Relationship between signal-averaged electrocardiography and dangerous ventricular arrhythmias in patients with left ventricular aneurysm after myocardial infarction

We performed signal-averaged electrocardiography (SAECG) andHolter monitoring, and subsequently followed-up 53 ambulatorypatients with left ventricular aneurysm (LVA) after myocardialinfarction (MI). A history of spontaneous episodes of sustainedventricular tachycardia (VT) v also analysed. Out of 53 patients, 25 (47%) had an abnormal SAECG. AbnormalSAECG correctly identified nine out of 10 cases with a historyof sustained VT. Complex ventricular arrhythmias were detectedon Holler monitoring in 23 patients: in five out of 28 withnormal SAECG (18%) and in 18 out of 25 with abnormal SAECG (72%)(P<0001). During follow-up (mean 19 months) sustained VTand/or sudden cardiac death (SCD) occurred in eight cases, outof which seven had an abnormal SAECG. The negative predictivevalue of SAECG (no VT or SCD during follow-up) was very high,96%. similar to the negative predictive value of a history ofsustained VT (93%). Using multivariate analysis only a historyof sustained VT twas an independent factor in predicting theoutcome of patients in this study. We conclude that an abnormal SAECG identifies those post infarctionpatients with LVA who are prone to complex ventricular arrhvthmias.A normal SAECG and an absence of a history of sustained VT stronglyindicate that the risk of developing arrhythmic events is verylow.     

Predicting arrhythmic events after acute myocardial infarction using the signal-averaged electrocardiogram.

To determine if the signal-averaged (SA) electrocardiogram (ECG) predicts the occurrence of sustained ventricular arrhythmia and sudden death after acute myocardial infarction, 182 consecutive patients underwent systematic noninvasive testing, including the SAECG. Seventy-one patients (39%) had an abnormal SAECG. The presence of an abnormal SAECG was not related to underlying left ventricular dysfunction or any other clinical or measured variable. There were 16 end points (sustained ventricular arrhythmia or sudden cardiac death) during 14-month follow-up. The SAECG was a significant predictor of these events (p less than 0.02), and an abnormal SAECG conferred a 2.7-fold increase in risk. The risk associated with an abnormal SAECG was independent of both left ventricular function and ventricular arrhythmia on Holter ECG. The SAECG had excellent negative predictive accuracy (95%), but the positive predictive accuracy was low (15%). When the results of the SAECG were combined with the results of the Holter ECG, a group of very high-risk patients was identified; at 18 months, the presence of abnormal SAECG and Holter ECG was associated with a risk of 26% compared with only 4% if both tests were normal. Furthermore, all published studies with a similar design were pooled for meta-analysis. The meta-analysis revealed a sixfold increase in risk, independent of left ventricular function, and an eightfold increase in risk, independent of Holter results when the SAECG was abnormal. The SAECG is a noninvasive test that can rapidly and easily provide potent prognostic information regarding the risk of sustained ventricular arrhythmias for patients after myocardial infarction.     

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.     

The value of time and frequency domain, and spectral temporal mapping analysis of the signal-averaged electrocardiogram in identification of patients with hypertrophic cardiomyopathy at increased risk of sudden death

Late potentials detected by the signal-averaged ECG (SAECG)identify post-infarction patients at risk from sustained ventriculartachycardia (VT) and sudden death. Hypertrophic cardiomyopathy(HCM) is also associated with increased risk of sudden death.In adults, episodes of non-sustained VT on ambulatory ECG monitoringare a marker of high risk patients. In children and adolescents,however, there is no reliable ECG marker, and clinical featureshave low predictive accuracy. The prognostic value of the SAECGin HCM has not been systematically evaluated. We examined the relation of detailed time domain, frequencydomain, and spectral temporal mapping analysis of the SAECGand clinical and echocardiographic features, and the resultsof 48 h ambulatory ECG monitoring in 121 consecutive patientswith HCM. Non-sustained VT on Holter monitoring was recordedin 27 (23%) patients. An abnormal time domain SAECG was presentin three (11%) patients with VT vs three (3%) without VT (ns).Of the SAECG variables, reduced (below 150 µ V) voltageof the initial 40 ms of the signal-averaged QRS complex wasthe best predictor for non- sustained VT (sensitivity: 95% specificity:74% ;positive predictive accuracy: 64%; negative predictiveaccuracy: 97%). Nine patients (of whom eight were 30 years ofage) experienced catastrophic events: three died suddenly andsix had been resuscitated from out-of-hospital ventricular fibrillation.None of them had an abnormal time domain SAECG. The frequencydomain analysis and spectral temporal mapping of the SAECG didnot improve the identification of patients with VT or patientswith catastrophic events. In conclusion, alterations of the initial portion of the signal-averagedQRS complex identified patients with HCM and non-sustained VT,but the SAECG was not useful in identifying young patients whosuffered cardiac arrest.     

Influence of the infarct site on the identification of patients with ventricular tachycardia after myocardial infarction based on the time-domain and spectral turbulence analysis of the signal-averaged electrocardiogram

In a significant proportion of patients with sustained ventricular tachycardia (VT) following anterior myocardial infarction, the areas of slow conduction are activated early during cardiac depolarization. Therefore, they may not be detected by the standard time-domain analysis of the signal-averaged electrocardiogram (SAECG) which is limited to the terminal part of the QRS complex. Spectral turbulence analysis of the SAECG is a new frequency domain technique which examines the whole QRS complex and may improve identification of patients with sustained VT following anterior infarction. We compared the results of time-domain and spectral turbulence analyses of the SAECG in 53 postinfarction patients with sustained VT and in 53 age-, gender- and infarct site-matched patients without VT. The receiver operator characteristic curves have shown that the time-domain analysis resulted in better identification of patients with VT following inferior than following anterior infarction (e.g., at the sensitivity level of 90%, the corresponding values of specificity were 96 and 90%, respectively), whereas the spectral turbulence analysis performed better in the anterior site of infarction. When both time-domain and spectral turbulence analyses were combined, the accuracy of the SAECG for identification of patients with VT following anterior infarction improved, reaching a specificity of 97% at the sensitivity level of 90%. In conclusion (1) spectral turbulence analysis of the SAECG results in better identification of patients with VT following anterior than following inferior infarction, and (2) the combination of time-domain and spectral turbulence analyses of the SAECG may improve identification of patients with VT following anterior infarction.     

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.     

Late fields of the magnetocardiographic QRS complex as indicators of propensity to sustained ventricular tachycardia after myocardial infarction

INTRODUCTION: Magnetocardiographic (MCG) mapping is a new method to record cardiac signals. This study examined the association of MCG late fields with the propensity to sustained ventricular tachycardia (VT) after myocardial infarction (MI). METHODS AND RESULTS: One hundred patients with remote MI were studied, 38 with and 62 without history of VT. High-resolution MCG and signal-averaged ECG (SAECG) as a comparative method were recorded. Time-domain parameters describing the abnormal low-amplitude end QRS activity, MCG late fields, and SAECG late potentials were analyzed. Late field parameters differed significantly between the patient groups: filtered QRS duration was 137 +/- 26 msec in the VT group and 110 +/- 18 msec in the control group (P < 0.001), and root mean square amplitude of the last 40 msec was 260 +/- 170 and 510 +/- 360 fT (P < 0.001), respectively. The optimal MCG parameter combination yielded a sensitivity of 92% and a specificity of 61% in classification to the VT group, whereas those for SAECG were 63% and 66%. In a subgroup of 63 patients with marked left ventricular dysfunction and comparable stage of coronary heart disease, only MCG (sensitivity 73%, specificity 67%) but not SAECG could assign a patient to the VT group. CONCLUSION: Late fields of the MCG QRS complex indicate propensity to life-threatening arrhythmias in post-MI patients. This discriminative ability persists in the presence of severe left ventricular dysfunction where ECG late potentials lose their informative value. MCG late field analysis is a potential new method for noninvasive risk assessment in post-MI patients.     

Comparative evaluation of the results of Holter monitoring and programmed ventricular stimulation in patients with ischemic heart disease

24-hour ECG Holter monitoring and programmed ventricular stimulation were performed in 81 patients (64 males and 17 females aged 35-65). No ++anti-arrhythythmic agents nor beta-blockers were administrated. 58 patients suffered from myocardial infarction in the past, and 38 had a history of ventricular tachycardia. Right atrial and ventricular stimulation (in 7 patients also left ventricular stimulation) was performed using stimuli of a 2 ms pulse width. 24-hour ECG Holter monitoring was recorded on a magnetic tape from two bipolar precordial leads. Both examinations results were compared to assess correlation between ECG Holter monitoring parameters and inducibility of VT or VF by programmed stimulation. Significant correlation was stated among occurrence of: 1) spontaneous sustained ventricular tachycardia and induced by stimulation monomorphic sustained VT (p less than 0.005) as well as estimated both sustained and nonsustained VT (p less than 0.010) 2) spontaneous nonsustained VT and induced by stimulation sustained or nonsustained monomorphic VT (p less than 0.025). There was no correlation between spontaneous ventricular arrhythmias estimated by Lown and Wolf's classification and possibility to induce monomorphic VT as well as between any of ECG Holter monitoring parameters and polymorphic VT or ventricular fibrillation induced by stimulation. Aggressiveness extent of stimulation protocol necessary to induce monomorphic VT was similar in patients with or without VT recorded by Holter method.     

Differences in electrophysiological substrate in patients with coronary artery disease and cardiac arrest or ventricular tachycardia. Insights from endocardial mapping and signal-averaged electrocardiography

BACKGROUND. Many studies have combined patients with hemodynamically well-tolerated ventricular tachycardia (VT) and those with cardiac arrest (CA) as a single, homogenous group. Recent studies suggest that these two groups have different electrophysiological substrates and responses to therapy. Most of these studies, however, enrolled patients with a variety of cardiac diagnoses. METHODS AND RESULTS. We used signal-averaged electrocardiography (SAECG) and endocardial catheter mapping to define the electrophysiological substrate in patients with coronary artery disease and VT or CA and correlate the results of the two methods. We also examined the usefulness of SAECG in CA patients to differentiate those with inducible arrhythmias from those who are noninducible. VT patients were more likely to have had a prior myocardial infarction (p = 0.0005) and to have inducible arrhythmias (p = 0.0001) than were CA patients. The induced arrhythmias in patients who presented with VT was VT in more than 90% of cases, whereas in CA patients, polymorphic ventricular tachycardia (PMVT) accounted for one third of induced arrhythmias. Mean filtered QRS duration was longer (135 versus 120 msec) and the terminal QRS voltage was smaller (20 versus 34 microV) in VT than in CA patients (p less than 0.01). Sixty-three percent of CA patients and 87% of VT patients had abnormal SAECG (p = 0.001). VT patients had more extensive endocardial abnormalities and more abnormal (53% versus 40%, p = 0.002), fractionated (8% versus 3%, p = 0.02), late (17% versus 8%, p = 0.0003), and late abnormal or fractionated (14% versus 4%, p = 0.0001) sites than CA patients. VT patients had a greater duration of the longest electrogram (129 versus 109 msec, p = 0.0006) and total endocardial activation time (68 versus 54 msec, p = 0.009). Among CA patients, those with induced VT had more extensive substrate than did those with induced PMVT and were similar to VT patients with induced VT. Among CA patients, the trend for more patients with inducible VT (77%) or PMVT (55%) than noninducible patients (47%) to have an abnormal SAECG did not reach statistical significance (p = 0.14). The positive and negative predictive values of an abnormal SAECG were 77% and 44%, respectively. CONCLUSIONS. VT patients have more extensive endocardial substrate than CA patients, which translates into greater and more frequent SAECG abnormalities. Among CA patients, there are significant differences in substrate between patients with induced VT and those with induced PMVT. SAECG is not useful in differentiating CA patients who have inducible VT or PMVT from those who do not.     

Treatment of malignant ventricular tachyarrhythmia with amiodarone: comparison of empirical administration and administration guided by Holter or ventricular stimulation. Results of the parallel test

To assess the most appropriate method of administering amiodarone and predicting its efficacy (empiric vs guided by Holter or by ventricular stimulation), 19 patients with sustained ventricular tachycardia or ventricular fibrillation underwent a "parallel study". Fifteen patients were men and 4 women, with a mean age of 65 years. A coronary artery disease with previous myocardial infarction was present in 15 patients, dilated cardiomyopathy in 3 and arrhythmogenic right ventricular dysplasia in 1 (mean left ventricular ejection fraction = 35%). All 19 patients had, as inclusion criteria, 1) frequent (greater than or equal to 30/hour) and/or repetitive (greater than or equal to 10/24 hours) ventricular premature beats during 24-hour Holter monitoring and 2) inducible sustained (greater than 30/sec) ventricular arrhythmias during programmed ventricular stimulation (1-3 extrastimuli from 2 right ventricular sites). Amiodarone was given at an initial dosage of 15 mg/kg/day for 2 weeks and then at a dosage of 5 mg/kg/day. After 15 days 24-hour Holter monitoring and programmed ventricular stimulation were repeated. The data of these tests, however, were not used to guide the therapy that remained empiric, but served only to assess retrospectively the predictive value of Holter monitoring and ventricular stimulation. The following main results were obtained: The mean duration of follow-up was 25 +/- 13 months. During this period 6 patients (32%) died, 3 from sudden and 3 from non-sudden cardiac death. Two other patients had recurrence of sustained ventricular arrhythmias. After 15 days of therapy amiodarone was effective at Holter monitoring in 15 patients (79%) and not effective in 4 (21%). Two of the 15 patients considered responders died suddenly during the follow-up and 2 had arrhythmic recurrence, vs 1 of the 4 non-responder patients who died suddenly (negative predictive value of Holter monitoring: 73%; positive predictive value: 25%; predictive accuracy: 63%). After 15 days of therapy amiodarone was effective at ventricular stimulation in 10 patients (53%) and not effective in 9 (47%). None of the 10 patients considered responders had arrhythmic events during the follow-up, vs 5 of the 9 non-responders, 3 of whom died suddenly and 2 of whom had arrhythmic recurrences (negative predictive value of ventricular stimulation: 100%; positive predictive value: 56%; predictive accuracy: 79%). Only 1 patient discontinued amiodarone after 25 months of follow-up because of development of an important blue-grey skin discoloration.(ABSTRACT TRUNCATED AT 400 WORDS)     

Long-term follow up of 115 patients with ischemic heart disease and ventricular flutter induced by programmed ventricular stimulation in the absence of ventricular arrhythmia

The clinical significance of rapid monomorphic ventricular tachycardia (VT) (> 270 beats/min), also called ventricular flutter, remains controversial in patients without documented spontaneous sustained VT. The aim of this study was to evaluate the outcome of 115 patients with ischaemic heart disease, aged 58 +/- 10 years, without spontaneous ventricular arrhythmias, but who had inducible ventricular flutter during programmed ventricular stimulation. The patients underwent stimulation to evaluate the prognosis after myocardial infarction or to investigate a malaise with or without loss of consciousness. Sustained ventricular flutter was the only inducible arrhythmia in all patients. The mean left ventricular ejection fraction (LVEF) was 42 +/- 14%. During an average follow-up period of 66 +/- 43 months, 31 deaths, including 27 of cardiac causes, were observed. The 1, 5, and 11 year survival of the whole population was 94, 79 and 64% respectively. In univariate analysis, anterior wall myocardial infarction, a low LVEF, the presence of non-sustained ventricular tachycardia (NSVT) on 24 hour Holter monitoring and Class III antiarrhythmic treatment, were poor prognostic factors (p 0.05). In multivariate analysis, the only independent predictive factors of mortality were low LVEF (p = 0.006), the presence of NSVT on Holter monitoring (p = 0.003) and the absence of betablocker therapy (p = 0.015). Medical therapy with betablockers or the implantation of an automatic defibrillator may be indicated in these patients at higher risk.     

Correlation between the signal-averaged electrocardiogram and electrophysiologic study findings in patients with coronary artery disease and sustained ventricular tachycardia

Ventricular late potentials at the end of the surface QRS, detected on the signal-averaged electrocardiogram (SAECG) have been shown to be markers for spontaneous and/or inducible ventricular tachycardia (VT) in patients with coronary artery disease (CAD). We examined the correlations between electrophysiologic study (EPS) findings and SAECG indexes in 50 patients with chronic CAD with documented spontaneous VT/ventricular fibrillation (VF), who had either syncope (24 patients) or aborted sudden cardiac death (SCD). The prevalence of late potentials was significantly higher in the syncope patients (75%) compared with the SCD group (46%) (p less than 0.05). No correlation was found between the ventricular refractoriness and the SAECG indexes. There was a significant difference in quantitative SAECG indexes comparing the induction mode of the sustained VT/VF by single and double versus triple extrastimuli; the types of the induced VT (sustained monomorphic, sustained pleomorphic or VF, noninducible); and the cycle length of the induced sustained monomorphic VT with the high frequency QRS duration (QRSD). In conclusion, differences in prevalence and characteristics of ventricular late potentials were found between patients with syncope and with SCD. The degree of abnormality of SAECG indexes correlated with the type and the mode of induction of sustained VT. The magnitude of QRSD of the SAECG correlated with the cycle length of monomorphic VT. The above findings suggest that in patients with CAD and sustained VT/VF the SAECG variables are related to the area of reentry.     

Programmed electrical stimulation of the heart in relation to left ventricular contractility in ischemic heart disease

To determine the relation between left ventricular contractility disorders and the inducibility of serious ventricular arrhythmias, 83 patients (pts) with ischaemic heart disease and ventricular tachycardia (VT) or fibrillation (VF) in history and/or Lown's class IVb arrhythmia in 24-hour Holter ECG monitoring were evaluated by means of echocardiography and programmed electrical stimulation (PES) of the heart. Inducible VT or VF were observed in 66% of pts: sustained monomorphic VT (SMVT) in 33%, nonsustained VT (NSVT) in 28% and VF in 6%. VT or VF were significantly more frequent in patients with VT/VF in history (91% vs 42%, p less than 0.001), SMVT (48% vs 17%, p less than 0.01) as well as NSVT (38% vs 17%, p less than 0.01). Low ejection fraction (EF less than 40%) was observed in 18 pts (22%), VT/VF was inducible in 94% of them, while only in 57% with EF greater than or equal to 40%, p less than 0.01, SMVT in 39% vs 30%, NSVT in 33% vs 25%. Among 21 pts (21%) with left ventricular (LV) dyskinesis in 91% of pts while only in 55% without it, p less than 0.01, SMVT in 53% vs 26%, p less than 0.05. We concluded that in patients with previous myocardial infarction, VT/VF in history and abnormal LV contractility full haemodynamic, angiographic and electrophysiologic examination should be performed to determine their risk of sudden death due to serious ventricular arrhythmia before final decision about the mode of treatment.     

Long-term incidence of malignant ventricular arrhythmia and shock therapy in patients with primary defibrillator implantation does not differ from event rates in patients treated for survived cardiac arrest

INTRODUCTION: Recent trials have demonstrated benefit of prophylactic defibrillator (ICD) implantation compared to conventional treatment in high-risk patients. However, many patients have rare or no sustained arrhythmias following implantation. Our study addresses the question, whether patients with prophylactic defibrillator implantation have a lower risk for life-threatening ventricular tachycardia (VT) or ventricular fibrillation (VF) compared to sudden cardiac death (SCD) survivors. METHODS AND RESULTS: Over 7 years we enrolled 245 patients. Occurrence of spontaneous sustained VT/VF resulting in adequate ICD treatment was the endpoint. Incidence, type, and treatment of sustained arrhythmia in 43 previously asymptomatic ICD recipients (group B) were compared to data of 202 survivors of imminent SCD (group A). All patients had severely impaired left ventricular ejection fraction (<45%). Group B patients had long runs (>6 cycles, <30 s) of VT during Holter monitoring and inducible sustained arrhythmia. Incidence of rapid VT and VF (cycle length <240 ms/heart rate >250 bpm) after 4 years (35% in both groups, P = ns) and adequate defibrillator therapies (57% vs 55%, P = ns) were similar in both groups after univariate and multivariate analysis. Cumulative mortality tended to be lower in group B compared to group A, but the difference was not statistically significant. CONCLUSION: During long-term follow-up, incidence of sustained rapid ventricular arrhythmia in prophylactically treated patients is as high as that of SCD survivors. Benefit from defibrillator implantation for primary prevention (group B) appears to be comparable to that for survived cardiac arrest (group A).     

Therapy for late post infarction ventricular tachycardia

Non-sustained ventricular tachycardia (VT) in the late post myocardial infarction (MI) period (7-21 days) has been reported to be a predictor of sudden death. We suspected that patients with 3 beat VT on Holter monitoring in the late infarction period would demonstrate electrical instability at electrophysiologic studies. Forty-seven patients were identified as having at least 3 beat VT on Holter monitoring. Eighteen patients refused electrophysiologic studies or were not referred by their attending physician. The mean ejection fraction of this group was 43 +/- 16%. Eight patients have died, 3 sudden deaths in 13 +/- 5 months, a 17% incidence of sudden death. Twenty-nine patients underwent invasive electrophysiologic studies. Their mean ejection fraction was 37 +/- 7%, and 28 had inducible, 18 sustained ventricular tachycardia and 10 non-sustained VT. No complications were noted with electrophysiological testing in the post infarction patients. Using programmed electrical stimulation studies an effective antiarrhythmic agent preventing VT induction (usually experimental) could be found for each patient. After a mean follow-up of 12.5 +/- 4 months, the patient without inducible VT is alive and 26 of the 28 "inducible" patients are alive and well. Two patients died, one of stroke and one due to pump failure following a second MI. No sudden deaths were observed in this group. Two patients had breakthrough arrhythmias and were treated by alternative antiarrhythmic therapy that was also effective at the initial electrophysiologic studies. Thus, PES studies post MI are safe and may be an effective way to assess therapy for patients in the early post MI period, identified at high risk for sudden death.     

Long-term follow-up of the signal-averaged ECG in arrhythmogenic right ventricular cardiomyopathy: correlation with arrhythmic events and echocardiographic findings.

AIMS: The aims of our study were to evaluate late potential changes during long-term follow-up in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) and to correlate these results with echocardiographic findings and sustained ventricular tachycardia (VT) occurrence. METHODS AND RESULTS: We studied 31 patients (22 males and 9 females; mean age 29+/-16) during 8 years of follow-up by signal-averaged ECG (SAECG) and echocardiography. Ten subjects experienced episodes of sustained VT. During follow-up, all the SAECG parameters showed a progressive significant increase in late potentials. In contrast, echocardiographic indices did not show evidence of relevant modifications. Patients with sustained VT were characterized by significantly lower left and right ventricular ejection fractions, longer values of filtered QRS at 25/40/80-250 Hz filters, and longer high-frequency low-amplitude (HFLA) signals at 25-250 Hz at baseline. The analysis of SAECG modification during follow-up indicated that only HFLA signals at 25-250 Hz increased significantly in the sustained VT group. CONCLUSION: We detected a progressive increase in delayed ventricular conduction by SAECG not associated with significant echocardiographic changes. Therefore, the conduction disturbance seems to increase independently from anatomical alterations. The baseline SAECG and echocardiographic parameters, more than their modifications during follow-up, appear to be useful in identifying patients with sustained VT.     

Ventricular late potentials and induced ventricular arrhythmias after surgical repair of tetralogy of Fallot.

Ventricular tachycardia (VT) and sudden death are rare but recognized complications after surgical repair of tetralogy of Fallot. We prospectively studied 31 patients (19 boys and 12 girls, mean age +/- standard deviation 7 +/- 4 years) with postoperative tetralogy of Fallot, by means of right-sided cardiac catheterization, 24-hour Holter monitoring, body-surface and intracavitary signal-averaging (gain 10(5) to 10(6), filters of 100 and 300 Hz) and programmed ventricular stimulation (1 and 2 extrastimuli, 3 basic cycle lengths, right ventricular apex and outflow tract). All patients were asymptomatic and none had documented or suspected ventricular arrhythmias. Ventricular late potentials were detected in 10 of 31 patients (32%) and spontaneous ventricular arrhythmias in 12 of 31 patients (39%). No sustained VT was induced by programmed ventricular stimulation but nonsustained VT was induced in 3 patients (10%). Patients with inducible VT more often had late potentials (3 of 3 vs 7 of 28, p less than 0.01), and spontaneous ventricular premature complexes (VPCs) during Holter monitoring (3 of 3 vs 9 of 28, p less than 0.05). To predict VT inducibility, late potentials had a sensitivity of 100%, a specificity of 75%, a positive predictive value of 30% and a negative predictive value of 100%. For spontaneous VPCs, the figures were 100, 68, 25 and 100%, respectively. It is concluded that shortly after repair of tetralogy of Fallot, the presence of both spontaneous VPCs and ventricular late potentials are associated with an increased incidence of inducible VT. Conversely, the absence of VPCs and ventricular late potentials may identify patients at low risk of subsequent ventricular arrhythmias.     

A new protocol of programmed stimulation for assessment of predisposition to spontaneous ventricular arrhythmias

We have devised a simple method for identifying predispositionto spontaneous sustained ventricular fibrillation (VF) and tachycardia(VT). A standardized protocol of programmed stimulation wasapplied to 111 control subjects without ventricular diseaseand with no history of VF or VT (Group I) and to 27 patientswith previous myocardial infarction and documented spontaneous(in the absence of evidence of further acute myocardial ischaemia)VF or VT (Group II). The stimulation protocol consisted of singleand paired ventricular extrastimuli introduced during ventriculardrive at the right ventricular apex and ouflow tract, at twicediastolic threshold current intensity and at 20 mA. None ofthe Group I subjects exhibited VF or sustained (more than 10s) VT. In contrast sustained arrhythmias were induced in 24(89%) of Group II patients. We conclude: In our study population,initiation of a sustained ventricular tachyarrhythmia at programmedstimulation was both a sensitive (89%) and specific (100%) indicatorfor predisposition to spontaneous VF and VT.     

Prognostic significance of sustained monomorphic ventricular tachycardia induced by programmed ventricular stimulation using up to triple extrastimuli in survivors of acute myocardial infarction

The prognostic significance of sustained monomorphic ventricular tachycardia (VT) induced by programmed ventricular stimulation using up to 3 extrastimuli was evaluated in 133 consecutive survivors of acute myocardial infarction (AMI) at a mean interval of 1.8 +/- 1.1 months after onset. This was compared with hemodynamic and angiographic abnormalities shown by cardiac catheterization and ventricular ectopic activity detected by Holter monitoring. Sustained monomorphic VT was induced in 25 (19%) patients, sustained polymorphic VT in 11 (8%) patients, nonsustained monomorphic VT (greater than or equal to 10 beats) in 12 patients (9%) and nonsustained polymorphic VT in 9 patients (7%). Multivariate logistic regression analysis of clinical, angiographic, hemodynamic and electrocardiographic variables showed that the presence of a left ventricular aneurysm (p = 0.005) and Lown grade 4B ventricular ectopic activity (p less than 0.001) were independent predictors of inducibility of sustained monomorphic VT. During a mean follow-up of 21 +/- 13 months, there were 8 (6%) sudden cardiac deaths and 3 (2.3%) spontaneous occurrences of life-threatening sustained VT. The 2-year probability of freedom from sudden cardiac death or sustained ventricular tachyarrhythmias was 53 +/- 13% for patients with inducible sustained monomorphic VT, 70 +/- 10% for those with a left ventricular ejection fraction less than 40% and 58 +/- 13% for those with Lown grade 4B ventricular ectopic activity.(ABSTRACT TRUNCATED AT 250 WORDS)     

Spontaneous and inducible ventricular arrhythmias in a canine model of chronic heart failure: relation to haemodynamics and sympathoadrenergic activation.

The relationship between the incidence, frequency and complexity of spontaneous ventricular arrhythmias and the extent of haemodynamic compromise and sympathoadrenergic hyperactivity was evaluated in a canine model of chronic heart failure produced by multiple sequential intracoronary microembolizations. Ambulatory ECG Holter monitoring recorded during chronic heart failure in 18 dogs revealed spontaneous ventricular arrhythmias ranging from single ventricular premature beats (VPBs) to non-sustained episodes of ventricular tachycardia (VT). Single VPBs were present in 94% of dogs, couplets in 67%, triplets in 28% and spontaneous episodes of non-sustained VT in 33%. Dogs with > 28 VPBs.h-1 (n = 9) had a markedly higher plasma norepinephrine (PNE) concentration (1001 +/- 185 vs 561 +/- 31 pg.ml-1) (P < 0.03), and a higher pulmonary artery wedge pressure (PAWP) (18 +/- 2 vs 12 +/- 1 mmHg) (P < 0.03) than dogs with < or = 28 VPBs.h-1 (n = 9). Dogs that developed spontaneous episodes of VT also had significantly higher PNE levels (1119 +/- 247 pg.ml-1) compared to dogs that did not develop VT (612 +/- 64 pg.ml-1) (P < 0.02). Programmed ventricular stimulation performed in seven of 18 dogs resulted in the development of sustained monomorphic VT in three and ventricular fibrillation in three dogs each (43%, 43%). Dogs with inducible sustained monomorphic VT had a significantly higher number of ambient arrhythmias and higher PAWP compared to dogs that did not develop sustained VT. The observed complexity, frequency and incidence of spontaneous and inducible ventricular arrhythmias in this canine model are similar to those described in patients with chronic heart failure.