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The relationship between structural and electrical remodeling in the heart, particularly after long-standing endurance training, remains unclear. Signal-averaged electrocardiogram (SAECG) may provide a more sensitive method to evaluate cardiac remodeling than a 12-lead electrocardiogram (ECG). Accurate measures of electrical function (SAECG filtered QRS duration (fQRSd) and late potentials (LP) and left-ventricular (LV) mass (cardiac magnetic resonance, CMR) can allow an assessment of structural remodeling and QRS prolongation. Endurance athletes (45-65 yr old,10 yr of endurance sport), screened to exclude cardiac disease, had standardized 12-lead ECG, SAECG, resting echocardiogram (ECHO), and CMR performed. SAECG fQRSd was correlated with QRS duration on the 12-lead ECG, and ECHO and CMR-derived LV mass. Participants (

Background Patients with serious mental illness (SMI) have an increased risk of sudden death. Higher rates of signal-averaged electrocardiogram (SAECG) abnormal late potentials (LP), which may be a predictor of sudden death risk, have been shown in patients with schizophrenia. We aimed to assess the prevalence and predictors of electrocardiograph (ECG) and SAECG abnormalities in a mixed SMI population. Methods Consecutive consenting inpatients with SMI had 12-lead ECG and SAECG recorded in addition to demographics, diagnoses and medications. Standard criteria for abnormal SAECG were applied. Multivariate regression analysis was performed to determine predictors of SAECG abnormalities including diagnoses, body mass index, ECG parameters, psychotropic medication use, and medications associated with Long QT or Brugada syndromes. Results Eighty (80) patients, 49% male, mean age 39±17 years were included. SAECG criteria abnormality for 1, 2 or 3 criteria were seen in 19, 3 and 5 cases (34% in total) respectively. Early repolarisation pattern was seen in 19% of patients. SAECG abnormality was associated with male gender (OR 7.3; 95% CI 2.3–23.4), and schizophrenia/schizoaffective disorder diagnosis (OR 7.4; 95% CI 1.9–29.0), but not with medication type or dose. Conclusions In the mixed SMI population studied, there was a high rate of SAECG-detected late potentials (34%) and early repolarisation pattern (19%). Schizophrenia/schizoaffective disorder diagnosis was the strongest multivariate predictor identified. Further studies are needed to define the mechanism and significance of these cardiac abnormalities in SMI patients.

Background Although some post myocardial infarction (post‐MI) and dilated cardiomyopathy (DCM) patients with mid‐range ejection fraction heart failure (HFmrEF/40%‐49%) face an increased risk for arrhythmic sudden cardiac death (SCD), current guidelines do not recommend an implantable cardiac defibrilator (ICD). We risk stratified hospitalized HFmrEF patients for SCD with a combined non‐invasive risk factors (NIRFs) guiding to programmed ventricular stimulation (PVS) two‐step approach. Methods Forty‐eight patients (male = 83%, age = 64 ± 14 years, LVEF = 45 ± 5%, CAD = 69%, DCM = 31%) underwent a NIRFs screening first‐step with electrocardiogram (ECG), SAECG, Echocardiography and 24‐hour ambulatory ECG (AECG). Thirty‐two patients with presence of one of three NIRFs (SAECG ≥ 2 positive criteria for late potentials, ventricular premature beats ≥ 240/24 hours, and non‐sustained ventricular tachycardia [VT] episode ≥ 1/24 hours) were further investigated with PVS. Patients were classified as either low risk (Group 1, n = 16, NIRFs−), moderate risk (Group 2, n = 18, NIRFs+/PVS−), and high risk (Group 3, n = 14, NIRFs+/PVS+). All in Group 3 received an ICD. Results After 41 ± 18 months, 9 of 48 patients, experienced the major arrhythmic event (MAE) endpoint (clinical VT/fibrillation = 3, appropriate ICD activation = 6). The endpoint occurred more frequently in Group 3 (7/14, 50%) than in Groups 1 and 2 (2/34, 5.8%). Logistic regression model adjusted for PVS, age, and LVEF revealed that PVS was an independent MAE predictor (OR: 21.152, 95% CI: 2.618‐170.887, P = .004). Kaplan‐Meier curves diverged significantly (log rank, P, We applied a combined non‐invasive risk factors (NIRFs) leading to programmed ventricular stimulation (PVS), a two‐step risk stratification algorithm, to detect the HFmrEF/40‐49% patients at risk for major arrhythmic events.This combined two‐step approach efficiently detected the patients at increased arrhythmic risk.

Background The majority of beta thalassemia major (β‐TM) patients suffer from cardiac disease, while a significant proportion of them die suddenly. Twelve‐lead and signal‐averaged electrocardiography (SAECG) are simple, inexpensive, readily available tools for identifying an unfavorable arrhythmiological substrate by detecting the presence of arrhythmias, conduction abnormalities, and late potentials (LPs) in these patients. Methods A total of 47 β‐TM patients and 30 healthy controls were submitted to 12‐lead and signal‐averaged electrocardiography. Basic electrocardiographic parameters and prevalence of LPs were recorded. Basic echocardiographic parameters were estimated by transthoracic echocardiography. T2* was calculated by cardiac magnetic resonance imaging wherever available. Results β‐TM patients demonstrated a more prolonged PR interval (167.74 msec vs 147.07 msec) (P = .043), a higher prevalence of PR prolongation (21.05% vs 0%) (P = .013), and a higher prevalence of LPs (18/47, 38.3% vs 2/30, 6.7%) (P = .002) compared with controls. The prevalence of atrial fibrillation among b‐TM patients was estimated at 10.64%. Patients had also greater E/e′ ratio (8.35, SD = 2.2 vs 7, SD = 2.07) (P = .012) and LAVI (30.7 mL/m2, SD = 8.76 vs 24.6 mL/m2, SD = 6.57) (P = .002) than controls. Regression analysis showed that QTc and LAVI could correctly predict the presence of LPs in the 80.9% of the patients. Conclusions β‐TM patients have a higher prevalence of a prolonged PR interval, atrial fibrillation, and LPs. Twelve‐lead and SAECG performance was feasible in all subjects and constitutes a readily available tool for assessing myocardial electrophysiological alterations in this patient group., A cross‐sectional study considering the value of conventional and signal‐averaged electrocardiography in assessment of the arrhythmiological substrate of β‐thalassemia patients.

Atrial fibrillation (AF) is the most common cardiac arrhythmia. Pharmacologic and non-pharmacologic rhythm control strategies impact on AF-related symptoms, while leaving largely unaffected the risk of stroke. Moreover, up to 20% of AF patients are asymptomatic during paroxysmal relapses of arrhythmia, thus underlying the need for early markers to identify at-risk patients and prevent cerebrovascular accidents. Indeed, non-invasive assessment of pre-clinical substrate changes that predispose to AF could provide early identification of at-risk patients and allow for tailored care paths. ECG-derived P wave analysis is a simple-to-use and inexpensive tool that has been successfully employed to detect AF-associated structural and functional atrial changes. Beyond standard electrocardiographic techniques, high resolution signal averaged electrocardiography (SAECG), by recording microvolt amplitude atrial signals, allows more accurate analysis of the P wave and possibly AF risk stratification. This review focuses on the evidence that support P wave analysis to assess AF substrates, predict arrhythmia relapses and guide rhythm-control interventions.

Aims Arrhythmogenic right ventricular cardiomyopathy (ARVC) is diagnosed by a complex set of clinical tests as per 2010 Task Force Criteria (TFC). Avoiding misdiagnosis is crucial to prevent sudden cardiac death as well as unnecessary implantable cardioverter-defibrillator implantations. This study aims to validate the overall performance of the TFC in a real-world cohort of patients referred for ARVC evaluation. Methods and results We included patients consecutively referred to our centres for ARVC evaluation. Patients were diagnosed by consensus of three independent clinical experts. Using this as a reference standard, diagnostic performance was measured for each individual criterion as well as the overall TFC classification. Of 407 evaluated patients (age 38 ± 17 years, 51% male), the expert panel diagnosed 66 (16%) with ARVC. The clinically observed TFC was false negative in 7/66 (11%) patients and false positive in 10/69 (14%) patients. Idiopathic outflow tract ventricular tachycardia was the most common alternative diagnosis. While the TFC performed well overall (sensitivity and specificity 92%), signal-averaged electrocardiogram (SAECG, P = 0.43), and several family history criteria (P ≥ 0.17) failed to discriminate. Eliminating these criteria reduced false positives without increasing false negatives (net reclassification improvement 4.3%, P = 0.019). Furthermore, all ARVC patients met at least one electrocardiogram (ECG) or arrhythmia criterion (sensitivity 100%). Conclusion The TFC perform well but are complex and can lead to misdiagnosis. Simplification by eliminating SAECG and several family history criteria improves diagnostic accuracy. Arrhythmogenic right ventricular cardiomyopathy can be ruled out using ECG and arrhythmia criteria alone, hence these tests may serve as a first-line screening strategy among at-risk individuals.

Signal-averaged electrocardiography (SAECG) has been known to be useful for prediction of lethal ventricular arrhythmias (VA). However, this technique has limitations in patients with intraventricular conduction disturbance (IVCD), which is common in cardiac sarcoidosis (CS). Meanwhile, wavelet-transformed ECG (WTECG) has been reported to be useful for detecting arrhythmogenic substrate hidden within QRS complex. The objective of this study was to assess the utility of WTECG for detecting arrhythmogenic substrate in patients with CS. Forty-four CS patients including 18 patients with VA were retrospectively investigated. The parameters on the signal-averaged electrocardiography (SAECG) and the power of frequency components on WTECG were compared between VA group and non-VA group. Eighteen patients have VA (VT: n = 17, VF: n = 1). LP were detected in 17 in VA group and 24 in non-VA group. WTECG showed that high-frequency components (HFC; 80-150 Hz) were developed in VA group. Peak power value at 150 Hz (P150) was significantly higher in VA group than that in non-VA group (442.9 ± 160.2 vs 316.7 ± 100.8, p = 0.006). The receiver operating characteristic (ROC) curve analysis showed an optimal cutoff point of 336 of P150 for detecting patients with VA, with 82.4% sensitivity, 61.5% specificity, and area under the curve of 0.74 (95% confidence interval [CI] 0.59-0.89). WTECG may be useful for detecting CS patients who are prone to VA.

Purpose Signal-averaged ECG (SAECG) can detect inhomogeneous myocardial conduction in patients presenting with ventricular tachycardia (VT) after myocardial infarction. Radiofrequency ablation (RFCA) aims at elimination of the endocardial late potentials and non-inducibility of VT. Previously, we demonstrated that abnormal SAECG at baseline can return to normal after a successful VT ablation. The present research investigates the post-ablation changes in SAECG after RFCA of VT and their relation to the procedural long-term outcomes. Methods Thirty-three patients (31 male; age 68 ± 9 years; EF 36 ± 12%) with ischemic VT were prospectively enrolled to receive RFCA. One VT (range 1–7) per patient was ablated using substrate-guided RFCA and complete success was achieved in 28 (85%) cases. SAECG was performed before (t1), immediately after (t2), and at least 6 months (t3) after the RFCA. Results After RFCA, the amount of patients showing abnormal SAECG decreased from 82% initially (t1) to 57.6% post-interventionally (t2); P = 0.008; and remained unchanged thereafter in 57% (t3). Patients who experienced VT recurrence (VT+) during the follow-up period had broader averaged QRS (t2): (VT+) 150 ± 26 vs. (VT−) 129 ± 21 ms; P = 0.015, as well as longer LAS40 (t2): (VT+) 60 ± 26 vs. (VT−) 43 ± 18 ms; P = 0.03. Abnormal SAECG (t2) was a strong predictor for VT recurrence: HR 5.4; 95% CI 1.5–21. SAECG detected more late potentials in patients with inferior than in those with anterior scars: 95% vs. 58%; P = 0.016. Conclusions RFCA of VT in the left ventricle can improve an abnormal SAECG in some patients after myocardial infarction. Normal SAECG after RFCA of VT is associated with a lower risk for VT recurrence and death.

BACKGROUND: Late potentials (LPs) identified on the signal averaged electrocardiogram (SAECG) are a marker for an increased risk of arrhythmias in Brugada syndrome (BrS). Procainamide is a sodium channel blocker used to diagnose BrS. The effects of Procainamide on the SAECG in those with BrS and the significance of Procainamide-induced LPs are unknown.METHODS: Procainamide provocation was performed for suspected BrS with 12-lead and SAECG pre- and post-infusion. Filtered QRS duration (fQRSd), duration of low amplitude signals RESULTS: Data from 150 patients were included in the analysis (mean age 44.5 years, 109 males). Procainamide increased fQRSd (Pre 118.8 ± 10.5 ms, post 121.2 ± 10.2 ms, p < 0.001) and LAS40 (Pre 38.7 ± 9.8 ms, post 40.2 ± 10.5 ms, p = 0.005) and decreased RMS40 (Pre 24.6 ± 12 ms, post 22.8 ± 12 ms, p = 0.002). LPs were present in 68/150 (45%) at baseline. Fifteen patients with negative baseline SAECGs had LPs unmasked by Procainamide, but six patients had LPs at baseline that were no longer present following Procainamide. Comparing those with normal hearts (n = 48) to those with a final diagnosis of BrS (n = 38), Procainamide prolonged fQRSd to a greater extent in those with BrS. Comparing those with Procainamide-induced LPs to those with no LPs at any time did not highlight any aspect of phenotype and did not correlate with a history of ventricular arrhythmias.CONCLUSIONS: Procainamide influences the SAECG, provoking LPs in a small proportion of patients. However, there is no evidence that Procainamide-induced LPs provide additional diagnostic information or aid risk stratification.

Introduction Brugada syndrome (BS) is a relevant cause of sudden death in individuals without structural heart disease. The accuracy of the available methods for risk stratification is very limited and the investigation of new methodologies to improve the identification of patients at risk is under intensive investigation. Recently the pathophysiological relevance of anomalous, fragmented and prolonged electrograms on the epicardial surface of the right ventricular outflow tract (RVOT) has been described. Therefore, the study of signal-averaged ECG (SA-ECG) has become attractive since it may allow the non-invasive evaluation of these electrical anomalies. In order to maximize the detection capacity and to focus the evaluation in the RVOT, we developed an alternative methodology of electrode positioning directed to this area of interest. Purpose To characterize the study of late potentials (LP) by SA-ECG in patients with SB and to evaluate its association with the occurrence of arrhythmia events. Methods Prospective single centre study of patients (pts) with BS. LP were evaluated by SA-ECG with determination of the total filtered QRS duration (fQRS), root mean square voltage of the 40 ms terminal portion of the QRS (RMS40) and duration of the low amplitude electric potential component (40 microV) of the terminal portion of the QRS (LAS40) in conventional and modified leads (addressed to RVOT). The association of LP with the risk of definite malignant dysrhythmias due to sudden death, ventricular fibrillation, ventricular tachycardia or appropriate shock of the implantable cardioverter defibrillator (ICD) was evaluated and the acuity of the prognostic stratification was determined by the area under the receiver operator characteristic curve (ROC). Results A total of 76 pts (69.7% men, age 48±12 years) were studied, of which 33 had a spontaneous type 1 pattern and 43 had a type 1 pattern induced by flecainide. During a median follow-up of 1.6 years, 13 pts (17.1%) had symptoms potentially related to BS and 6 (10.5%) had malignant arrhythmias [including two pts who suffered sudden death (2.6%). The pts who had malignant dysrhythmias presented higher values of fQRS (125±23 vs. 108±18, p=0.046) and LAS40 (54±13 vs. 40±11, p=0.014), and lower values of RMS40 only in the modified leads (11±5 vs. 22±19, p=0.041). The parameters of the SA-ECG were significant prognostic predictors. The acuity of each of the parameteres alone was moderate and the parameters that were identified as more powerful predictors of risk were those derived from the modified leads (Figure). Conclusion The LP evaluated by SA-ECG may be relevant in the prognostic stratification of patients with BS, since it seems to be associated with the risk of malignant ventricular arrhythmias. Funding Acknowledgement Type of funding sources: None.

Introduction: Postoperative atrial fibrillation (POAF) is common after cardiac surgery and associated with increased hospital length of stay, patient morbidity and mortality. We aimed to identify factors associated with POAF and evaluate the accuracy of available POAF prediction models. Methods: We screened articles from Ovid MEDLINE® and PubMed Central® (PMC) and included studies that evaluated risk factors associated with POAF or studies that designed or validated POAF prediction models. We only included studies in cardiac surgical patients with sample size n ⩾ 50 and a POAF outcome group ⩾20. We summarised factors that were associated with POAF and assessed prediction model performance by reviewing reported calibration and discriminative ability. Results: We reviewed 232 studies. Of these, 142 fulfilled the inclusion criteria. Age was frequently found to be associated with POAF, while most other variables showed contradictory findings, or were assessed in few studies. Overall, 15 studies specifically developed and/or validated 12 prediction models. Of these, all showed poor discrimination or absent calibration in predicting POAF in externally validated cohorts. Conclusions: Except for age, reporting of factors associated with POAF is inconsistent and often contradictory. Prediction models have low discrimination, missing calibration statistics, are at risk of bias and show limited clinical applicability. This suggests the need for studies that prospectively collect AF relevant data in large cohorts and then proceed to validate findings in external data sets.

Considering the importance of ventricular arrhythmias in the prediction of sudden cardiac death in chronic Chagas heart disease, the aim of the present study was to associate late potentials observed in the signal-averaged electrocardiogram (SAECG) with either non-sustained ventricular tachycardia in the 24-hour Holter monitoring or reduced left ventricular ejection fraction in the 2-dimension echocardiogram.This was a retrospective transversal study. The medical charts of 49 patients with chronic Chagas heart disease that underwent 24-hour Holter monitoring at our institution from September 2012 to December 2015 were reviewed. In the univariate analysis, variables associated with SAECG at a p value0.05 were entered a multivariate stepwise logistic regression analysis through the model forward. A p value0.05 was considered to have statistical significance.In the univariate analysis, right bundle branch block, left atrial diameter, left ventricular systolic diameter, and left ventricular ejection fraction were associated with late potential in the SAECG. In the multivariate analysis, however, right bundle branch block and left atrial diameter were retained as independent predictors of late potentials in the SAECG.Neither ventricular arrhythmias in the 24-Holter monitoring nor reduced left ventricular ejection fraction in the 2-D echocardiogram were associated with late potentials in the SAECG of patients with chronic Chagas heart disease.

Atrial arrhythmias occur at a higher than expected prevalence amongst endurance athletes. Few studies have examined both atrial structure and arrhythmias in middle-aged endurance athletes. We examined the relationship between P-wave duration, atrial dimensions, and the presence of atrial ectopy in long-standing, middle-aged endurance athletes.Middle-aged athletes with a minimum of 10 years of competitive endurance sport history and no history of structural heart disease or clinical atrial arrhythmias, had 12-lead ECGs to assess P-wave duration, signal-averaged ECGs (SAECG) to assess filtered P-wave duration, a 24 h Holter monitor to assess atrial ectopy, and echocardiography and cardiac magnetic resonance imaging to assess atrial structural characteristics.Amongst endurance athletes (n = 104; mean age = 54 ± 5 years; 63% male), filtered P-wave duration on SAECG was correlated with P-wave duration on 12-lead ECG (r = 0.36, p, 0.0001), as well as with larger CMR-derived RA areas (r = 0.30, p = 0.01) and volumes (r = 0.24, p 0.05). There was no correlation between filtered P-wave duration and any LA measures on imaging (p 0.05). There was no correlation between the incidence of atrial ectopy (premature atrial contractions or atrial tachycardia) and any electrocardiographic or structural measures.Longer filtered P-wave duration was associated with larger RA areas and volumes, without an increase in atrial ectopy.

Introduction Several noninvasive risk factors for ventricular arrhythmias have been described in postmyocardial infarction (MI) patients, whose relationships with scar characteristics and modifications by ablation are unknown. Methods Twenty-two patients with previous MI referred for ventricular tachycardia ablation were prospectively included. ECG, heart rate variability (HRV), signal-averaged ECG (SA-ECG), and T wave alternans (TWA) were performed before and after radiofrequency ablation. Scar areas were correlated to preablation parameters. Pre and postablation parameters were furthermore compared. Results Left ventricular ejection fraction and some spectral and time-domain HRV parameters were significantly correlated to the scar areas. QRS duration was larger after vs before ablation (120 ± 29 vs 105 ± 22 msec, P = .01). No significant modification in time or spectral domain of HRV was observed. There was no significant change in TWA and SA-ECG before and after ablation. Borderline decreases in quantitative TWA parameters were noted in patients with positive TWA and successful ablation procedure. Conclusion Some noninvasive risk factors were linked to the scar areas, but few were significantly modified after ablation. Larger populations are needed to demonstrate significant differences or correlations.

Introduction While cardiac sarcoidosis (CS) carries a risk of ventricular arrhythmias (VAs) and sudden cardiac death (SCD), risk stratification of patients with CS and preserved left ventricular/right ventricular (LV/RV) systolic function remains challenging. We sought to evaluate the role of electrophysiologic testing and programmed electrical stimulation of the ventricle (EPS) in patients with suspected CS with preserved ventricular function. Methods One hundred twenty consecutive patients with biopsy-proven extracardiac sarcoidosis and preserved LV/RV systolic function underwent EPS. All patients had either probable CS defined by an abnormal cardiac positron emission tomography or cardiac magnetic resonance imaging, or possible CS with normal advanced imaging but abnormal echocardiogram (ECG), SAECG, Holter, or clinical factors. Patients were followed for 4.5 ± 2.6 years for SCD and VAs. Results Seven of 120 patients (6%) had inducible ventricular tachycardia (VT) with EPS and received an implantable cardioverter defibrillator (ICD). Three patients (43%) with positive EPS later had ICD therapies for VAs. Kaplan-Meier analysis stratified by EPS demonstrated a significant difference in freedom from VAs and SCD (P = 0.009), though this finding was driven entirely by patients within the cohort with probable CS (P = 0.018, n = 69). One patient with possible CS and negative EPS had unrecognized progression of the disease and unexplained death with evidence of CS at autopsy. Conclusions EPS is useful in the risk stratification of patients with probable CS with preserved LV and RV function. A positive EPS was associated with VAs. While a negative EPS appeared to confer low risk, close follow-up is needed as EPS cannot predict fatal VAs related to new cardiac involvement or disease progression.

Introduction A spontaneous type I electrocardiogram (ECG) pattern and/or unheralded syncope are conventionally used as risk markers for primary prevention of sudden cardiac arrest/death (SCA/SCD) in Brugada syndrome (BrS). In this study, we determine the prevalence of conventional and newer markers of risk in those with and without previous aborted SCA events. Methods All patients with BrS were identified at our institute. History of symptoms was obtained from medical tests or from interviews. Other markers of risk were also obtained, such as presence of (1) spontaneous type I pattern, (2) fractionated QRS (fQRS), (3) early repolarization (ER) pattern, (4) late potentials on signal‐averaged ECG (SAECG), and (5) response to programmed electrical stimulation. Results In 133 patients with Bars, 10 (7%) patients (mean age = 39 ± 11 years; nine males) were identified with a previous ventricular fibrillation/ventricular tachycardia episode (n = 8) or requiring cardio‐pulmonary resuscitation (n = 2). None of these patients had a prior history of syncope before their SCA event. Only two (20%) patients reported a history of palpitations or dizziness. None had apneic breathing and three (30%) patients had a family history of SCA. From their ECGs, a spontaneous pattern was only found in one (10%) of these patients. Further, 10% of patients had fQRS, 17% had late potentials on SAECG, 20% had deep S waves in lead I, and 10% had an ER pattern in the peripheral leads. No significant differences were observed in the non‐SCA group. Conclusion The majority of BrS patients with previous aborted SCA events did not have a spontaneous type I and/or prior history of syncope. Conventional and newer markers of risk appear to only have limited ability to predict SCA.

Funding Acknowledgements Type of funding sources: None. Introduction The 2010 Task Force Criteria (TFC) for the diagnosis of arrhythmogenic right ventricular cardiomyopathy (A(R)VC) in 1st degree relatives includes an abnormality in a single parameter of the signal averaged ECG (SAECG). SAECG normal ranges were derived predominately from ischaemic heart disease patients, so may not be applicable in an A(R)VC population. There remain concerns that the SAECG is not specific enough and its role in the diagnosis of A(R)VC is under scrutiny. Purpose to improve the diagnostic utility of the SAECG Methods Patients with an A(R)VC diagnosis and 1st degree family members (FM) under follow-up at a single inherited cardiac conditions (ICC) centre were included. All cases were independently reviewed by 3 cardiologists experienced in the diagnosis and management of A(R)VC. All SAECGs included were free from artefact. TFC clinical variables and genetic status were recorded for each patient. Where tests had been repeated the most recent values were used. Because of concerns about the use of a single abnormal SAECG parameter in making a clinical diagnosis we required ≥2 abnormal SAECG parameters, or a confirmed genetic mutation to make a diagnosis. A diagnosis of false positive SAECG was made with ≥2 abnormalities when the individual was known not to carry the familial pathogenic mutation. Results A study population of 160 patients (male 103 (64%), age 46yrs (range 18-85yrs); 41 pro-bands and 119 FM. 62(52%) FM had a clinical diagnosis of AVC, with ARVC the pre-dominant phenotype 51(82%). A pathogenic genetic variant was identified in 24(47%) of FM with ARVC. The SAECG data is presented graphically for each parameter. A clinical diagnosis of ARVC was made on the basis of an affected 1st degree FM and an abnormal SAECG in 24(47%) of FM. Of these, 16(67%) had three abnormal SAECG parameters, 6(25%) two and 2(8%) a single abnormal parameter. Both patients with only one abnormal SAECG parameter carry a pathogenic variant. In total 88% of FM with ARVC, and 32% of FM without AVC had an abnormal SAECG as per current TFC. False positive values were mainly in fQRS duration (17/18), but also LAS40 (5/18), and RMS40 (2/18). By redefining an abnormal fQRS duration to be ≥118ms, false positives are reduced from 17 to 4. In addition, if there is a requirement for a 2nd abnormality then the false positives are reduced to 2 (4%). By adjusting the diagnostic criteria to fQRS duration ≥118ms, with a 2nd abnormal parameter or known pathogenic gene carrier status none of the 24 FM with a clinical diagnosis on abnormal SAECG alone would change diagnostic classification. Conclusion The SAECG is useful in family screening as it is frequently the only test to show an abnormality. However, the current TFC reference values lack specificity. By redefining an abnormal fQRS as ≥118ms with the requirement of a 2nd abnormal parameter, specificity is increased to 96%, with no significant change in sensitivity. Abstract Figure. SAECG Parameters in Family Members

Introduction The clinical utility of inferolateral early repolarisation (ER) and late potentials (LP) in children with Brugada Syndrome (BrS) has not been previously evaluated. The aim of this study was to determine the prevalence of electrocardiographic (ECG) abnormalities in children with BrS, and to investigate their relationship with clinical outcomes. Methods 43 patients with BrS and 47 controls aged ≤18 undergoing systematic clinical and ECG evaluation, including signal-averaged ECG (SAECG) and pharmacological provocation testing, between 2003 and 2019 were included. Results Four patients with BrS (9%) presented with a spontaneous type 1 Brugada pattern; the remaining 39 (91%) were diagnosed following ajmaline provocation testing. Twelve BrS patients (28%) had late potentials (LP) on SAECG compared to 1 (2%) in controls (p = 0.001). LP were more common in 5 patients with a high-risk phenotype (60% vs 24%) but this was not statistically significant. Twelve patients with BrS (28%) had inferolateral early repolarisation (ER) and 2 (5%) had fractionated QRS (f-QRS), but there were no statistically-significant differences with controls in these parameters. A significant arrhythmia (non-sustained ventricular tachycardia or atrial fibrillation) was seen in 4 patients (9%). Conclusions This study shows a high prevalence of SAECG abnormalities in children with BrS compared with controls, but this was not significantly associated with a high-risk phenotype.

Background Early detection of cardiac involvement in patients with sarcoidosis is important but currently unresolved. The aim of this study was to elucidate the utility of frequency domain microvolt T‐wave alternans (TWA), signal‐averaged ECG (SAECG), and heart rate turbulence (HRT) using 24‐hour Holter ECG for detecting cardiac involvement in patients with pulmonary sarcoidosis. Methods This study consisted of consecutive 40 pulmonary sarcoidosis patients (11 males, 62 ± 13 years) who underwent 24‐hour Holter monitoring with and without cardiac involvement. All patients underwent frequency domain TWA, SAECG, and HRT using 24‐hour Holter monitoring. Patients with atrial fibrillation pacing or wide QRS electrocardiogram were excluded. Results After 14 patients were excluded, a total of 26 patients (six males, 59 ± 14 years) were evaluated. Seven patients had cardiac involvement (cardiac sarcoidosis [CS] group). On the Holter SAECG, duration of low‐amplitude signals, Holter‐based signal‐averaged ECG showed high prevalence of positive late potentials (LP) in cardiac sarcoidosis (CS) patients.

Background The peri‐outflow tract region could be the origin of ventricular tachycardia (VT) after aortic valve replacement (AVR). However, the clinical characteristics of outflow tract ventricular tachycardias (OTVTs) after AVR are yet to be clarified. This study investigated the incidence, risk factors, and clinical characteristics of patients with OTVTs after AVR. Methods We retrospectively analyzed the clinical course of 120 patients who had undergone surgical AVR (SAVR) between April 1980 and October 2018. The patients had no ischemic or diagnosed cardiomyopathies other than primary aortic valve diseases. Results Six patients (5.0%) developed OTVTs after SAVR. The average onset was at 10.8 ± 5.7 years after SAVR. All cases of VT arose from the inferior axis and included left and right bundle branch block configuration. Two patients who underwent cardiac magnetic resonance imaging (MRI) had late gadolinium enhancement (LGE) in the midlayer of the left ventricle basal anteroseptal wall. Patients with periaortic VTs had significantly larger left ventricular (LV) diameter at systole, lower LV ejection fraction, higher positive rates of signal‐averaged electrocardiogram (SAECG), and nonsustained VTs on Holter monitoring. On ablation, local fragmented potentials with low voltage zones were observed in accordance with the LGE distribution. Multiple VTs originating from the periaortic region were provoked in the sessions. Conclusions Acute OTVT was found in 5% of patients after SAVR. Arrhythmia risk stratification by SAECG, Holter ECG, and cardiac MRI should be considered for a long period in patients after SAVR., Based on our results, acute onset of OTVT was found in 5% of patients who received SAVR. Therefore, we suggest that arrhythmic risk stratification should be considered for patients who have undergone SAVR for a long period.

Introduction The sudden cardiac death risk in Brugada Syndrome (BrS) is higher in patients with spontaneous type 1 pattern. Brugada diagnosis is also established in patients with induced type 1 morphology after provocative test with intravenous administration with a sodium blocker channel. Nevertheless, this group of patients is known to be at a lower risk of SCD, and their risk stratification is still a matter of discussion. Late potentials (LP) detected on signal-averaged ECG (SAECG) on the RVOT have been previously proposed as a predictor factor for BrS, even though data is lacking on its value. Purpose To evaluate the association between positive LP (LMS40> 38ms) on SAECG with modified Brugada leads and a positive flecainide test in patients with non-type 1 BrS. Methods Retrospective single-center study of non-type 1 BrS patients referred for the performance of a flecainide provocative test. Patients presenting with spontaneous type 1 morphology were excluded from the study. Study of LP on SAECG with modified leads for Brugada were evaluated before administration of flecainide [2mg/kg (maximum150mg), for 10minutes] with determination of filtered QRS duration (fQRS), root mean square voltage of the last 40ms of the QRS complex (RMS40) and duration of low amplitude signals Results 126 patients (47.3 ± 14.1 years, 61.9% males) underwent study with LP SAECG and flecainide test. Among these patients, 7.9% were symptomatic and 16.7% had familiar history of BrS. Flecainide test was positive in 46.8% of patients. In patients with a positive flecainide test, 64.4% presented LMS40 > 38ms whereas LMS40 > 38ms was present in only 46% of those with a negative flecainide test (p = 0.031). The presence of positive LMS40 was a positive predictor for a positive flecainide test, associated with a two-fold increase likelihood in the induction of a Brugada pattern (OR: 2,12; IC95% 1,025-4,392; P = 0,043). There was no association between fQRS or RMS40 and a positive flecainide test (p = NS). fQRS > 114ms and RMS40 Conclusion In patient with non-type 1 Brugada syndrome, LMS40 > 38ms in SAECG was a predictor for a positive flecainide test, suggesting that this finding could be helpful on the risk stratification of patients undergoing diagnostic study for Brugada syndrome. Abstract Figure. Effect of LMS 40 in flecainide test

BACKGROUND QRS abnormalities may not be apparent in sinus rhythm in electrically stable cardiomyopathy patients who can have quiescent but highly arrhythmogenic substrate. Here, we test the hypothesis that differential changes in QRS construction during right-ventricular apex pacing (RVP) as opposed to atrial pacing (AP) will identify latent substrate for ventricular arrhythmias (VA) and death. METHODS Forty patients with cardiomyopathy free of VA underwent baseline 114-electrode body-surface electrocardiogram during AP (100 beats per minute [bpm]) and RVP (100 and 120 bpm). The filtered-averaged QRS at each electrode was deconstructed into individual intra-QRS and post-QRS ventricular myopotentials (VMP ). The primary outcome was VA or death. Prognostic accuracy of VMP was validated using V1 to V6 leads in another prospective cohort of 44-cardiomyopathy patients. RESULTS Twenty-six patients were eligible for initial analysis. After 5 ± 2 years of follow-up, eight (31%) patients had VA (VAPos ) while rest were uneventful (VANeg ). During AP100 , VAPos patients expressed more VMP than VANeg patients (16 ± 1 vs 12 ± 1, P = 0.02). RVP100 and RVP120 in VAPos patients introduced an additional 5.5 ± 0.5 and 6.0 ± 0.5 VMP (P

The Centers for Diseases Control and Prevention estimates that 5.7 million adults in the United States suffer from heart failure and 1 in 9 deaths in 2009 cited heart failure as a contributing cause. Almost 50% of patients who are diagnosed with heart failure die within 5 years of diagnosis. Cardiovascular disease is a public health burden. The prognosis of patients with heart failure has improved significantly. However, the risk for death remains high. Managing sudden death risk and intervening appropriately with primary or secondary prevention strategies are of paramount importance.

Background Arrhythmogenic right ventricular cardiomyopathy (ARVC) is traditionally considered as primarily affecting the right ventricle. Mutations in genes encoding desmosomal proteins account for 40–60% of cases. Genotype-phenotype correlations are scant and mostly non gene-specific. Accordingly, we assessed the genotype-phenotype correlation for desmoplakin ( DSP ) missense and non-missense mutations causing ARVC. Methods and results We analyzed 27 ARVC patients carrying a missense or a non-missense DSP mutation, with complete clinical assessment. The two groups were compared for clinical parameters, basic demographics such as sex, age at diagnosis, age at disease onset, as well as prevalence of symptoms and arrhythmic events. Missense DSP variants were present in 10 patients and non-missense in 17. Mean age at diagnosis and at first arrhythmic event did not differ between the two groups. Also the prevalence of symptoms, either major (60% vs 59%, p=1) or all (80% vs 88%, p=0.61), did not differ. By contrast, left ventricular (LV) dysfunction was significantly more prevalent among patients with non-missense mutations (76.5% vs 10%, p=0.001), who were also much more likely to have a structural LV involvement by Cardiac Magnetic Resonance (CMR) (92% vs 22%, p=0.001). Conclusions For ARVC patients, both missense and non-missense DSP mutations carry a high arrhythmic risk. Non-missense mutations are specifically associated with left-dominant forms. The presence of DSP non-missense mutations should alert to the likely development of LV dysfunction. These findings highlight the clinical relevance of genetic testing even after the clinical diagnosis of ARVC and the growing clinical impact of genetics.

Background: Ventricular fibrillation and atrial fibrillation are well-known arrhythmias in patients with Brugada syndrome. This study evaluated the characteristics of the atrial arrhythmogenic substrate using the signal-averaged electrogram (SAECG) in patients with Brugada syndrome. Methods: SAECGs were performed during normal sinus rhythm in 23 normal volunteers (control group), 21 patients with paroxysmal atrial fibrillation (PAF; PAF group), and 21 with Brugada syndrome (Brugada group). Results: The filtered P wave duration (fPd) in the control, Brugada, and PAF groups was 113.9 ± 12.9 ms, 125.3 ± 15.0 ms, and 137.1 ± 16.3 ms, respectively. The fPd in the PAF group was significantly longer compared to that in the control and Brugada groups (p

Background The changes of signal averaged ECG (SAECG) in patients with arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) undergoing radiofrequency catheter ablation (RFCA) of ventricular arrhythmias (VAs) remains unknown. Methods Between 2010 and 2014, a total of 81 ARVD/C patients underwent endocardial and/or epicardial RFCA for drug-refractory VAs. Seventy patients (mean age 46.2±14.1years, 37 males) achieving acute procedure success (negative inducibility) were enrolled. Baseline characteristics, non-invasive examinations and SAECG (before and 3months after RFCA) were collected retrospectively. Results After successful RFCA, the electrical parameters of SAECG changed in 39 patients (55.7%), including 28 patients (40%) with electrical regression (group 1), and 11 patients (15.7%) with electrical progression (group 3). Thirty-one patients (44.3%) showed no significant SAECG change (group 2). During a mean follow-up of 17.8±10.7months, 23 patients (32.9%) had VA recurrences, including 4 in group 1, 12 in group 2, and 7 in group 3. In comparisons with groups 2 and 3, group 1 patients had a significantly better VA recurrence-free survival ( P =0.02). In multivariable Cox regression analysis, electrical regression was found to be associated with fewer VA recurrences ( P =0.02, OR: 0.28, 95% CI: 0.10–0.83). Conclusions Electrical regression of SAECG after RFCA in ARVD/C was found to be associated with fewer VA recurrences.

Aims Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart-muscle disease primarily affecting the right ventricle (RV) and potentially causing sudden death in young people. The natural history of the disease is firstly characterized by a concealed form progressing over a biventricular involvement. Three different cases coming from the same family are presented together with a review of the literature. Methods and results Multi-parameter analysis including imaging and electrocardiographic analysis is presented since the first medical referral with follow-up ranging from 11 to 38years. Case 1 presented a typical RV involvement in agreement with the ECG pattern. Case 2 presented a prevalent left ventricular involvement leading from the beginning to a pattern of dilated cardiomyopathy in agreement with his ECG evolution over the years. On the other side, Case 3 came to observation with a typical RV involvement (similar to Case 1) but with ECG evolution of typical left ventricle involvement (similar to Case 2). The genetic analysis showed a mutation in desmoglein-2 ( DSG2 ) gene: p. Arg49His. Comparison between size and localization of ventricular dyskinesia at cardiovascular imaging and the surface 12 lead electrocardiography are proposed. Conclusions ARVC may lead to an extreme phenotypic variability in clinical manifestations even within patients coming from the same family in which ARVC is caused by the same genetic mutation. ECG progression over time reflects disease evolution and in particular cases may anticipate wall motion abnormalities by years.

Ventricular tachyarrhythmias include potentially lethal episodes of sustained ventricular tachycardia (VT) and ventricular fibrillation (VF) as well as hemodynamically tolerated ventricular ectopic activity. Sustained VT or VF may develop in the setting of acute myocardial infarction or as clinical sequelae of advanced cardiomyopathy. The incidence of these serious arrhythmias is estimated from retrospective and observational studies and registries of sudden cardiac arrest and sudden cardiac death. Over the past few decades, there has been a gradual decline in the incidence of life-threatening ventricular tachyarrhythmias which has been largely driven by upstream treatments for and prevention of coronary artery disease and its sequelae. In addition primary prevention implantable cardioverter-defibrillators (ICDs) have improved survival in patients at risk for malignant ventricular arrhythmias and sudden cardiac death. Improved understanding, and improved diagnostic and imaging methods have elucidated many of the previously classified "idiopathic" ventricular arrhythmias as inherited arrhythmic syndromes and occult cardiomyopathies. In addition, improved sensitivity and duration of ECG monitoring has allowed increased detection of ventricular ectopic activity.

The presence of fragmented QRS is a known marker of heterogeneous ventricular activation around the myocardial scar area. We validated whether fragmented QRS shows any association with ventricular dysfunction, fibrosis, or ventricular arrhythmias in patients with Duchenne muscular dystrophy (DMD). Thirty-seven patients with DMD were evaluated using electrocardiography (ECG), echocardiography, cardiac magnetic resonance, and 24-h Holter monitoring. Associations between fragmented QRS and ventricular dysfunction, fibrosis, or ventricular arrhythmia were investigated. Fragmented QRS complexes were present in 31 of 37 (83.7%) patients, and they were associated with a significantly lower left ventricular ejection fraction along with an increased left ventricular Tei index as evaluated by echocardiography, and more frequent ventricular arrhythmia as indicated using 24-hour Holter monitoring compared with patients without fragmented QRS. The number of leads with fragmented QRS correlated negatively with left ventricular ejection fraction both using echocardiography (r = -0.616) and CMR (r = -0.516). Further, the number of leads with fragmented QRS showed a significant correlation with several other echocardiographic measurements (mitral Em and Sm, and left ventricular Tei index), and 2-dimensional speckle-tracking echocardiography derived global left ventricular longitudinal strain. The frequency of ventricular arrhythmia observed using Holter monitoring showed a significant positive correlation with the frequency of fragmented QRS on ECG (r = 0.674). There was a positive trend of correlation between fragmented QRS and the amount of myocardial fibrosis as assessed by late gadolinium enhancement using CMR, but the statistical significance of the relationship was low (r = 0.433, p = 0.056). Fragmentation of QRS complexes is associated with degrees of left ventricular dysfunction, fibrosis, and ventricular arrhythmias in patients with DMD.

Non-invasive risk stratification for ventricular fibrillation (VF) in Brugada syndrome (BrS) has not been fully evaluated. The aim of this study was to assess the utility of signal-averaged Holter electrocardiogram (Holter SAECG) and 12-lead Holter electrocardiogram (Holter ECG) after a pilsicainide provocation test for non-invasive risk stratification in BrS. We enrolled 30 consecutive patients with BrS [divided into 2 groups: the VF group, those with a previous history of VF (n = 10); and the non-VF group, those without a history of VF (n = 20)] and 10 control subjects without type 1 ECG. We evaluated late potentials [LP: filtered QRS (f-QRS), RMS40, and LAS40] on the Holter SAECG for 4 h after the pilsicainide provocation and in the same patients on another day without performing the pilsicainide provocation. Furthermore, we measured QRS duration and QTc interval in leads V2 and V5, and J amplitude in lead V2 on the Holter ECG after the pilsicainide provocation. On the Holter SAECG, the f-QRS at 1 h and LAS40 at 3 h after the pilsicainide provocation were significantly larger in the VF group than in the non-VF group (f-QRS at 1 h: 113.9 ± 8.9 vs. 104.9 ± 8 ms; p = 0.01, LAS40 at 3 h: 45.4 ± 5.9 vs. 35.5 ± 7.4 ms; p

Very narrow QRS have been reported in sudden death survivors but prevalence and prognosis role of narrow QRS is unknown.546 healthy men between 50 and 60 years (group 1) and 373 similar patients with coronary artery disease (368 men, group 2) underwent signal averaged ECG (SA-ECG) allowing precise measurement of QRS duration. All cause-mortality was determined after 18 ± 3 years follow-up. Mean QRS duration was 97 ± 13 ms in group 1 and 103 ± 16 ms in group 2. Tenth percentile was 84 ms in group 1 and 85 ms in group 2. All cause-mortality in group 1 was 10.4% (57/546): 6/85 in case of QRS 85 ms (7%) and 2/23 (9%) in case of QRS 120 ms (ns). HR for all-cause mortality was 0.75 (95% CI 0.32-1.76, P = 0.52) for QRS 85 ms and 0.86 (95% CI 0.21-3.53, P = 0.84) for QRS 120 ms. All cause mortality in group 2 was 29% (109/373): 7/44 in case of QRS 85 ms (16%) and 22/44 (50%) in case of QRS 120 ms (P = 0.002). HR for all-cause mortality was 0.65 (95% CI 0.29-1.45, P = 0.29) for QRS 85 ms and 1.73 (95% CI 1.02-2.94, P = 0.05) for QRS 120 ms.QRS duration 80-85 ms can be observed in a significant proportion of middle-aged healthy males and in similar patients with ischemic heart disease. Narrow QRS were not linked to prognosis in any group.

QRS duration has been associated with the response to cardiac resynchronization therapy (CRT). However, the methods for defining QRS duration to predict the outcome of CRT have discrepancies in previous reports. The aim of this study was to determine an optimal measurement of QRS duration to predict the response to CRT.Sixty-one patients who received CRT were analyzed. All patients had class III-IV heart failure, left ventricular ejection fraction not more than 35%, and complete left bundle branch block. The shortest, longest, and average QRS durations from the 12 leads of each electrocardiogram (ECG) were measured. The responses to CRT were determined using the changes in echocardiography after 6 months. Thirty-five (57.4%) patients were responders and 26 (42.6%) patients were non-responders. The pre-procedure shortest, average, and longest QRS durations and the QRS shortening (ΔQRS) of the shortest QRS duration were significantly associated with the response to CRT in a univariate logistic regression analysis (P = 0.002, P = 0.03, P = 0.04 and P = 0.04, respectively). Based on the measurement of the area under curve of the receiver operating characteristic curve, only the pre-procedure shortest QRS duration and the ΔQRS of the shortest QRS duration showed significant discrimination for the response to CRT (P = 0.002 and P = 0.038, respectively). Multivariable logistic regression showed the pre-procedure shortest QRS duration is an independent predictor for the response to CRT.The shortest QRS duration from the 12 leads of the electrocardiogram might be an optimal measurement to predict the response to CRT.

Purpose of review Tetralogy of Fallot (TOF) carries a long-term risk of arrhythmias and sudden death after surgical repair. Risk stratification is still less accurate than desired. Recent findings Several factors have been studied as risk predictors for ventricular arrhythmias and sudden death. Clinical parameters include age at surgery, time since repair, types of previous surgeries, and symptoms such as syncope and palpitations. Electrocardiographic parameters that have been studied include QRS interval, ventricular arrhythmias assessed with Holter monitors, signal averaged ECG, QRS fragmentation, QRS vector magnitude, and microvolt T-wave alternans. Exercising testing has been shown to have prognostic significance. Ventricular function assessment with imaging studies including echocardiography and magnetic resonance imaging (MRI) plays a significant role. Invasive hemodynamic and electrophysiologic studies, in addition to assessment for inducible tachycardia, can provide information regarding the electroanatomic substrate of VT. Summary Risk stratification for TOF has improved over the last years with several clinical, electrocardiographic, imaging, and invasive electrophysiologic findings showing promise, but there still a lack of uniformity in approach between various investigators and reproducibility of findings is difficult in larger populations. With use of a combination of factors, a more informed decision can be made.

Background Approximately 10–25% of ischemic strokes are of unknown origin. Determining their potential association with subclinical atrial fibrillation (SCAF) is important for proper secondary prevention. We investigated whether SCAF can be predicted by assessing the atrial substrate with signal-averaged electrocardiography (SAECG). Methods Between April 2015 and February 2018, we recruited 125 consecutive patients with embolic stroke of undetermined source (ESUS) and 125 patients with paroxysmal atrial fibrillation (AF) patients as control. All participants underwent P wave SAECG at baseline and ESUS patients were followed up with ECG and Holter ECG, at baseline, 3, 6, and 12 months after discharge, and every 12 months thereafter. Results In the ESUS group (69 males, 68.4±12.1 years), 32 (25.6%) patients were diagnosed with SCAF during follow-up. There were no significant differences between both groups in terms of P wave duration [PWD] (ESUS vs. AF, P=0.321). PWD demonstrated a significant predictive efficacy for SCAF detection during follow-up (C-index of standard PWD=0.657, 95% confidence interval (CI) 0.552–0.761, P=0.008). Stroke recurrence occurred in 22 patients (17.6%) and was significantly associated with PWD but not SCAF (odds ratio 2.756, 95% CI 1.061–7.161, P=0.037). Conclusion PWD, an ECG biomarker associated with atrial substrate directly contributes to AF and ESUS, is useful for predicting SCAF. The potential for using this simple ECG biomarker for screening for SCAF amongst ESUS patients merits further exploration.

Background The mechanisms involved in changes in P wave following catheter ablation for atrial fibrillation (AF) are uncertain. This study aimed to assess the relationship between changes in P‐wave morphology and pulmonary vein (PV) reconnection following ablation by the assessment of 12‐lead surface electrocardiogram and signal‐averaged electrocardiogram. Methods This retrospective study included 115 consecutive patients with paroxysmal AF that underwent repeat ablation for recurrence following initial ablation. We investigated changes in P‐wave morphology between baseline and repeat procedure in patients with and without PV reconnection. The study also included as validation group without recurrence (n = 67) following initial ablation. Results The maximum P‐wave duration (PWD) was significantly decreased from baseline to just after the procedure in all groups. However, for the PV reconnection group (n = 100), the maximum PWD was significantly increased again at the repeat procedure. In contrast, the maximum PWD was significantly reduced between baseline and repeat procedure in the non‐PV reconnection group (n = 15). The signal‐averaged PWD was significantly decreased from baseline to repeat procedure in the non‐PV reconnection group, but, conversely, was increased in the PV reconnection group. In the non‐PV reconnection group, the disappearance of notched P wave was detected in 8 of 15 patients (53%), which was significantly higher than in other groups (p = .001). A new or delayed notched P wave was identified in the PV reconnection group only. These results were confirmed in the validation group. Conclusions The reverse dynamics of PWD after initial shortening directly following ablation were significantly associated with PV reconnection.

Signal-averaged electrocardiogram (SAECG) provides not only diagnostic information but also the prognostic implication of ablation in arrhythmogenic right ventricular cardiomyopathy (ARVC).This study aimed to validate the role of SAECG in identifying arrhythmogenic substrates requiring an epicardial approach in ARVC.Ninety-one patients with a definite diagnosis of ARVC who underwent successful ablation for drug-refractory ventricular arrhythmia were enrolled and classified into 2 groups: group 1 who underwent successful ablation at the endocardium only and group 2 who underwent successful ablation requiring an additional epicardial approach. The baseline characteristics of patients and SAECG parameters were obtained for analysis.Male predominance, worse right ventricular (RV) function, higher incidence of syncope, and depolarization abnormality were observed in group 2. Moreover, the number of abnormal SAECG criteria was higher in group 2 than in group 1. After a multivariate analysis, the independent predictors of the requirement of epicardial ablation included the number of abnormal SAECG criteria (odds ratio 2.8, 95% confidence interval 1.4-5.4; P = .003) and presence of syncope (odds ratio 11.7; 95% confidence interval 2.7-50.4; P = .001). In addition, ≥2 abnormal SAECG criteria were associated with larger RV endocardial unipolar low-voltage zone (P.001), larger RV endocardial/epicardial bipolar low-voltage zone/scar (P.05), and longer RV endocardial/epicardial total activation time (P.001 and P = .004, respectively).The number of abnormal SAECG criteria was correlated with the extent of diseased epicardial substrates and could be a potential surrogate marker for predicting the requirement of epicardial ablation in patients with ARVC.

Aims Brugada syndrome (BrS) represents a major cause of sudden cardiac death in young individuals. The risk stratification to forecast future life-threatening events is still controversial. Non-invasive assessment of late potentials (LPs) has been proposed as a risk stratification tool. However, their nature in BrS is still undetermined. The purpose of this study is to assess the electrophysiological determinants of non-invasive LPs. Methods and Results Two hundred and fifty consecutive patients with (Group 1, n = 96) and without (Group 2, n = 154) BrS-related symptoms were prospectively enrolled in the registry. Signal-averaged electrocardiogram (SAECG) was performed in all subjects before undergoing epicardial mapping. Group 1 patients exhibited larger arrhythmogenic substrates (AS; 5.8 ± 2.8 vs. 2.6 ± 2.1 cm2, P Conclusion The results of this study support the role of the epicardial AS as an electrophysiological determinant of non-invasive LPs, which may serve as a tool in the non-invasive assessment of the BrS substrate, as SAECG-LPs could be considered an expression of the abnormal epicardial electrical activity. ClinicalTrials.gov number (NCT02641431; NCT03106701).

Background Although several prognostic factors of atrial fibrillation (AF) recurrence after pulmonary vein isolation (PVI) have been investigated, the accurate prediction of AF recurrence remains difficult. We propose an electrocardiogram (ECG) index, the P-wave force (PWF), which is the product of the amplitude of the negative terminal phase of the P wave in the V1 electrode and the filtered P-wave duration, obtained by a signal-averaged P-wave analysis. This study was conducted to evaluate the impact of the PWF on the recurrence of AF after PVI. Methods We retrospectively evaluated 79 paroxysmal AF patients (64 ± 9 years, 56 males) who underwent PVI by cryoballoon ablation. Standard 12-lead ECG and a P-wave signal-averaged electrocardiogram (SAECG) were recorded the day before and 1 month after the PVI procedure. Results During the mean follow-up of 10.2 months, AF recurred in 11 (14%) patients. The PWF 1 month after ablation was significantly higher in the recurrence group compared to that in the nonrecurrence group (8.8 ± 3.1 mVms vs 6.5 ± 2.9 mVms, P = 0.017). The patients with a PWF value ≥9.3 mVms had a significantly greater risk of recurrence after the ablation compared to the patients with a PWF value

Exercise-induced ventricular tachycardia (VT) rarely occurs in the absence of organic heart disease. Idiopathic monomorphic VT has an excellent prognosis. The main aspect of the risk stratification process is recognizing subtle forms of organic heart disease, particularly arrhythmogenic right ventricular cardiomyopathy. Exercise-induced polymorphic VT is potentially malignant. Exercise-induced polymorphic VT has also been seen in mitral valve prolapse. Some patients with stable coronary disease, and even healthy athletes, sometimes have short bursts of polymorphic VT during exercise tests but these arrhythmias are usually not reproducible during repeated testing and have unknown long-term clinical significance.

Primary electrical diseases manifest with polymorphic ventricular tachycardia (PMVT) and ventricular fibrillation (VF) and along with idiopathic VF contribute to about 10% of sudden cardiac deaths (SCDs) overall. These disorders include long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia, short QT syndrome, and early repolarization syndrome. This article reviews the clinical electrophysiological management of PMVT/VF in a structurally normal heart affected with these disorders.

Background Cardiac resynchronisation therapy (CRT) is an accepted device therapy in patients with low ejection fraction. Beneficial effects of CRT result from mechanical remodelling. Some controversial reports suggest that CRT may also induce electrical remodelling with intrinsic QRS narrowing but still the effect of CRT on electrical remodelling is an issue for debate. The aim of our study was to evaluate the effects of CRT on intrinsic QRS duration. For clarity, our analysis was performed by the signal averaged electrocardiogram (SAECG) which is a high resolution electrocardiographic signal suitable for accurate measurement of QRS duration. Signal averaged electrocardiogram provides a better value of QRS duration compared to 12-lead ECG by the ability to detect ventricular late potentials. Methods A total of 48 consecutive patients with severe systolic dysfunction and typical left bundle branch block (LBBB) were enrolled in the study prospectively. Patients were scheduled for CRT-D implantation according to the current guidelines. Intrinsic QRS duration was accurately measured by SAECG before and at least 14 months after CRT implantation. Results The mean intrinsic QRS duration remained unchanged during follow-up (from 149.9 ± 13.8 ms to 149.6 ± 18.4 ms; P= 0.3). Among 32 CRT responder patients, the mean intrinsic QRS duration remained unchanged during follow-up. Also, the mean intrinsic QRS duration showed no significant changes in 16 CRT non-responders. Conclusion Structural remodelling induced by CRT does not necessarily translate into decrease of intrinsic ventricular activation. Despite significant left ventricular recovery, electrical characteristics of the left ventricular conduction system cannot generally be expected to recuperate.

Background Increased QRS score and wide spatial QRS-T angle are independent predictors of cardiovascular mortality in the general population. Our main objective was to assess whether a QRS score ≥5 and/or QRS-T angle ≥105° enable screening of patients for myocardial scar features. Methods Seventy-seven patients age ≤70 years with QRS score ≥5 AND/OR spatial QRS-T angle ≥105° as well as left ventricular ejection fraction (LVEF) >35% were enrolled in the study. All participants underwent complete clinical examination, signal averaged ECG (SAECG), 30-minute ambulatory electrocardiogram recording for T-wave alternans (TWA), and late gadolinium enhancement cardiac magnetic resonance (LGE-CMR). Relationship between QRS score, QRS-T angle with scar presence and pattern, as well as gray zone, core, and total scar size by LGE-CMR were assessed. Results Myocardial scar was present in 41 (53%) patients, of whom 19 (46%) exhibited a typical ischemic pattern. QRS score but not QRS-T angle was related to total scar size and gray zone size (R2 = 0.12, P = 0.002; R2 = 0.17; P ≤ 0.0001, respectively). Patients with QRS scores ≥6 had significantly greater myocardial scar and gray zone size, increased QRS duration and QRS-T angle, a higher prevalence of late potentials presence, increased LV end-diastolic volume and decreased LVEF. There was a significant independent and positive association between TWA value and total scar (P = 0.001) and gray zone size (P = 0.01). Conclusion Patients with preserved LVEF and myocardial scar by CMR also have electrocardiographic features that could be involved in ventricular arrhythmogenesis.

BACKGROUND: Current noninvasive risk stratification methods offer limited prediction of arrhythmic events when selecting patients for ICD implantation. Our laboratory has recently developed a signal processing metric called Layered Symbolic Decomposition frequency (LSDf) that quantifies the percentage of hidden QRS wave frequency components in signal‐averaged ECG (SAECG) recordings. The purpose of this pilot study was to determine whether LSDf can be predictive of ventricular arrhythmia or death in an ICD patient cohort. METHODS AND RESULTS: Fifty‐two ICD patients were recruited from 2008 to 2009. These were followed for a mean of 8.5 ± 0.4 years for the primary outcome of first appropriately treated ventricular arrhythmia (VT/VF) or death. Thirty‐four subjects met the primary outcome. LSDf was significantly lower, and 12‐lead QRS duration was significantly greater in patients meeting the primary outcome (12.14 ± 3.97% vs. 16.45 ± 3.73%; p = 0.001) and (111.59 ± 14.96 ms vs. 97.69 ± 13.51 ms; p = 0.012) respectively. A 13.25% LSDf threshold (0.74 sensitivity and 0.85 specificity) was selected based on an ROC curve. Kaplan–Meier survival analysis was conducted; patients above the 13.25% threshold demonstrated significantly better survival outcomes (log‐rank p

Background A novel signal-averaged electrocardiogram (SAECG) device and a novel ambulatory SAECG device are clinically available, but reference values have not been established. This study aimed to validate the novel SAECG and the novel ambulatory-based SAECG devices by comparison with the conventional SAECG device. Methods and results High-resolution SAECGs were recorded consecutively in 83 healthy volunteers using the 3 devices. A novel ambulatory SAECG device was used as real-time recording within 15 min for validation study (15 min ambulatory-based SAECG). We examined the concordance of positive results (at least 2/3 abnormal SAECG parameters) and negative results (0 or 1/3 abnormal parameters), as well as the correlations between SAECG parameters (filtered QRS duration [fQRS]); duration of low-amplitude signals Qualitative analysis showed excellent concordance among the novel SAECG, the 15 min ambulatory-based SAECG, and the conventional SAECG methods (novel SAECG vs. conventional SAECG = 94%; 15 min ambulatory-based SAECG vs. conventional SAECG = 91.6%; p = 0.755), while quantitative analysis indicated strong correlations between the novel SAECG and the conventional SAECG values for fQRS, LAS40, and LnRMS40 (r = 0.838–0.805, p Conclusion In healthy subjects, the parameters of either the novel SAECG or the 15 min ambulatory-based SAECG and those of the conventional SAECG were strongly correlated. Relatively good agreements were observed among 3 SAECGs, especially better between the 15 min ambulatory-based SAECG and the conventional SAECG probably due to similar measurement system of 2 methods.

This review aims to give an update on the pathogenesis, clinical manifestations, and diagnosis of arrhythmogenic right ventricular cardiomyopathy (ARVC). Arrhythmogenic right ventricular cardiomyopathy is mainly an autosomal dominant inherited disease linked to mutations in genes encoding desmosomes or desmosome-related proteins. Classic symptoms include palpitations, cardiac syncope, and aborted cardiac arrest due to ventricular arrhythmias. Heart failure may develop in later stages. Diagnosis is based on the presence of major and minor criteria from the Task Force Criteria revised in 2010 (TFC 2010), which includes evaluation of findings from six different diagnostic categories. Based on this, patients are classified as having possible, borderline, or definite ARVC. Imaging is important in ARVC diagnosis, including both echocardiography and cardiac magnetic resonance imaging for detecting structural and functional abnormalities, but importantly these findings may occur after electrical alterations and ventricular arrhythmias. Electrocardiograms (ECGs) and signal-averaged ECGs are analysed for depolarization and repolarization abnormalities, including T-wave inversions as the most common ECG alteration. Ventricular arrhythmias are common in ARVC and are considered a major diagnostic criterion if originating from the RV inferior wall or apex. Family history of ARVC and detection of an ARVC-related mutation are included in the TFC 2010 and emphasize the importance of family screening. Electrophysiological studies are not included in the diagnostic criteria, but may be important for differential diagnosis including RV outflow tract tachycardia. Further differential diagnoses include sarcoidosis, congenital abnormalities, myocarditis, pulmonary hypertension, dilated cardiomyopathy, and athletic cardiac adaptation, which may mimic ARVC.