a shorter baseline QRS duration and the degree of drug-induced prolongation of filtered QRS duration. Amiodarone prolonged the QRS duration, LAS duration and decreased RMS 40; this effect was more important in patients with no inducible VT and in those with only slowed VT, than in patients with unchanged or accelerated VT. The absence of changes of QRS duration predicted the induction of a more rapid or not slowed VT with amiodarone with a sensitivity of 87% and a specificity of 83%. Therefore, SAECG appears as an useful and simple means to predict the effects of amiodarone in patients with myocardial infarction and VT.     

Quantitative improvement in signal-averaged electrocardiography after coronary artery bypass grafting.

Abnormal signal-averaged electrocardiography (SAECG) reflects slow and heterogeneous myocardial conduction, predicting ventricular arrhythmia and sudden cardiac death in patients with ischemic heart disease. The purpose of this study was to investigate the quantitative effect of coronary artery bypass grafting (CABG) on SAECG, which is still controversial, and to identify the factors that are related to it. Pre- and postoperative SAECGs were recorded in 100 patients who underwent CABG. Compared parameters included filtered QRS duration (dQRS), root mean square voltage in the terminal 40 ms of the QRS complex (RMS40), and duration of the terminal low-amplitude signal less than 40 microV (LAS40). All 3 parameters in SAECG improved significantly after CABG (dQRS: 105+/-21 ms-->99+/-18 ms, RMS40: 55+/-45 microV-->65+/-41 microV, LAS40: 29+/-19 ms-->25+/-12 ms). The improvements in SAECG were greater in patients who underwent complete revascularization and in those without prior myocardial infarction. In conclusion, CABG improved SAECG quantitatively, even in patients with normal SAECG. However, this improving effect was variable and closely related to the presence of prior myocardial infarction and the completeness of revascularization.     

Role of bandpass filters in optimizing the value of the signal-averaged electrocardiogram as a predictor of the results of programmed stimulation

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.     

Quantitative Comparison of Temporal and Spatial High-Resolution Recordings of Terminal QRS

Beat-by-Beat Recording of Terminal QRS. Introduction: Beat-by-beat recordings of quasiorthogonal leads were performed in 82 normal subjects (35 male and 47 female) with normal standard electrocardiograms (ECGs) in order to: (1) establish normal values for parameters that were similar to those used in signal-averaged ECG; (2) compare these data with the signal-averaged ECG; and (3) assess the noise level in beat-by-beat recording. Methods and Results: Low-noise recordings were achieved by special instrumentation, preparation of subjects, and screening recording sites for an optimal magnetic field at 60 Hz or its harmonics without using a shielded room. Using a 40-Hz bidirectional high-pass filter, 95% of normal subjects had a beat-by-beat duration of vector magnitude complex ≤ 107 msec, a duration of low-amplitude signal under 40 μV ≤ 37 msec, and a root mean square (RMS) voltage of last 40 msec ≥ 24.1 μV. Significant difference was found in duration of vector magnitude complex (P < 0.0001) between gender groups; this difference disappeared after normalization for height (P > 0.3). Although the beat-by-beat and signal-averaged data were highly correlated in all three parameters, the beat-by-beat recordings exhibited a shorter duration of low-amplitude signal (P < 0.0004) and a higher RMS voltage of last 40 msec (P < 0.002), and no significant variation in duration of vector magnitude complex (P > 0.2). The mean RMS noise in the vector magnitude lead from the normal group was 1.52 ± 0.65 μV (mean ± SD) while over 80% of the subjects had RMS noise under 1 μV in an individual lead. Conclusion: The normal values from beat-by-beat recordings are correlated to but different from those of signal-averaged ECGs. Every-beat high-resolution recordings of terminal QRS are stable and reproducible in normal subjects. Also, the use of individual lead (s) with lower noise is recommended for better detection of low-level terminal QRS. (J Cardiovasc Electrophysiol, Vol. 3, pp. 109–118, April 1992)     

Effects of exposure to hypoxia on the signal-averaged electrocardiogram in healthy subjects

The effects of hypoxia on the signal-averaged ECG (SAECG) wereinvestigated in 26 healthy active subjects with no suggestionof cardiac disease. The SAECG was recorded in each resting subjectin normoxic and hypoxic normobaric conditions (inspired O₂ fraction20.7 vs 10.0%) which lowered resting arterial O₂ saturationfrom 98.6 +0.6% to 77.7 ± 8%. Recordings from four subjects(three men) met the definition of abnormal late potentials atbaseline; in all these subjects but one, who exhibited an improvedbut still abnormal QRS duration, these parameters returned tonormal in hypoxic conditions. The duration of the filtered QRSwas significantly reduced (from 107.6 ±13.2 to 101.6± 11.3 ms, P<001), the duration of the low amplitudesignals in the terminal portion of the QRS <40 µ V(LAS) significantly decreased (from 26.5 ± 9.5 to 22.7± 7.9 ms, P<005) and the root mean square voltagein the last 40 ms (Term-RMS) increased non-significantly (from55.8±40.2 to 69.1±38.3 µV, P=0.058). Hypoxiadetermined a higher (P<0.05) heart rate increase in subjectswith abnormal records than in normal subjects. These data could be related to a sympathic discharge. They suggestthat: (1) variation in heart rate could affect the SAECG; (2)exposure to hypoxia improves SAECG parameters in healthy subjects,possibly related to sympathetic discharge; (3) abnormal recordscollected during sinus bradycardia could represent a type offalse-positive expression of late potentials in young activeadults.     

The effect of glucose-insulin-potassium solution on ventricular late potentials and heart rate variability in acute myocardial infarction.

BACKGROUND: Blunted heart rate variability (HRV) and presence of ventricular late potentials (VLPs) are known to correlate with an increased risk of ventricular tachycardia and sudden cardiac death in acute myocardial infarction (AMI). In the present study, we investigated the effect of glucose-insulin-potassium (GIK) solution on the VLPs and HRV in AMI. METHODS: Seventy-two consecutive patients with first Q wave AMI were randomized to GIK solution and placebo. HRV analysis and ambulatory electrocardiographic recordings were taken in all patients between 24 and 48 h. Sub-maximal exercise testing and echocardiography were performed and signal-averaged electrocardiography (SAECG) was recorded before discharge. RESULTS: Total filtered QRS duration (FQRS: 102 +/- 7 versus 108 +/- 11 ms; P < 0.05), low-amplitude signal (LAS: 25 +/- 8 versus 32 +/- 11 ms; P < 0.01) and frequency of VLPs (21 versus 45%; P < 0.05) were found to be significantly lower while root-mean-square voltage of the terminal 40 ms of QRS (RMS-40: 45 +/- 18 versus 36 +/- 20 microV; P < 0.05), and left ventricular ejection fraction (EF: 55 +/- 6 versus 48 +/- 7; P < 0.05) were significantly higher in the GIK group when compared to placebo. During the hospital period, the presence and frequency of post-myocardial infarction angina were significantly lower in the GIK group (15 versus 29%, P < 0.05), whereas an insignificant decrease in frequency of ventricular arrhythmias was observed in these patients. On HRV analysis, there was no significant difference between two groups in either time domain (SD, SDNN, RMS-SD) or frequency domain (HF, LF, LF/HF ratio) parameters. CONCLUSION: GIK solution may be beneficial to VLPs, ischaemic events, and left ventricular systolic performance in the early period of AMI. This therapy has no significant effect on HRV in AMI patients.     

Impact of diabetes mellitus on the improvement in signal-averaged electrocardiography after coronary artery bypass grafting.

BACKGROUND: Although it has been reported that coronary artery bypass grafting (CABG) for multivessel disease markedly improves several parameters of signal-averaged electrocardiography (SAECG), its beneficial effect on SAECG is variable. The hypothesis of the present study was that the presence of diabetes mellitus (DM) affects the improvement in SAECG after CABG. METHODS AND RESULTS: Pre- and post-operative SAECGs were recorded in 100 consecutive patients who underwent complete surgical revascularization. Changes in the following parameters were compared between the diabetic (n=43) and non-diabetic (n=57) patients: filtered QRS duration (dQRS), root mean square voltage in the terminal 40 s of the QRS complex (RMS40), and duration of the terminal low-amplitude signal lower than 40 microV (LAS40). Although baseline characteristics and the occurrence of late potentials were similar in both groups, quantitative improvements in the SAECG parameters after CABG were significantly greater in non-diabetic than in diabetic patients (dQRS: 109 +/- 22 ms vs 102 +/- 19 ms in diabetics and 106 +/- 21 ms vs 88 +/- 11 ms in non-diabetics; p=0.028, RMS40: 55 +/- 46 microV vs 65 +/- 38 microV in diabetics and 50 +/- 37 microV vs 76 +/- 37 microV in non-diabetics; p=0.037, LAS40: 31 +/- 20 ms vs 26 +/- 17 ms in diabetics and 32 +/- 12 ms vs 17 +/- 8 ms in non-diabetics; p=0.007, respectively). CONCLUSIONS: The presence of DM limits the CABG-induced improvement in SAECG. In diabetic patients, therefore, perioperative changes of the SAECG must be interpreted with caution.     

Lack of Impact of Myocardial Ischemia on the Signal‐Averaged ECG Assessment by Time‐Domain Analysis

Background: Late potentials represent an arrhythmogenic substrate in chronically infarcted myocardium. It is hypothesized that acute transient ischemia enhances anisotropic electrical ventricular activation and facilitates reentry mechanisms. Study aim was the prospective assessment of the impact of dipyridamole‐induced myocardial ischemia on the signal‐averaged ECG. Methods: Dipyridamole stress thallium‐201 SPECT imaging was utilized to avoid noise contamination of the signal‐averaged ECG from exercise and to document evidence and localization of myocardial ischemia or persistent perfusion defects in 68 patients with suspected coronary artery disease. Before and during dipyridamole‐induced vasodilatation serial signal‐averaged ECG was performed to evaluate the influence of transient ischemia on the occurrence of late potentials. Results: There was a significant difference between heart rate at rest and heart rate under dipyridamole influence in patients with inducible ischemia (70 ± 13 vs. 87 ± 13; P < 0.0001) in contrast to patients without dipyridamole‐induced ischemia (74 ± 20 vs. 80 ± 16; n.s.). The number of averaged beats and achieved noise level was comparable between both groups. Thirty‐three of 68 patients (49%) revealed dipyridamole‐induced ischemia; however, no changes of the SAECG parameters, such as QRS, RMS, LAS at 25–250 and 40–250 Hz bandpass filtering in the leads X, Y, Z and vector magnitude, respectively, were observed as a result of ischemia. Conclusion: These results suggest that transient myocardial ischemia does not affect the signal‐averaged ECG. Clinically, the signal‐averaged ECG analysis seems not to be helpful in identifying patients with silent ischemia. A.N.E. 2002;7(3):191–197     

Predictive Value of Late Potentials after Myocardial Infarction in the Thrombolytic Era

Background: The value of the signal-averaged electrocardiogram (ECG) for prediction of arrhythmic events (AE) after myocardial infarction (MI) has been well established. The current incidence of AE in the first year after Ml is remarkably lower than that reported in the 1980s. In this study, we compared the prevalence and the predictive value of late potentials (LP) in patients with Ml treated with either conventional or reperfusion therapy. Methods: A total of 433 patients (age 62 ± 10 years, 350 men) recovering from acute Ml were prospectively analyzed. Two hundred seven patients had conventional therapy (group A), and 226 had reperfusion therapy (group B) within 12 hours of the onset of symptoms: 145 of group B patients received thrombolytic agents, whereas 81 underwent direct or rescue angioplasty. Standard signal-averaged variables were recorded (filter range 40–250 Hz) 10 ± 6 days (range 5–30 days) after Ml. LP were defined as being present if 2 of the following were met: fQRS <114 ms, RMS40 20 μV, LAS40 <38 ms (criterion 1), and if QRS 120 ms (criterion 2). Results: LP were found in 33% versus 21%, P = 0.004 (criterion 1) and in 13% versus 8%, P = 0.057 (criterion 2) of group A and group B patients, respectively. During a mean follow-up of 24 ± 19 months (range 5 days to 48 months), there were 22 AE (5%). The AE rate for patients with conventional therapy was significantly higher in those with LP than in those without LP: 12% versus 4%; P = 0.03 (criterion 1) and 30% versus 3%; P = 0.00003 (criterion 2). The AE rate for patients with reperfusion therapy was similar in patients with and without LP: 9% versus 3%, P = 0.09 (criterion 1) and 12% versus 3%, P = 0.14 (criterion 2). Multivariate analysis indicated that the presence of LP based on criterion 2 was the strongest independent predictor of AE in patients with Ml treated with conventional therapy. Conclusion: In this study, reperfusion therapy influenced the prevalence of LP. The predictive value of LP for serious AE in the postinfarction period was remarkably affected by thrombolysis and/or interventional catheter therapy.     

Slowed Conduction with Antiarrhythmic Drugs Reduces High Frequency Energy of the Signal-Averaged Electrocardiogram

Background: We have previously demonstrated that high frequency QRS energy decreases after experimental myocardial infarction (Ml) and is lower in patients who have had MI compared to controls. The mechanism for this decrease in high frequency QRS energy is unclear. The objective of this study was to evaluate the effect of slowed myocardial conduction on high frequency QRS energy measured on the signal-averaged SAECG. We hypothesized that slowed conduction in the infarcted ventricle may be responsible for the decrease in high frequency QRS energy. In order to test this hypothesis, we examined antiarrhythmic drug therapy known to slow conduction (propafenone) compared to drug therapy with minimal effects on conduction (sotalol). Methods: In patients with sustained ventricular tachyarrhythmias undergoing serial drug testing, SAECGs were obtained before and after antiarrhythmic therapy. After filtering the leads with a spectral band-pass (15–40 Hz, 40–80 Hz, and 80–300 Hz) filter, the vector magnitude was con structed, and the energy (in μV sec) was calculated for the entire QRS by integrating the area under the filtered QRS complex. Results: Propafenone significantly prolonged QRS duration (+17%, P > 0.001) and significantly reduced QRS energy (-16.1% to 21.8%, P > 0.0001) in all three band widths. Sotalol did not have either effect (P = ns). There was a strong correlation between the prolongation of the filtered QRS and the drop in QRS energy for all three band widths (r values ranging from 0.64–0.90, all P > 0.05). When the changes in QRS energy were corrected for QRS duration, the results did not change. Conclusion: The Class IC antiarrhythmic drug propafenone, known to decrease myocardial conduction velocity, significantly reduced QRS energy in all three band widths, whereas the Class III drug sotalol did not. These data are consistent with the hypothesis that decreases in low and high frequency QRS energy after Ml result in part from slowed conduction.     

Value of non-invasive and invasive studies in patients with bundle branch block, syncope and history of myocardial infarction.

The prognosis of patients with bundle branch block (BBB) and myocardial infarction (MI) is poor, particularly for patients suffering from syncope. The purpose of this study was to investigate the diagnostic value of some techniques for the evaluation of the mechanism of syncope in patients with MI and BBB and their prognosis. METHODS: We prospectively obtained the results of clinical history, 24 h Holter monitoring, left ventricular ejection fraction (LVEF), signal-averaged ECG (SAECG) and programmed ventricular stimulation in 130 patients with syncope, MI and BBB. 81 of them had right (R)BBB and 49-left (L)BBB. RESULTS: Ventricular tachycardia (VT) was identified as the main cause of syncope in patients with MI and BBB: 68% of them had inducible VT. The sensitivity (se) and specificity (sp) of non sustained VT on Holter monitoring for the detection of VT were respectively 42.5 and 47% in patients with RBBB, 62 and 36% in those with LBBB; se and sp of LVEF <40% were 67.5% and 65% in patients with RBBB, 85 and 9% in those with LBBB; se and sp of the combination of 2 of the 3 SAECG criteria, QRS duration > 155 ms, LAS duration >30 ms and RMS 40 < 17 microV were respectively 50 and 57% in patients with RBBB; se and sp of the combination of 2 of the 3 criteria QRS duration >165 ms, LAS duration >40 ms and RMS 40 <17 microV were 73 and 55.5%) in patients with LBBB. During the follow-up (4.7 years +/- 2.5), 12 patients died suddenly and 12 patients died from heart failure. Univariate and multivariate analysis revealed than only the induction of VT was a significant predictor of sudden death. A long QRS duration (> 165 ms) and induction of VT were independent predictors of total cardiac mortality. CONCLUSION: Among noninvasive studies, only the determination of filtered QRS duration was a significant predictor of cardiac mortality in the case of a prolongation (> 165 ms). Sudden death was only predicted by the induction of sustained VT. Because of the high incidence of inducible sustained VT, the low value of Holter monitoring and decreased LVEF for the prediction of ventricular arrhythmias and the poor prognosis of patients with inducible VT and low LVEF, systematic programmed ventricular stimulation is indicated in patients with MI, syncope and BBB, whatever the non-invasive studies results.     

Is the Change of Late Potential Over Time Related to Enzyme Levels?Ichemic Burden in Acute Myocardial Infarction

Background: The ventricular late potential (VLP) detected using the technique of signal average electrocardiography (SAECG) interacts with several factors, primarily time. Method: In this study, we examined the interaction, over time, of VLP with the initial ischemic burden and enzyme levels in acute myocardial infarction. Patients diagnosed as having acute myocardial infarction were included in the study. On the first day, the patients underwent enzyme analysis and electrocardiography (ECG) follow‐up every 6 hours. A 24‐hour ambulatory ECG was performed on the seventh day in order to determine the ischemic burden. SAECG findings (TQRS, RMS, LAS were obtained on the seventh day, in the first and third months. The study was continued with the patients who did not require angioplasty as decided with angiographic evaluation in the first month. Results: The study included 30 patients with acute myocardial infarction (mean age 51 ± 12, 28 males and 2 females). The initial mean CK‐MB levels and the mean ischemic burden were 98 ± 31 U/L and 44 ± 96 minutes. The TQRS (ms), LAS (ms), and RMS (μV) values (mean ± SD) obtained at day 7, month 1, and month 3 are 97 ± 12, 96 ± 9, 103 ± 11, P = 0.01; 31 ± 10, 31 ± 11, 32 ± 10, P = 0.46; 43 ± 28, 41 ± 26, 33 ± 25, P = 0.01, respectively. We observed that the TQRS and RMS values changed significantly with time, but these levels of significance disappeared when adjusted for the initial ischemic burden and CK‐MB levels (P = 0.06; P = 0.53). The VLP frequency was 33% at day 7 and 23% at month 3. Unlike the CK‐MB level, the initial ischemic burden was significantly different between the patients with and without VLP at month 3 (150.85 ± 149.28, 12.34 ± 26.48, P = 0.001). When tested together with age and gender, it was found that the high initial ischemic burden increased the possibility of VLP (OR: 24, Cl: 2.09–279.52, P = 0.01) at month 3. Conclusion: SAECG findings in patients with myocardial infarction changed with time; however, this change occurred depending on the initial ischemic burden and CK‐MB levels. Of these, only the initial ischemic burden, especially in high levels, was a determinant for the presence of VLP in the late period of myocardial infarction. A.N.E. 2002;7(3):242–246