Signal-averaged electrocardiography: a new noninvasive test to identify patients at risk for ventricular arrhythmias

Signal-averaged electrocardiography (ECG) is a new noninvasive test for identifying patients at risk for ventricular arrhythmias. This computerized method of analyzing standard ECGs identifies particular microvolt-level signals called late potentials. Late potentials have been correlated with clinical ventricular tachycardia, are predictive of ventricular tachycardia inducibility at the time of electrophysiologic testing, and are predictive of arrhythmic events after myocardial infarction. In this review, we describe late potentials, the method of obtaining and processing the signal-averaged ECG, and clinical studies in various patient groups that have assessed the predictive value of the signal-averaged ECG for identification of patients at risk for subsequent ventricular arrhythmias.     

Magnetic Resonance Imaging and Signal-Averaged Electrocardiography in Patients with Repetitive Monomorphic Ventricular Tachycardia and Otherwise Normal Electrocardiogram

Early or localized forms of arrhythmogenic right ventricular dysplasia (ARVD) have been proposed as the arrhythmogenic substrate of repetitive monomorphic ventricular tachycardia (RMVT) originating in the right ventricular outflow tract in patients without any underlying cardiac abnormality on clinical examination and echocardiography. To further examine this hypothesis, magnetic resonance imaging (MRI) and signal-averaged electrocardiography (SAECG) were performed on 23 patients with RMVT and normal 12-lead standard ECG of conducted sinus beats. MRI was performed using ECG-gated turbo spin-echo images of the heart in order to detect signs of early or localized forms of ARVD, such as localized wall thickness reductions, signal intensity increase indicating adipose tissue infiltrates, and regional bulgings or aneurysms. MRI was normal in 22 (96%) of 23 study patients. In the remaining patient (4%), MRI demonstrated signal intensity increase in the intraventricular septum but not in the right ventricular outflow tract. Time-domain analysis of the SAECG was normal in 21 (91 %) of 23 patients and revealed ventricular late potentials in 2 study patients (9%). Frequency-domain analysis of the SAECG was normal in 22 (96%) of 23 patients and revealed ventricular late potentials in one study patient (4 %). We conclude that normal MRI findings of the heart and absence of ventricular late potentials in the SAECC in most patients with RMVT and otherwise normal ECG do not support the hypothesis that early or localized forms of ARVD create the arrhythmogenic substrate in the majority of these patients.     

Arrhythmogenic Right Ventricular Cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) has evolved from postmortem pathology at to a diagnosable clinical condition, and holds promise for definitive genetic diagnosis. Its prevalence is between 1/1,000 and 1/5,000, with 10% of deaths occurring before age 19 and 50% before age 35. When analyzed against age-specific norms, the electrocardiography (ECG) and signal-averaged ECG (SAECG) have moderate sensitivity for ARVC. Endomyocardial biopsy in young individuals with ARVC demonstrates fibrosis more frequently than fatty infiltration, and is convincing for the diagnosis in approximately 1/3 (often in patients who would not otherwise be diagnosed), but has a recognized complication rate of 2%. Newer technologies of magnetic resonance imaging and voltage mapping hold promise but require further assessment in young individuals suspected to have ARVC. Genetic diagnosis of one of several desmosomal mutations is positive in an approximately 50% of suspected patients, and may provide clues to the pathophysiology of the disease. Serial studies of myocardial function, ambulatory electrocardiography, and SAECG parameters may be useful in risk stratification of identified patients, although their applicability to genetically identified asymptomatic individuals has not been studied.     

Late Potentials and Arrhythmogenesis *

There are three current prognostic indicators of ventricular electrical instability. (1) categorization and siratification of sponlaneous ventricular arrhythmias from standard ECG recordings; (2) programmed electrical stimulation; (3) direct recording of delayed depolarization potentials, usually re/erred to as late potentials. Of the three, the latter offers a new and promising approach. Late potentials represent delayed activation potentials of diseased myocardial zones and may prove to be a strong independent marker of the propensity to develop reentrant ventricular arrhythmias and sudden cardiac electrical death. The problem in identifying late potentials on the body surface is that the signal is smaller than the electrical noise produced by various sources. Two different techniques have been utilized to improve the signal-to-noise ratio: first, signal averaging, which is applicable to regular repelifive electrocardiographic signals but cannot detect moment-to-moment dynamic changes in the signal; second, low-noise or high-resolution electrocardiography that utilizes spatial averaging techniques as well as other noise-reducing measures to record the late potentials on a beat-to-beat basis. This technique has the potential of directly identifying malignant “reentrant” versus benign “focal” ventricular rhythms. The present report discusses the electrophysiologic basis of late potentials and the clinical results of both signal-averaged and low-noise recordings for evaluation of ventricular electrical instability, particularly in patients with ischemic heart disease.     

Within- and Between-Patient Variation of the Signal-Averaged P Wave in Coronary Artery Disease

Objectives: To estimate interobserver, within-patient and between-patient variation of the signal-averaged P wave. To determine whether demographic, clinical, conventional ECG information, and coronary angiographic data are associated with the signal-averaged P wave duration in patients with documented coronary artery disease. Background: A prolonged signal-averaged P wave may indicate the presence of a substrate for atrial tachyarrhythmias and may predict subsequent development of atrial fibrillation. However, information on variation, reproducibility, and determinants of the signal-averaged P wave are sparse. Methods: One hundred ninety-three patients with angiographically documented coronary artery disease underwent two consecutive procedures of signal-averaging of P waves (SAECG1 and SAECG2). Interobserver, within-patient, and between-patient variation of the signal-averaged P wave was estimated (coefficient of variation: SD/mean). Multiple linear regression analysis was applied to identify parameters independently associated with signal-averaged P wave duration (SA-P). Atrial late potentials were considered if SA-P > 140 ms, and logistic regression analysis was applied to identify parameters associated with the presence of atrial late potentials. Results: The interobserver, within-patient, and between-patient coefficients of variation for the signal-averaged P wave duration were 7.5%, 6.0%, and 8.4%, respectively. The signal-averaged P wave duration correlated significantly with standard ECG P wave duration and height of the patient (r = 0.59). Forty-nine percent of the patients had atrial late potentials. P wave duration in the standard ECG correctly classified 73% (140/188) of the patients with respect to atrial late potential positivity or negativity. The sensitivity was 67% and the specificity was 78%. Agreement on the presence or absence of atrial late potentials between two observers was present in 71% (136/193) of the patients, and in 78% (151/193) between SAECG1 and SAECG2. Conclusions: The signal-averaged P wave has limited reproducibility in patients with coronary artery disease, and a normal or abnormal signal-averaged P wave can be predicted from the conventional ECG with high accuracy. It is recommended that the signal-averaged P wave be compared with the standard ECG P wave duration in follow-up studies with the aim of predicting atrial fibrillation.     

Prediction of Arrhythmic Events After Acute Myocardial Infarction Using Two Methods for Late Potentials Recording

One hundred consecutive patients recovering from an acute myocardiai infarction underwent, prior to home discharge, signal-averaged electrocardiography (ECG), left ventriculography. and 24-hour Holter ECG recording. The signal-averaged ECG was recorded and analyzed using two procedures: the orthogonal bipolar XYZ lead configuration with a bidirectional filter: and a precordial unipolar lead configuration with a uonrecursive digital filter. An abnormal signal-averaged ECG was seen in 40% of patients with the XYZ system and in 30% of patients in the precordial method, abnormal ejection fraction (< 40%) in 24% of patients and high grade ectopy activity in 22%. During the 24-month follow-up period, 12 patients (12%) had an arrhythmic event defined as either sudden death (11 patients) or sustained ventricular tachycardia (1 patient). Neither the signal-averaged ECG with the XYZ configuration, the abnormal ejection fraction, nor the high grade ectopy were able to statistically predict a higher arrhythmic event rate. The signal-averaged ECG with the precordial configuration was able to statistically predict a higher arrhythmic event rate, P < 0.03; odds ratio = 3.96. The combination of the orthogonal XYZ configuration signal-averaged ECG with the ejection fraction (P < 0.01, odds ralio = 7.33), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio = 6.17) was able to predict a higher arrhythmic event rate. The combination of the precordial configuration signal-averaged ECG with the ejection fraction (P < 0.002, odds ratio = 14.4), or with ejection fraction and Holter monitoring (P < 0.06. odds ratio =10) was able to better predict a higher arrhythmic event rate. The combination of a normal or abnormal signal-averaged ECG and ejection fraction gave a sensitivity, specificity, positive, or negative value prediction of arrhythmic events of 60%, 90.6%, 37.5%, and 96%, respectively. It must be emphasized that the number of arrhythmic events during the 2-year follow-up was small and further study is required to determine the true predictive value of each method for arrhythmic events.     

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.     

Endocardial Fragmented Electrogram and Prediction of Ventricular Tachycardia by Body Surface Signal-Averaged Electrocardiographic Mapping

Signal-averaged (SA) electrocardiography and SA electrocardiographic mapping were performed in 50 patients with old myocardial infarction, 19 of whom had left ventricular aneurysm and 11 of whom had clinical sustained ventricular tachycardia.The SA electrocardiogram and SA electrocardiographic mapping data were then compared with those obtained by endocardial catheter mapping in patients with or without fragmented electrograms, sustained ventricular tachycardia, and ventricular aneurysm. Compared to SA electrocardiography, the SA map correlates with sustained VT with improved sensitivity but decreased specificity. However, SA electrocar diographic mapping had the advantage of displaying the extent of the body surface area that was positive for late potentials. In addition, the site of the longest endocardial fragmented electrogram could be predicted by SA electrocardiographic mapping, suggesting that this technique deserves wider clinical application.signal-averaged electrocardiography, signal-averaged electrocardiographic mapping, late potential, sustained ventricular tachycardia     

Ventricular Arrhythmia Factors in Mitral Valve Prolapse

To assess tbe prevalence of ventricular arrhythmias and late potentials (LPs) in mitral valve prolapse (MVP) and to identify clinical, ECG, and echocardiographic markers of spontaneous ventricular arrhythmias, we studied 58 consecutive patients (mean age 46.6 ± 17.8 years; 29 males, 29 females) with MVP diagnosed by echocardiography. Patients underwent ambulatory ECG recording (n = 58), exercise stress test (n = 56), signal-averaged ECG (n = 58), and programmed ventricular stimulation (n = 52). Ten patients (17.2%) had spontaneous nonsustained ventricular tachycardia (NSVT), 26 patients (44.8%) had premature ventricular contractions (PVGs), Lown grade ≥ 3 during 24-hour EGG, and 19 had Lown grade ≥ 3 PVCs during exercise stress test; 13 patients had LPs (22.4%). We provoked sustained VT in one case and NSVT in ten cases. Patients with complex ventricular arrhythmias during 24-hour EGG and exercise stress test were older and more often had mitral regurgitation. There was a statistical correlation between the presence of LPs and spontaneous VT (46.1 % vs 8.9%; P < 0.005) and induced ventricular arrhythmias (50% vs 12.8%; P < 0.005). No correlation was found between spontaneous ventricular arrhythmias and thickness or posterior displacement of the mitral valve. In conclusion, complex ventricular arrhythmia (especially VT) and LPs are frequent in MVP. Patient age and mitral regurgitation seem to be determinant factors of complex ventricular arrhythmias in MVP. On signal-averaged EGG, absence of LPs seems to be a good additional marker to identify MVP patients without spontaneous VT. On the other hand, programmed ventricular stimulation does not appear valuable in determining a MVP subgroup with a high risk of ventricular arrhythmias.     

Modification of Late Potentials by Intracoronary Ethanol Infusion

Antiarrhythmic drugs have no consistent effects on the signal-averaged electrocardiogram (ECG) while successful surgical ablation of ventricular tachycardia is known to abolish late potentials. Ten patients with prior myocardial infarction had successful ablation of recurrent sustained ventricular tachycardia by selective ethanol infusion into a small coronary vessel supplying the tachycardia origin. Signal-averaged ECGs were performed before and after initially successful ablation in patients without pacemaker dependence or infra-ventricular conduction delay to assess the effects on late potentials and to determine if the signal-averaged EGG could predict ventricular tachycardia recurrence. Only four of ten patients were eligible for study and all four had late potentials prior to ethanol ablation. Late potentials were abolished in one patient who has not had an arrhythmia recurrence in 25 months. One patient with sudden death and another patient with ventricular tachycardia recurrence had persistent late potentials post procedure that were modified by a reduction in terminal voltage and lengthening of terminal low amplitude signal. The fourth patient who receives chronic amiodarone had no arrhythmia recurrence in spite of persistent but modified late potentials. Thus, the abolition of late potentials after ethanol ablation may predict freedom from arrhythmia recurrence.     

Diagnosis and treatment of idiopathic ventricular tachycardia

Idiopathic ventricular tachycardia in patients with an anatomically normal heart is a distinct entity whose management and prognosis differs from ventricular tachycardia associated with structural heart disease. The tachycardia's QRS morphology on surface electrocardiogram (ECG) predicts the site of origin and is commonly classified as right ventricular tachycardia or left ventricular tachycardia. The tachycardia is further characterized by clinical features such as repetitive monomorphic ventricular tachycardia (VT), paroxysmal sustained VT, or catecholamine dependent VT. The responsiveness of VT to adenosine or verapamil is useful in differentiating the mechanism, which may be reentry or triggered activity.Patients generally tolerate the tachycardia but may present with dizziness, syncope, or palpitations. Sudden cardiac death is rare in this patient population. Patient work-up should include 12-lead ECG, signal-averaged ECG, ambulatory ECG recording, stress testing, and tests to rule out structural heart disease such as echocardiography, cardiac angiography, endomyocardial biopsy, or magnetic resonance imaging. Treatment options include pharmacotherapy or catheter ablation. Although the prognosis of these patients remains excellent, they should continue to have periodic cardiac follow-up to rule out latent progressive heart disease such as arrhythmogenic right ventricular dysplasia or cardiomyopathy or other forms of cardiomyopathies.     

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.     

Prevalence of cardiomyopathy in asymptomatic patients with left bundle branch block referred for cardiovascular magnetic resonance imaging

The diagnostic evaluation of patients with isolated left bundle branch block (LBBB) is challenging due to limitations of several non-invasive tests. Our aim was to evaluate the diagnostic value of cardiovascular magnetic resonance (CMR) in asymptomatic patients with LBBB. Sixty-one asymptomatic patients with complete LBBB who were referred for CMR from January 2005 to November 2010 were identified. 29 patients (18 men) had normal echocardiograms (echo) whereas 25 (18 men) had abnormal findings on echo. Six had no echo and one had poor echo windows, and these patients were excluded from further analysis. Patients with cardiac symptoms or known coronary artery disease at the time of referral were also excluded. Of the 29 patients with normal echo, 9 (31%) were found to have pathological findings on CMR. The most common abnormalities were dilated cardiomyopathy-DCM (n = 6, 21%) followed by left ventricular hypertrophy (n = 2, 7%). Of the 25 patients who had an abnormal echo, CMR confirmed the diagnosis in 19 (76%) and provided clinically relevant additional information in 13 (52%) subjects. Of these 13 patients, 9 (69%) had characteristic patterns of myocardial late gadolinium enhancement (8 mid-wall and 1 patchy distribution consistent with DCM and cardiac sarcoid, respectively). CMR detects sub-clinical cardiomyopathy in a third of asymptomatic patients with LBBB despite normal echocardiograms. In those with abnormal echocardiograms, CMR provides additional clinically relevant information in over 50% of patients, including a high prevalence of mid-wall fibrosis in patients with impaired left ventricular function. These findings support the use of CMR as a valuable adjunct to conventional investigations in asymptomatic LBBB.     

Characteristics of arrhythmia and late ventricular potentials in patients with cardiological syndrome X

AIM: A comparative study of late ventricular potentials (LVP) in patients with cardiological syndrome X (SX) and stenotic atherosclerosis of coronary arteries (ACA) as well as their relations with arrhythmia, cardiac contractility, lipid metabolism and morphological characteristics of the myocardium. MATERIAL AND METHODS: The examination of 52 SX and 77 ACA patients as well as 17 healthy subjects included coronaroventriculography, bicycle exercise, 24-h ECG monitoring, echocardiography, signal-averaged high-resolution (SAHR) ECG, investigation of blood lipoproteins. Endomyocardial biopsy was made in 5 ACA and 5 SX patients. RESULTS: No differences were registered between SX and ACA patients by frequency and severity of arrhythmic episodes, percentage of patients with registered LVP, quantitative parameters of SAHR ECG. Frequency of high-gradation ventricular arrhythmia episodes was significantly higher in SX and ACA patients with LVP than such patients free of LVP. SX patients had correlation between parameters of SAHR ECG, myocardial contractility and lipid metabolism. Foci of diffuse cardiosclerosis are most probable anatomic substrate of LVP. CONCLUSION: The risk of prognostically unfavourable high-gradation ventricular arrhythmia episodes in SX and ACA patients is the same. LVP may predict severe ventricular arrhythmia episodes both in SX and ACA patients.     

Ventricular arrhythmias and cardiac late potentials inpatients with acute coronary syndrome after reperfusion therapy

The prognostic value of ventricular late potentials (VLP) and the character of rhythm disturbance were studied in 64 patients with acute coronary syndrome. 8 hours after system thrombolysis procedure VLP rate increased from 68.6% up to 85.7%. In all cases of reperfusion arrhythmia deterioration of signal-averaged ECG (SAECG) parameters and VLP were observed. Within the hospital treatment period VLP rate in the 1st group (patients receiving thrombolytic therapy) was lower than in the 2nd (no thrombolytic therapy). In the 1st group VLP was observed in 31.4% of the patients on the 10th day and in 11.4% by the end of hospital treatment; in the 2nd group--in 48.3% and 41.4% of the patients, respectively (p < 0.05). Administration of beta-adrenoblockers in both groups allowed improvement of SAECG parameters and cardiac rhythm variability.     

Study of Late Potentials and Ventricular Arrhythmias in Hypertensive Patients with Normal Electrocardiograms

Introduction: Although an increase in the occurrence of ventricular arrhythmias has been observed in hypertensive patients, some basic questions remain unresolved regarding the prevalence and the pathophysiology of these arrhythmias. The basic aims of this study were as follows: (1) to examine the incidence and severity of ventricular arrhythmias in a substantial number of hypertensive patients without electrocardiographic indications of hypertrophy; and (2) to examine the correlation between late potentials, hypertrophy, and ventricular arrhythmias in these patients. Materials and Methods: We studied 78 consecutive patients (31 men, 47 women), aged 60.5 ± 7.8 years, with a history of hypertension but a normal electrocardiogram. All patients had an echocardiographic study, 24-hour ambulatory monitoring, exercise test, and signal-averaged electrocardiogram. The latter was analyzed using a 40-to 250-Hz filter and with a noise level ± 0.3 μV. Results: Of the 78 patients studied, 21 (26.9%) had severe ventricular arrhythmias, while 57 (73.1 %) had either no ventricular ectopics or sporadic isolated ventricular extrasystoles. Left ventricular hypertrophy, defined by echocardiography, was found in 58 patients (74.3%), of which 16 (27.58%) had severe ventricular arrhythmias. Five (25%) of the 20 patients without hypertrophy also had severe ventricular arrhythmias (P = NS). Ventricular late potentials were recorded in 19 (24.5%) of the 78 patients. Of these, 11 (57.89%) had severe arrhythmias, while of the 59 patients without late potentials 10 (16.94%) had severe ventricular ectopic activity. Conclusions: In hypertensive patients without electrocardiographic signs of hypertrophy, the higher prevalence of ventricular arrhythmias does not appear to be related to left ventricular hypertrophy but is correlated with the existence of ventricular late potentials.     

Loss of Late Potentials After Radiofrequency Catheter Ablation of Recurrent Ventricular Tachycardia in a Patient with Right Bundle Branch Block

The case of a patient with a history of myocardial infarction and recurrent ventricular tachycardia undergoing attempted radiofrequency catheter ahlation with loss of late potentials is described. Prior to energy delivery fractionated, late activation could be found using the signal-averaged ECC despite the presence of a right bundle branch block. After successful catheter ablation, the clinical ventricular tachycardia was no longer inducible and the signal-averaged ECG, recorded the next day, showed marked changes indicating loss of late potentials. Our report emphasizes the possibility of late potential recordings despite the presence of bundle branch block.     

Time-Domain Signal-Averaged Electrocardiogram in Nonischemic Ventricular Tachycardia

The prevalence of late ventricular potentials (LVPs) detected by signal averaged ECG (SAECG) is variable in nonischemic heart diseases. In idiopathic dilated cardiomyopathy, the prevalence increases from about 25% to 70%-90% in cases of spontaneous sustained ventricular tachycardia (VT), is not significantly correlated with hemodynamic and Holter data, and has a good positive predictive value for induced and spontaneous sustained VT. However, its predictive value for cardiac death has not been established. In primary hypertrophic cardiomyopathy, LVPs are rare (about 10%), not correlated to hemodynamic data, enhanced in cases of spontaneous sustained VT (up to 77%), and have a good predictive value of induced VT. LVP-SAECG are frequent in arrhythmogenic right ventricular dysplasia (ARVD) (70%-80%). They can identify patients with VT and an unapparent or limited form of this disease, or ARVD with few ventricular arrhythmias. The prevalence (26%-37%) of LVPs in mitral valve prolapse is clearly higher than in normal individuals or in other valvular diseases and is enhanced in cases of spontaneous and induced VT. Its significance remains speculative. After surgical repair of tetralogy of Fallot, LVPs can identify a group of patients with higher probability of induced and spontaneous risk of VT. The usefulness and significance of LVPs in other nonischemic cardiac diseases have not to date been established. In "true" idiopathic VT, without proved structural cardiac disease, the prevalence of LVPs does not exceed that observed in normal individuals (0%-5%), but in "apparent" idiopathic VT the prevalence of LVPs rises to 20%-40%. In these latter cases more invasive techniques must be used to discover a limited form of myocardiopathy.     

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.     

Correlation between ECG abnormalities and cardiac parameters in highly trained asymptomatic male endurance athletes: evaluation using cardiac magnetic resonance imaging

Intensive endurance training can induce abnormal ECG patterns at rest. These alterations are differentiated into minor, mildly or distinctly abnormal ECG patterns. Echocardiographic data imply a correlation between the extent of these alterations and cardiac parameters like cardiac volume or wall thickness. In comparison to echocardiography, cardiac magnetic resonance imaging (MRI) is characterized by high reproducibility and accuracy. The aim of this study was to investigate the correlation between ECG alterations and cardiac parameters in highly trained asymptomatic male endurance athletes as assessed using cardiac MRI. Forty-five asymptomatic male endurance athletes (mean age 40 ± 8.9 years., range 19–59 years., 13 ± 5 h of training per week) underwent a cardiac MRI examination in addition to a resting ECG. Based on the ECG patterns at rest, the athletes were divided into groups with normal or minor (group 1) and mild or distinct (group 2) alterations. Steady-state free-precession cine MRI was used to calculate left and right ventricular end-diastolic volume, end-systolic volume, stroke volume, ejection fraction, and myocardial mass (MM). Late enhancement imaging was used to exclude structural alterations or myocardial scarring. Athletes in group 1 and 2 did not differ significantly in terms of age, height, body weight, body mass index or hours of training per week. Athletes with mildly or distinctly abnormal ECG patterns showed a significantly higher MM than athletes with minor ECG alterations at rest or normal resting ECG values (156.4 ± 18.4 g vs. 140.5 ± 20.0 g; p = 0.0103). The differences persisted when the values were corrected for body surface area (80.0 ± 7.4 g/m² vs. 73.4 ± 8.3 g; p = 0.0093). All other assessed cardiac parameters did not differ between the two groups. Pathological myocardial enhancement was detected only in one patient with a minor abnormal ECG. Male asymptomatic endurance athletes with mildly or distinctly abnormal ECG patterns at rest are characterized by a higher myocardial mass than comparable athletes with minor alterations or normal ECG at rest. Thus, the extent of ECG-abnormalities seems to be mainly the result of an increase in myocardial mass. Additionally, the absence of mild or distinct ECG alterations does not exclude the presence of pathological late gadolinium enhancement.