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Aim. To study the signal-averaged ECG (SA-ECG) parameters of atrial complex and supraventricular arrhythmias (SVA) in patients with coronary heart disease (CHD) and chronic heart failure (CHF), treated with diuretics (D) torasemide and furosemide. Material and methods. The study included 107 patients with CHD and CHF. All participants underwent 24-hour ECG monitoring and the registration of SA-ECG atrial complex parameters. In total, 52 patients received furosemide, and 55 were administered torasemide. Results. In both groups, D therapy was associated with some increase in the duration of filtered P and LAS5, as well as a decrease in RMS20. These changes were more pronounced in the furosemide-treated patients. Torasemide demonstrated better effects on the SVA dynamics, which manifested in the decreased numbers of single, paired, and grouped SV extrasystoles. Conclusion. In CHD and CHF patients, the disturbed atrial depolarisation was manifested in negative dynamics of SA-ECG atrial complex parameters. Torasemide therapy did not affect the atrial complex parameters and also reduced SVA incidence, which made torasemide a medication of choice for patients with CHD and CHF.

Background: Signal-averaged electrocardiography of the P wave (P wave SAECG) is a noninvasive method for evaluating the risk of atrial fibrillation (AF). We aimed to study P wave SAECG parameters in a large number of apparently healthy subjects and to compare them with patients with converted AF. Methods: We examined 591 individuals; P wave SAECG were recorded in 330 normal subjects, 31 patients with converted persistent AF and 57 patients with converted paroxysmal AF immediately after conversion, at 12 and 24 hours after conversion, then after 3 and 6 months. P wave SAECG were recorded using a commercially available machine aiming to obtain a noise level

Summary Purpose: There has been growing interest in cardiac disturbances in epilepsy patients and their etiologic role in the context of sudden death. Ventricular late potentials (VLPs) recorded on signal-averaged electrocardiography (SAECG) reflects delayed ventricular depolarization and identifies the structural or functional substrate for the ventricular tachycardia in the reentry mechanism. Therefore, abnormal SAECG poses the potential of identifying patients at increased risk of malignant ventricular arrhythmias and sudden cardiac death. The aim of this exploratory study was to screen epilepsy patients who were treated with established doses of antiepileptic drugs (AEDs) on the presence of VLPs. Methods: Forty-five consecutive patients with the diagnosis of epilepsy and 19 healthy volunteers, aged younger than 46 years, participated in the study. Exclusion criteria included symptoms or signs of diseases other than epilepsy, in particular relating to heart disease or medication influencing the cardiovascular system, as well as seizure reported by patients that occurred

The Selvester QRS score translates subtle changes in ventricular depolarization measured by the electrocardiogram into information about myocardial scar location and size. This estimated scar has been shown to have a high degree of correlation with autopsy-measured myocardial infarct size. In addition, multiple studies have demonstrated the value of the QRS score in post-myocardial infarct patients to provide prognostic information. Recent studies have demonstrated that increasing QRS score is predictive of increased implantable defibrillator shocks for ventricular tachycardia and fibrillation as well as decreased response to cardiac resynchronization therapy. Although QRS scoring has never achieved widespread clinical use, increased interest in patient selection and risk-stratification techniques for implantable defibrillators and cardiac resynchronization therapy has led to renewed interest in QRS scoring and its potential to identify which patients will benefit from device therapy. The QRS score criteria were updated in 2009 to expand their use to a broader population by accounting for the different ventricular depolarization sequences in patients with bundle-branch/fascicular blocks or ventricular hypertrophy. However, these changes also introduced additional complexity and nuance to the scoring procedure. This article provides detailed instructions and examples on how to apply the QRS score criteria in the presence of confounding conduction types to facilitate understanding and enable development and application of automated QRS scoring.

Symptomatic sustained cardiac arrhythmias are frequently observed in in the coronary care unit and often lead to hemodynamic compromise, especially in the presence of multisystem disease. The predominant arrhythmias noted in intensive care units are tachyarrhythmias, particularly atrial fibrillation and flutter, and ventricular tachycardia. Bradycardias, arguably less life-threatening than tachyarrhythmias, can arise from sinus node dysfunction or atrioventricular conduction block; transient vagally-mediated bradycardias are frequently encountered as well. Prompt diagnosis of the patient with tachycardia is critical as treatment depends on the accurate diagnosis of tachycardia mechanism. The electrocardiogram remains the most important diagnostic tool for the evaluation of both wide and narrow complex tachycardia. The electrocardiographic diagnosis of wide complex tachycardia is based on evaluation of atrioventricular relationship and QRS morphology while the diagnosis of narrow complex tachycardia is based on the location and morphology of P waves. It is important for critical care specialists to understand the principles of cardiac arrhythmia diagnosis and remain current with the recent advances in the pharmacologic and non-pharmacologic management of patients with arrhythmias.

Background: Several studies have showed that fragmented QRS complexes (f - QRS, defined as different RSR′ patterns) on a routine 12 - lead electrocardiogram were associated with increased mortality and arrhythmic events in patients with coronary artery disease, but relatively little data were available regarding idiopathic dilated cardiomyopathy (IDCM). Objective: The purpose of this study was to evaluate the relationship between fragmentation of QRS and the combined end point of all-cause mortality and ventricular arrhythmias in patients with IDCM. Methods: One hundred twenty-eight patients with IDCM and left ventricular dysfunction (ejection fraction, EF ≤ 40%) were analyzed, respectively. According to QRS duration and the existence of f - QRS on 12-lead electrocardiograph (ECG), the study populations were divided into three groups: (1) the f - QRS group (QRS

Background: Atrial fibrillation (AF) is observed in patients with Brugada syndrome (BS), especially those showing coved-type electrocardiogram (ECG) pattern. Using P-wave signal-averaged ECG (P-SAE), we investigated whether increased intraatrial conduction abnormality contributed to AF generation in BS patients. Methods: Twenty BS patients and 20 age- and gender-matched healthy controls were enrolled. At the P-SAE recording, 12 of the 20 BS patients showed coved-type (C-BS) and eight showed saddleback-type (S-BS). The total duration (Ad) and root mean square voltage for the terminal 20 ms (LP20) of the filtered P wave were measured. P-wave dispersion (P-disp) was defined as the difference between the maximum and minimum, measured from 16 precordial recording sites. Results: BS patients had a significantly longer Ad (128.2 ± 7.6 vs 116.3 ± 8.2 ms, P < 0.0001), lower LP20 (2.6 ± 0.9 vs 3.4 ± 0.8 μV, P < 0.01), and greater P-disp (15.5 ± 7.0 vs 7.4 ± 3.2 ms, P < 0.0001) than the controls. C-BS patients had significantly longer Ad (131.0 ± 7.2 vs 124.1 ± 6.8 ms, P < 0.05) and lower LP20 (2.2 ± 0.6 vs 3.2 ± 1.0 μV, P < 0.05) than S-BS patients. All C-BS patients and only three S-BS patients had atrial late potential (100% vs 38%, P < 0.01). Conclusion: Intraatrial conduction delay and its heterogeneity may exist in BS patients, especially those showing coved-type ECG patterns. These atrial electrical abnormalities could be a substrate for atrial reentrant tachycardia such as AF. (PACE 2011; 34:1138–1146)

Background: Ventricular arrhythmias are one of the main causes of sudden death in cardiac sarcoidosis (CS). Little is known about the efficacy of corticosteroid therapy for ventricular arrhythmias in CS. Methods: Thirty-one CS patients presenting premature ventricular contractions (PVCs, ≥300/day) were investigated. Fourteen patients had nonsustained ventricular tachycardia (NSVT). All of patients were treated with corticosteroid, and the initial dosage is 30 mg/day of prednisone, which was tapered over a period of 6 months to a maintenance dosage of 10 mg/day. Twenty-four hour Holter monitoring, signal averaged electrocardiography (SAECG), echocardiography, gallium-67 scintigraphy, serum angiotensin converting enzyme (ACE) and plasma B-type natriuretic peptide (BNP) concentrations were assessed before and after corticosteroid therapy. Results: As a whole, there were no significant differences in the number of PVCs and in the prevalence of NSVT before and after steroid therapy. However, the less advanced LV dysfunction patients (EF ≥ 35%, n = 17) showed significant reduction in the number of PVCs (from 1820 ± 2969 to 742 ± 1425, P = 0.048) and in the prevalence of NSVT (from 41 to 6%, p = 0.039). Late potentials on SAECG were abolished in 3 patients. The less advanced LV dysfunction group showed a significantly higher prevalence of gallium-67 uptake compared with the advanced LV dysfunction group (EF < 35 %, n = 14). In the advanced LV dysfunction patients, there were no significant differences in these parameters. Conclusions: Corticosteroid therapy may be effective for ventricular arrhythmias in the early stage, but less effective in the late stage. Ann Noninvasive Electrocardiol 2011;16(2):140–147

Ventricular tachyarrhythmias commonly occur in trained athletes during ambulatory Holter electrocardiography and are usually associated with a benign course. Such arrhythmias have been demonstrated to be sensitive to short periods of athletic deconditioning; however, their response to retraining is not known. Twenty-four hour Holter electrocardiographic monitoring was performed at peak training and after 3 to 6 months of deconditioning and was repeated in the present study after 2, 6, and 12 months of retraining in 37 athletes with frequent and complex ventricular tachyarrhythmias and without cardiovascular abnormalities. These subjects showed partial (101 to 500 ventricular premature complexes [VPCs]/24 hours) or marked (

Ventricular mural aneurysms especially in the left ventricle represent an increased risk for life-threatening arrhythmias. We present a case of ventricular tachycardia originating from an inferobasal left ventricular aneurysm. A 25-year-old male patient presented with complaints of palpitation, breathlessness, and dizziness of two-hour onset. The electrocardiogram showed wide-QRS tachycardia at which time his blood pressure was 80/40 mmHg. The patient suddenly developed collapse and ventricular tachycardia was diagnosed on the monitor, and he returned to sinus rhythm following successful cardioversion. He remained stable during hospitalization. The electrocardiogram was in sinus rhythm with right bundle branch block and small Q waves in inferior leads. He had an eight-year history of surgery for ventricular septal defect closure, during which a ventricular aneurysm was detected but left untreated. Echocardiographic examination showed a dyskinetic aneurysmal region extending from the inferobasal segment to the posterior wall of the left ventricle. Coronary arteries were normal on angiography, and ventriculography confirmed the aneurysm. Electrophysiologic study was recommended, but the patient refused any treatment. He remained asymptomatic during 18 months of follow-up.

Arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D) is an inherited disease that causes structural and functional abnormalities of the right ventricle (RV). The presence of late potentials as assessed by the signal-averaged electrocardiogram (SAECG) is a minor task force criterion.The purpose of this study was to examine the diagnostic and clinical value of the SAECG in a large population of genotyped ARVC/D probands.We compared the SAECGs of 87 ARVC/D probands (age 37 ± 13 years, 47 males) diagnosed as affected or borderline by task force criteria without using the SAECG criterion with 103 control subjects. The association of SAECG abnormalities was also correlated with clinical presentation, surface ECG, ventricular tachycardia (VT) inducibility at electrophysiologic testing, implantable cardioverter-defibrillator therapy for VT, and RV abnormalities as assessed by cardiac magnetic resonance imaging (cMRI).Compared with controls, all three components of the SAECG were highly associated with the diagnosis of ARVC/D (P.001). They include the filtered QRS duration (97.8 ± 8.7 ms vs 119.6 ± 23.8 ms), low-amplitude signal (24.4 ± 9.2 ms vs 46.2 ± 23.7 ms), and root mean square amplitude of the last 40 ms of the QRS (50.4 ± 26.9 μV vs 27.9 ± 36.3 μV). The sensitivity of using SAECG for diagnosis of ARVC/D was increased from 47% using the established 2 of 3 criteria (i.e., late potentials) to 69% by using a modified criterion of any 1 of 3 criteria, while maintaining a high specificity of 95%. Abnormal SAECG as defined by this modified criterion was associated with a dilated RV volume and decreased RV ejection fraction detected by cMRI (P.05). SAECG abnormalities did not vary with clinical presentation or reliably predict spontaneous or inducible VT and had limited correlation with ECG findings.Using 1 of 3 SAECG criteria contributed to increased sensitivity and specificity for the diagnosis of ARVC/D. This finding is incorporated in the recent modification of the task force criteria.

Introduction: Cardiac sarcoidosis (CS) occurs in up to 25% of patients with pulmonary involvement. Early diagnosis is critical because sudden death from ventricular arrhythmias can be the initial presentation. We sought to evaluate the diagnostic utility of signal-averaged ECG (SAECG) for detection of cardiac involvement of sarcoidosis. Methods: Subjects with biopsy proven sarcoidosis and symptoms suggestive of possible cardiac involvement were included in the cohort. Standard criteria for SAECG were used. Subjects were considered to have CS if they met criteria established by the Japanese Ministry of Health and Welfare modified to include cardiac MRI. Results: Of the 88 patients in the cohort 27 had evidence of CS independent of the SAECG results. The SAECG was abnormal in 14 of these 27 patients and 11 of the 61 of the subjects without cardiac involvement (P < 0.01). The sensitivity of SAECG detection of CS was 52% with a specificity of 82%. For the entire cohort, SAECG had a positive predictive value (PPV) of 0.56 and a negative predictive value (NPV) of 0.79. Within a subgroup of 67 patients with an unfiltered QRS duration of

Background. Levosimendan is an inotropic drug with unique pharmacological advantages in patients with acute heart failure. Scope of this study is to determine whether longer infusion patterns without the hypotension-inducing loading dose could justify an effective and safe alternative approach.Methods. 70 patients admitted to the emergencies with decompensated chronic heart failure received intravenously levosimendan without a loading dose up to 72 hours. Clinical parameters, BNP (Brain Natriuretic Peptide) and signal-averaged-ECG data (SAECG) were recorded up to 72 hours.Results. The 48-hour group demonstrated a statistically significant BNP decrease (P<.001) after 48 hours, which also maintained after 72 hours. The 72-hour group demonstrated a bordeline decrease of BNP after 48 hours (P=.039), necessitating an additional 24-hour infusion to achieve significant reduction after 72 hours (P<.004). SAECG data demonstrated a statistically significant decrease after 72 hours (P<.04). Apart from two deaths due to advanced heart failure, no major complications were observed.Conclusion. Prolonged infusion of levosimendan without a loading dose is associated with an acceptable clinical and neurohumoral response.

Ventricular tachycardia (VT) and ventricular fibrillation (VF) leading to sudden cardiac death remains responsible for significant mortality in patients with prior myocardial infarction (MI). The study population consisted of 50 normal controls and 50 patients with prior MI. The MI subjects were divided into 3 groups: VT/VF (-) group; 25 patients without ventricular tachyarrhythmia, VT group; 13 patients with sustained VT, and VF group; 12 patients with resuscitated VF. The parameters on the signal-averaged ECG and the frequency components recorded from the wavelet-transformed ECG were compared. The high-frequency components (HFC; 80-150 Hz) were developed in the MI group to a greater extent than those in the control group. Among the MI patients, the HFC were more developed in the VT and VF groups than in the VT/VF (-) group. In the VF group, the positive rate of LP was 50%. Meanwhile, when the peak power value at 150 Hz > 300 was defined as abnormal, the HFC was detected in 13 (100%) patients in the VT group and 12 (91.7%) in the VF group. The sensitivity of the abnormal HFC in identifying patients with VT/VF was higher than that of SAECG (96% versus 72%), although the specificity remained similar (68.5% versus 64.3%). Abnormal HFC recorded from the wavelet-transformed ECG may be a novel factor in detecting patients who are prone to VT/VF.

The non-therapeutic use of androgenic anabolic steroids (AAS) is associated with sudden cardiac death. Despite this, there is no proposed mechanism by which this may occur. Signal-averaged ECG (SAECG) allows the assessment of cardiac electrical stability, reductions of which are a known risk factor for cardiac arrhythmias. The aim of the present study was to examine cardiac electrical stability using SAECG in a group (n = 15) of long-term AAS users (AAS use 21.3 ± 3.1 years) compared with a group (n = 15) of age-matched weight lifters (WL) and age-matched sedentary controls [C (n = 15)]. AS, WL and C underwent SAECG analysis at rest and following an acute bout of exercise to volitional exhaustion. SAECGs were analyzed using a 40 Hz filter and were averaged over 200 beats. Results indicate a non-significant trend for increased incidence of abnormal SAECG measures at rest in AS (P = 0.55). However, AS demonstrated a significantly higher incidence of abnormalities of SAECG following exercise than C or WL (P < 0.05). In conclusion, the higher incidence of abnormal SAECG measurements immediately post-exercise in the AAS group places them at a greater risk of sudden death. The present study provides a strong contraindication to the use of AAS.

It has been reported that bepridil prevents ventricular fibrillation (VF) in patients with Brugada syndrome, but the comparative efficacy with and without mutation in the SCN5A gene has not been elucidated. The purpose of this study was to assess the efficacy of low-dose bepridil (100 mg/day) for VF prevention in patients with Brugada syndrome with and without SCN5A mutation. Among 130 patients with Brugada-type electrocardiogram (ECG), low-dose bepridil was administered to seven patients because of repetitive VF episodes, including three with and four without SCN5A mutation. Preventive effect for VF recurrence and changes of the ECG and the signal-averaged ECG were evaluated. Frequencies of VF episodes were reduced after treatment with low-dose bepridil in all three patients with the SCN5A mutation (before: 0.33 versus after: 0.02 episodes/month, P < 0.01), but not in all four patients without the SCN5A mutation (before: 0.43 versus after: 2.94 episodes/month, P = nonsignificant). Levels of ST-segment elevation at J points and duration of low-amplitude signals less than 40 µV in the terminal filtered QRS complex (LAS40) in signal-averaged ECG were improved exclusively in patients with the SCN5A mutation. Treatment with bepridil prevented recurrence of VF along with improvement of ST elevation and LAS40 in patients with Brugada syndrome with the SCN5A mutation.

Background Patients in the intensive care unit (ICU) setting are prone to malignant ventricular arrhythmias. We sought to test whether electrocardiographic (ECG) markers of autonomic tone, ventricular irritability, and repolarization lability could be used in short-term prediction of ventricular arrhythmias in this patient population. Methods We studied 38 patients with sustained (>30 seconds) monomorphic ventricular tachycardia, polymorphic ventricular tachycardia, or ventricular fibrillation while monitored in the ICU and 30 patients without arrhythmia in the ICU who served as controls. All patients had at least 12 hours of continuously recorded multilead ECG before arrhythmic event. Mean heart rate and measures of heart rate variability, QT variability, and ventricular ectopy were quantified in 1-hour epochs for the 12 hours before the arrhythmic event and in 5-minute epochs for the last hour preevent (and using a random termination time point in controls). Results A modest downward trend in QT variability and a rise in heart rate were observed hours before polymorphic ventricular tachycardia and ventricular fibrillation events, although no significant changes heralded monomorphic ventricular tachycardia and no changes in any parameter predicted imminent ventricular arrhythmia of any type. There were no significant differences in ECG parameters between arrhythmia patients and controls. Conclusions In ICU patients, sustained ventricular arrhythmias are not preceded by change in ECG measures of autonomic tone, repolarization variability, and ventricular ectopy. Short-term arrhythmia prediction may be difficult or impossible in this patient population based on ECG measures alone.

Background: Recurrent atrial arrhythmias (RAAs) following posterior left atrial isolation (PLAI) for atrial fibrillation are common and are associated with reconnection of the PLA and pulmonary veins. We aimed to show that P-wave duration (PWD) and P-wave area under the curve (PWAUC) changes in patients undergoing PLAI can be measured using signal-averaged electrocardiogram (SAECG), and that reversal of these changes in patients with RAAs can be used to noninvasively detect reconnection. Methods: SAECG recordings before and after PLAI in 52 patients were analyzed for changes in PWD and PWAUC and also in 26 of these patients who had a repeat procedure for RAA. Results: PWD and PWAUC reduced significantly in most leads following PLAI (mean 104 ± 11 ms to 93 ± 15 ms [P −0.29 μVs for detecting reconnection had a sensitivity of 94% and specificity of 100% (receiver operator characteristic area under the curve 0.97, P = 0.005). Conclusions: PLAI reduces PWD and PWAUC while reconnection increases them both. SAECG may be able to detect reconnection of the PLA noninvasively. (PACE 2010; 1324–1334)

BACKGROUND: Commercial spaceflight participants on orbital flights typically are older than career astronauts and they often have medical conditions that have not been studied at high g or in microgravity. This is a case report of a 56-yr-old orbital spaceflight participant with essential tremor and frequent premature ventricular contractions that occurred at rates up to 7000 per day. Before training and spaceflight, he was required to complete extensive clinical investigations to demonstrate normal cardiac structures and the absence of cardiac pathology. The evaluation included signal averaged ECG, transthoracic stress echocardiography, exercise tolerance tests, electrophysiological studies, cardiac MRI, electron beam CT, Holter monitoring, and overnight oximetry. While no cardiac pathology was demonstrated, the Russian medical team required that the PVCs be treated prior to training and spaceflight. For the initial flight, a selective beta-1 receptor beta blocker was used and for the second a calcium channel blocker was used in combination with a nonselective beta blocker for tremor control. Analogue environment testing assured that this combination of medications was compatible. CONCLUSION: The spaceflight participant's PVCs were incompletely suppressed with a low-dose selective beta-1 blocker, but were well suppressed by a calcium channel blocker. He tolerated in-flight periodic use of a nonselective beta blocker in combination with a calcium channel blocker. In-flight ECG and blood pressure monitoring results were normal, and an ECG obtained midmission and on landing day showed successful PVC suppression. He did not have any cardiac difficulty with launch, on-orbit operations, entry, or recovery

Signal averaged electrocardiogram (SAECG) is considered an important noninvasive indicator identifying patients at risk for ventricular arrhythmias. The aim of this study was to improve noninvasive prediction of CAD by integrating SAECG with the result of exercise tests in diabetic patients. Diabetic patients with stable angina pectoris underwent exercise testing and SAECG. Then a diagnostic score was derived that combined results of exercise testing and SAECG. A diagnostic score (0 to 2 points) was calculated by assigning 1 point for a positive exercise test result and 1 point for a positive SAECG. One hundred and seventy patients were included in the study. In patients with a score of 0, the likelihood of CAD is 18% whereas the likelihood of CAD is 95% in patients with a score of 2. Triple vessel CAD is present in 54%, 7% and only 1.5% of patients with score 2, 1 and 0 respectively. Therefore, patients with score 2 have a poor prognosis compared with score 1 or 0. A diagnostic score combining exercise testing and SAECG can distinguish patients with CAD from those without CAD with high accuracy in diabetic patients.

Instead of extracting the abnormal intra-QRS potentials (AIQP) waveform, this study proposes the analysis of the unpredictable intra-QRS potentials (UIQP) based on an autoregressive moving average (ARMA) prediction model to detect the signals with sudden slope change within the QRS complex for the diagnosis of high-risk patients with ventricular tachycardia (VT). The UIQP is detected as the slope changes at slope discontinuities by the prediction error of the ARMA prediction model. Because of the linearity of the ARMA prediction model, the UIQP is also proportional to the amplitude of the QRS complex if the input QRS waves have the same shapes. Hence this study further defines the UIQP-to-QRS ratio to normalize the UIQP by the root-mean-square (RMS) value of the QRS complex. The study subjects were composed of 42 normal Taiwanese and 30 patients with sustained VT. The clinical results show that the UIQP-to-QRS ratios of the VT patients in leads X, Y and Z were significantly higher than those of the normal subjects. The logical combination of any 4 of the UIQP-to-QRS ratios and conventional time-domain parameters can increase the diagnosis performance of VT patients to 92.9% specificity, 93.3% sensitivity and 93.1% total prediction accuracy.

Purpose We investigated the prevalence of LV strain impairment as estimated by 2D speckle-tracking imaging, Late potentials on signal averaged ECG (SAECG) and QRS fragmentation inpatients with diagnosed sarcoidosis without cardiac involvement according to the current guidelines. Methods and results Thirty-three patients with biopsy-proven extracardiac sarcoidosis were analyzed. We performed a prospective case–control longitudinal study including 33 patients with diagnosed extracardiac sarcoidosis and normal cardiac function as assessed by standard transthoracic echocardiography and 33 healthy age- and gender-matched controls. All patients underwent a twelve lead ECG and comprehensive echocardiographic study. Mean age of patients was 45.9 ± 13.4 years old (32 women). Compared with controls, global LV longitudinal strain (LV GLS) was reduced in sarcoidosis patients: (−18.2 ± 2.5 vs −22.4 ± 1.7%, P Conclusion Speckle-tracking echocardiography revealed decreased longitudinal LV strain in extracardiac sarcoidosis patients. QRS fragmentation was also frequently identified in this population. QRS fragmentation and LV GLS may represent an early marker of myocardial involvement in extracardiac sarcoidosis patients and should be integrated in a more sensitive and simple diagnostic algorithm criterion.

A 15-year-old boy without structural heart disease was admitted for the treatment of frequent episodes of premature ventricular contractions (PVCs). Left ventricular mapping revealed that the origin of PVC was at the posterior papillary muscle. Diastolic small potentials were observed during sinus rhythm with a constant interval following QRS beats. This potential eventually coupled with the ventricular myocardium, resulting in the generation of PVC, and thus preceded QRS by 31 msec. Catheter ablation to this site induced non-sustained ventricular tachycardia, followed by transient ventricular fibrillation. Repeated application of radiofrequency energy eliminated PVC accompanied by the split of the diastolic potential.

Background: Electrical storm (ES) is a serious problem in patients with an implantable cardioverter defibrillator (ICD). However, insufficient reports have indicated the predictors of ES in ICD patients with idiopathic dilated cardiomyopathy (DCM). The purpose of this study was to clarify the predictors of ES for risk stratification in DCM patients with an ICD. Methods and Results: Of 446 ICD patients, 53 DCM patients were included in this study. During a mean follow-up of 55±36 months, ES (≥3 times appropriate ICD therapy within 24 h) occurred in 18/53 (34%) patients. According to multivariate Cox proportional hazard regression analysis, a duration of the terminal low amplitude signals of

OBJECTIVES: : Cocaine use is associated with cardiac arrhythmias. Markers of ventricular late potentials, which may be a precursor to malignant ventricular arrhythmias, can be detected by signal-averaged electrocardiography (SA-ECG) but not by standard ECG. METHODS: : We evaluated SA-ECG parameters in 60 medically screened, physically healthy, recently abstinent cocaine users (53 males, mean [SD] age, 34.0 [4.6] years; 10.1 [6.0] years of use) and 54 nondrug-using controls (21 males, mean [SD] age 28.4 [7.8] years). SA-ECGs were done periodically for ≤12 weeks of monitored abstinence in 25 cocaine users. We analyzed 3 SA-ECG parameters considered markers of ventricular late potentials: duration of filtered QRS complex, duration of low-amplitude potentials during terminal 40 ms of QRS complex (LAS40), and root mean square voltage during terminal 40 ms of QRS complex (RMS40). RESULTS: : Cocaine users differed significantly from controls in filtered QRS complex (118.5 [11.2] ms versus 111.9 [11.4] ms; P = 0.03) but not in LAS40 (28.9 [8.2] ms versus 30.8 [8.3] ms; P = 0.40) or RMS40 (40.0 [19.8] μV versus 30.2 [20.1] μV; P = 0.06) values. The proportion of subjects with abnormal SA-ECG parameters did not differ significantly between male cocaine users and male controls. There were no significant changes over time in either the mean values or proportion of subjects with abnormal values for any SA-ECG parameter. There were significant gender differences among controls but not among cocaine users. CONCLUSION: : These findings suggest that chronic cocaine use is not associated with a higher prevalence of abnormal SA-ECG parameters in physically healthy users.

Whether T-wave morphology descriptors on the 12-lead electrocardiogram (ECG) can predict the occurrence of life-threatening ventricular arrhythmia in patients with advanced congestive heart failure is unclear.Standard 12-lead ECGs were photoscanned and digitized for analysis in 27 heart failure patients with ventricular tachycardia/ventricular fibrillation (VT/VF; study group), as well as in 54 age- and sex-matched heart failure patients without life-threatening ventricular arrhythmia as a control group. Novel T-wave morphology descriptors were compared.The results showed that the temporal descriptor, the lead dispersion (LD; 426.5 +/- 279.8 vs 189.0 +/- 125.7, P0.001), was significantly higher in the study than in the control group. The other T-wave morphology parameters, such as the T-wave morphology dispersion (45.7 +/- 20.1 vs 44.9 +/- 18.6), the total cosine between QRS and T wave (TCRT; -0.4 +/- 0.4 vs -0.5 +/- 0.3), and the normalized T-loop area (NTLA; 0.5 +/- 0.1 vs 0.4 +/- 0.1), were not significantly different between the two groups (all P value0.05). After an adjustment for other clinical variables, increased LD (odds ratio: 9.9, 95% confidence interval [CI]: 2.9-33.4, P0.001) or decreased NTLA (odds ratio: 0.4, 95% CI: 0.1-1.0, P =0.05) was associated with VT/VF.The novel T-wave morphology analysis may help in identifying heart failure patients at high risk for VT/VF.

AIMS: Patients with isolated left ventricular non-compaction (IVNC) are at high risk for developing ventricular tachyarrhythmias. However, no analysis of invasive electrophysiological (EP) findings in these patients has yet been performed. METHODS AND RESULTS: We performed a retrospective analysis of EP findings in 24 patients with IVNC. Ventricular tachyarrhythmias were inducible in nine patients; of these, two patients had sustained monomorphic ventricular tachycardia (VT) and two patients had ventricular fibrillation. No specific electrocardiographic or echocardiographic finding was predictive of VT inducibility. Three of the 9 patients with inducible VT experienced ventricular tachyarrhythmias during the follow-up of 61.4+/-50 months, whereas no tachyarrhythmias or sudden deaths were noted in 12 patients without inducible VT during the follow-up of 30+/-19 months (3 patients in the latter group were lost to follow-up). Supraventricular tachyarrhythmias were inducible in seven patients. CONCLUSION: Our present study provides the first comprehensive analysis of EP findings in patients with IVNC. Ventricular and supraventricular arrhythmias can readily be induced in these patients, whereas the inducibility of a sustained monomorphic VT is relatively low. Further studies including long-term follow-up are required to investigate the role of EP testing for arrhythmic risk stratification in these patients.

Background: Preimplantation left ventricular dyssynchrony is considered a prerequisite for a beneficial response to cardiac resynchronization therapy (CRT). However, electrical dyssynchrony estimated by QRS duration (QRSd) on ECG has not been proven to be an optimal surrogate of mechanical dyssynchrony. We evaluated the correlation of mechanical dyssynchrony with QRSd as measured by signal-averaged electrocardiography (SAECG) in comparison with measurements based on conventional surface ECG and with onscreen measurements based on digital ECG. Methods: We included 49 consecutive patients with decompensated heart failure (40 men, aged 66.8 ± 9.5 years), New York Heart Association (NYHA) class II–IV, and LVEF ≤ 40%. QRSd was calculated by manual measurement of 12-lead ECG, on-screen measurement of computer-based ECG, and calculation of total ventricular activation time on SAECG. Results: Only 60.4% of the studied patients had QRS ≥ 120 ms based on measurements derived by SAECG compared to 69.4% by using on-screen measurement of computer-based ECG and 73.5% based on surface ECG (P = 0.041). Interventricular but not intraventricular delay was correlated with QRSd. The correlation of interventricular dyssynchrony with QRSd was stronger when measured by SAECG than by surface ECG (r = 0.45, P = 0.001 vs r = 0.35, P < 0.01). Among patients with ischemic cardiomyopathy, no significant correlation was demonstrated between mechanical dyssynchrony and QRSd. In nonischemic patients, interventricular delay was significantly correlated with QRSd measured by surface ECG (r = 0.45, P < 0.05) and SAECG (r = 0.46, P < 0.05). Conclusions: The use of SAECG results in different patient classification in wide QRS complex category as compared to surface ECG. Furthermore, QRSd measured by SAECG is correlated with interventricular but not intraventricular dyssynchrony in heart failure patients.

Ventricular tachycardia and ventricular fibrillation are the most important causes of sudden cardiac death (SCD), particularly in those with structural heart disease and reduced left ventricular function. It is important to distinguish ventricular tachycardia from supraventricular tachycardia. A wide spectrum of ventricular arrhythmias exists, from those where the heart is structurally normal to those with structural heart disease. Each entity has a distinctive pathophysiology, treatment plan and prognostic outcome. Treatment modalities include simple beta-blockade to implantation of implantable cardiac defibrillator and ablative approaches. In general, those ventricular arrhythmias associated with a structurally normal heart are more benign than those associated with structural heart disease.

Several invasive and noninvasive tests for risk stratification of sudden cardiac death have been studied, mostly in the context of structural heart disease such as coronary artery disease (CAD), cardiomyopathy, and heart failure. Tests such as MTWA (repolarization abnormality) and SAECG (depolarization abnormality) have high negative predictive values but a low positive predictive value in patients with myocardial infarction or cardiomyopathy. Recently, we described the presence of a fragmented QRS complexes (fQRS) on a routine 12-lead electrocardiogram as another marker of depolarization abnormality. fQRS represents conduction delay caused by myocardial scar in patients with CAD. However, fQRS is not specific for CAD and is also encountered in other myocardial diseases such as cardiomyopathy and congenital heart disease. fQRS is associated with increased mortality and arrhythmic events in patients with CAD. fQRS has also been defined as a marker of arrhythmogenic right ventricular dysplasia/cardiomyopathy and Brugada syndrome. In Brugada syndrome, the presence of fQRS predicts episodes of ventricular fibrillation during follow-up. Therefore, the utility of fQRS in risk stratification of sudden cardiac death needs to be explored further, especially in nonischemic cardiomyopathy and heart failure.

Objectives We prospectively compared the predictive value of cardiac iodine-123 metaiodobenzylguanidine (MIBG) imaging for sudden cardiac death (SCD) with that of the signal-averaged electrocardiogram (SAECG), heart rate variability (HRV), and QT dispersion in patients with chronic heart failure (CHF). Background Cardiac MIBG imaging predicts prognosis of CHF patients. However, the long-term predictive value of MIBG imaging for SCD in this population remains to be elucidated. Methods At entry, cardiac MIBG imaging, SAECG, 24-h Holter monitoring, and standard 12-lead electrocardiography (ECG) were performed in 106 consecutive stable CHF outpatients with a radionuclide left ventricular ejection fraction (LVEF) Results During a follow-up period of 65 ± 31 months, 18 of 106 patients died suddenly. A multivariate Cox analysis revealed that WR and LVEF were significantly and independently associated with SCD, whereas the SAECG, HRV parameters, or QT dispersion were not. Patients with an abnormal WR (>27%) had a significantly higher risk of SCD (adjusted hazard ratio: 4.79, 95% confidence interval: 1.55 to 14.76). Even when confined to the patients with LVEF >35%, SCD was significantly more frequently observed in the patients with than without an abnormal WR (p = 0.02). Conclusions Cardiac MIBG WR, but not SAECG, HRV, or QT dispersion, is a powerful predictor of SCD in patients with mild-to-moderate CHF, independently of LVEF.

To assess the association of electrocardiographic repolarization and depolarization patterns to vulnerability to ventricular tachyarrhythmias.In the present case-control study, a 12-lead ECG, signal-averaged ECG (SAECG), T-wave and QRS morphology, and T-wave alternans (TWA) were analyzed in post-MI patients with and without documented sustained ventricular tachycardia (VT) or fibrillation (VF) (VT/VF group, n=40, Non-VT/VF group, n=37, respectively) and healthy subjects (n=41).The QRS complex duration, measured from standard ECG (128 +/- 32 ms vs. 102 +/- 21 ms, p0.001) or SAECG (125 +/- 25 ms vs. 99 +/- 20 ms, p0.001), was significantly longer in the VT/VF than Non-VT/VF group. Several T-wave morphology variables, e.g., the total cosine of the angle between the main vectors of T-wave and QRS loops (TCRT), were different in the VT/VF (-0.13 +/- 0.58) and Non-VT/VF group (-0.11 +/- 0.48) compared to the healthy controls (0.47 +/- 0.50, p0.001). However, there were no significant differences in any of the T-wave morphology variables including TWA between the two post-MI groups.Abnormalities in ventricular depolarization are more common among post-MI patients with prior VT/VF than in those without documented ventricular tachyarrhythmias. Abnormal T-wave morphology and TWA seem to reflect the heart disease rather than specifically vulnerability to VT/VF.

Background: It is important to follow up patients surviving acute myocardial infarction (MI), to detect the presence of any life-threatening arrhythmias. Various non-invasive examinations, such as signal-averaged ECG (SAECG), have been reported to predict the fatal ventricular tachycardia (VT); however, these conventional methods have limitations in detecting VT occurring in patients with complete right bundle branch block (CRBBB) QRS. Wavelet transform has been increasingly reported as a superior time-frequency analysis on the surface ECG in detecting abnormal high-frequency components (HFCs), thus suggesting abnormal myocardial conductions; however, it remains unclear whether wavelet-transformed ECG (WTECG) is useful in patients with CRBBB. Objective: The purpose of this study is to assess the predictive value of WTECG for detecting arrhythmogenic substrates in MI patients with CRBBB. Methods: Both the WTECG and SAECG were evaluated in 22 subjects with CRBBB, including 10 subjects without cardiovascular diseases (control group), 7 prior MI patients without VT (Non-VT group), and 5 prior MI patients with sustained VT (VT group). A 12-lead ECG (10 kHz sampling) was recorded and the representative QRS complex (300 ms) was transformed at a frequency range of 40-280 Hz using the Gabor function as the analyzing wavelet. In the power curve along a time course, the percentages of the peak power values at each frequency (60, 80, 120, 150, and 200 Hz) in the corresponding power values at 40 Hz (P60/40, P80/40, P120/40, P150/40, and P200/40, respectively) were calculated. 'The power percentages (P120/40, P150/40, or P200/40) ≥50%' was defined as an abnormal HFC (AHFC), and the number of the leads in which an AHFC was detected (NL-AHFC) of 8 leads (I, aVF, V1-V6) was counted for comparison of the two MI groups. Results: There was no significant difference among the three groups in the SAECG recording. The power percentages of HFCs (P120/40, P150/40, and P200/40) in Non-VT group were significantly higher than those in control group (48.2 ± 36.5 vs. 30.6 ± 7.7, P

Background: Intra-atrial reentrant tachyarrhythmia (IART) after surgical repair for congenital heart diseases (CHD) has not been noninvasively characterized. Methods and Results: The 28 patients after surgery for CHD and 14 patients without surgery were investigated by 87-lead body surface mapping (BSM), 12-lead electrocardiogram (ECG), 20-lead signal averaged ECG (SAECG) and endocardial electroanatomical mapping (CARTO) during clockwise (CW: n=9) or counterclockwise (CCW: n=5) incisional atrial tachycardia (Incision-AT), CCW (n=23) or CW (n=4) cavotricuspid isthmus-dependent atrial flutter (CTI-AFL), and double-loop reentry (n=4). On the BSM, the isopotential map pattern and its locus of the minimum potential could differentiate the reentrant circuits, and the activation map revealed the reentrant circuits, which were highly coincident with those obtained from CARTO. On the 12-lead ECG, negative-positive polarity in the inferior leads or a discordant pattern in the precordial leads was observed in all cases of CTI-AFL, but 3/14 Incision-AT, positive polarity in lead V1 was observed in all cases of CCW, but none of CW CTI-AFL, positive polarity in lead I was observed in all cases of CW, but none of CCW Incision-AT. Conclusions: Flutter-wave isopotential map and its activation sequence from the BSM predict reentrant circuits of IART after surgery for CHD. Flutter-wave polarity on the 12-lead ECG could differentiate these reentrant patterns. (Circ J 2009; 73: 451 - 460)

Background: The correlation between parameters of two-dimensional echocardiography and signal-averaged ECG (SAECG) in patients with arrhythmogenic right ventricular cardiomyopathy (ARVC) is not known well. Methods: Thirty-three patients (13 females, 40.3 ± 14.4 years old) were included in this study. Both the right and left ventricular dimensions and systolic function were assessed with two-dimensional echocardiography. The SAECG was performed with high-gain amplification and filtered using bidirectional Butterworth filters between 40 and 250 Hz. We evaluated the correlation between the parameters of the SAECG and two-dimensional echocardiography. Results: The right ventricular (RV) outflow tract was the most frequently (n = 18, 54%) involved segment. Six (18%) patients had only mildly decreased RV systolic function. All the other patients had normal RV systolic function. Although localized left ventricular wall motion abnormalities were observed in 14 (42%) patients, the left ventricular ejection fraction was normal in most (n = 32, 97%). Late potentials were positive in 22 (63%) patients. There was no significant correlation between parameters of the SAECG and two-dimensional echocardiography for the entire patient population. Conclusions: The SAECG parameters exhibited no correlation to any of two-dimensional echocardiography parameters in the patients with ARVC. Fragmented electrical activity may develop with no significant relation to the anatomical changes in the patients with ARVC.

Objective To identify electrocardiographic predictors of mortality in patients with familial dysautonomia (FD). Methods Ten-minute resting high-fidelity 12-lead electrocardiograms (ECGs) were obtained from 14 FD patients and 14 age/gender-matched healthy subjects. Multiple conventional and advanced ECG parameters were studied for their ability to predict mortality over a subsequent 4.5-year period, including representative parameters of heart rate variability (HRV), QT variability (QTV), T-wave complexity, signal averaged ECG, and 3-dimensional ECG. Results Four of the 14 FD patients died during the follow-up period, three with concomitant pulmonary disorder. Of the ECG parameters studied, increased non-HRV-correlated QTV and decreased HRV were the most predictive of death. Compared to controls as a group, FD patients also had significantly increased ECG voltages, JTc intervals and waveform complexity, suggestive of structural heart disease. Conclusion Increased QTV and decreased HRV are markers for increased risk of death in FD patients. When present, both markers may reflect concurrent pathological processes, especially hypoxia due to pulmonary disorders and sleep apnea.

Background: Ventricular late potentials (LPs) obtained by the signal-averaged electrocardiogram (SAECG) have prognostic significance as independent predictors of arrhythmic events after an acute myocardial infarction (AMI). Angiotensin receptor blockers reduce the overall mortality and risk of sudden cardiac death in postinfarction patients. The aim of this study was to investigate the effect of early losartan therapy on ventricular LPs, a noninvasive method for the evaluation of arrhythmogenic substrates in AMI patients. Methods: The study included 97 patients with their first AMI. Forty-eight patients (39 men and 9 women, aged 58.8 ± 13.19 years), received early losartan therapy. The control group consisted of 49 patients (38 men and 11 women, aged 59.55 ± 11.0 years), did not received early losartan therapy. The SAECG was performed at admission and day 14. Results: The baseline clinical, angiographic characteristics, and reperfusion methods were similar in both groups. The baseline SAECG findings were also similar in the two groups. There was a significant decrease in the rate of LP, between the first and last SAECG recordings, after reperfusion therapy in the losartan group. All of the parameters of LPs were significantly improved in the losartan group on the last SAECG recordings. Conclusion: The results of this study showed that losartan treatment, early after an AMI, reduced the incidence of LP and may thus favorably affect arrhythmia substrates.

L arge clinical trials 2,3 have shown that prophylactic implantable cardioverter/defibrillator (ICD) implantation reduces mortality in patients with severe left ventricular dysfunction. However, even in this “high-risk” population, only a minority of patients with ICDs ever receive lifesaving therapy. Although broad application of a strategy of relying on left ventricular dysfunction to select patients for prophylactic ICD implantation is marginally cost effective, implementation of this therapy in all patients meeting eligibility criteria presents a significant economic burden, particularly outside the United States and western Europe. Furthermore, current selection criteria for ICD implantation fail to address the large number of patients with less severe left ventricular dysfunction or normal ventricular function who go on to experience sudden cardiac death—in fact, only a minority of sudden deaths occur in patients with severe left ventricular dysfunction at baseline. These considerations highlight the importance of developing new tools for risk stratification for

This work analyzes and attempts to enhance the accuracy and reproducibility of parametric modeling in the discrete cosine transform (DCT) domain for the estimation of abnormal intra-QRS potentials (AIQP) in signal-averaged electrocardiograms. One hundred sets of white noise with a flat frequency response were introduced to simulate the unpredictable, broadband AIQP when quantitatively analyzing estimation error. Further, a high-frequency AIQP parameter was defined to minimize estimation error caused by the overlap between normal QRS and AIQP in low-frequency DCT coefficients. Seventy-two patients from Taiwan were recruited for the study, comprising 30 patients with ventricular tachycardia (VT) and 42 without VT. Analytical results showed that VT patients had a significant decrease in the estimated AIQP. The global diagnostic performance (area under the receiver operating characteristic curve) of AIQP rose from 73.0% to 84.2% in lead Y, and from 58.3% to 79.1% in lead Z, when the high-frequency range fell from 100% to 80%. The combination of AIQP and ventricular late potentials further enhanced performance to 92.9% (specificity = 90.5%, sensitivity = 90%). Therefore, the significantly reduced AIQP in VT patients, possibly also including dominant unpredictable potentials within the normal QRS complex, may be new promising evidence of ventricular arrhythmias.

Abnormal QT prolongation with the associated arrhythmias is a significant predictor of mortality in diabetic patients. Gap junctional intercellular communication allows electrical coupling between heart muscle cells. The effects of streptozotocin (STZ)-induced diabetes mellitus on the expression and distribution of connexin 43 (Cx43) in ventricular muscle have been investigated. Cx43 mRNA expression was measured in ventricular muscle by quantitative PCR. The distribution of total Cx43, phosphorylated Cx43 (at serine 368) and non-phosphorylated Cx43 was measured in ventricular myocytes and ventricular muscle by immunocytochemistry and confocal microscopy. There was no significant difference in Cx43 mRNA between diabetic rat ventricle and controls. Total and phosphorylated Cx43 were significantly increased in ventricular myocytes and ventricular muscle and dephosphorylated Cx43 was not significantly altered in ventricular muscle from diabetic rat hearts compared to controls. Disturbances in gap junctional intercellular communication, which in turn may be attributed to alterations in balance between total, phosphorylated and dephosporylated Cx43, might partly underlie prolongation of QRS and QT intervals in diabetic heart.

Background: The autonomic nervous system is thought to be involved in the initiation of atrial fibrillation (AF). However, there is a distinct entity of vagal AF characterized by episodes occurring at rest, postprandially, or during sleep. The purpose of this study was to compare intraatrial conduction in patients with vagally mediated AF to those with nonvagal AF, using the signal-averaged electrocardiogram (SAECG) of P wave. Methods: SAECG of P wave was performed in 58 patients with AF using the Marquette Medical System, and the mean filtered P-wave duration (SAPW) was measured. Nine patients were categorized as having pure vagal AF (Group I), and 42 patients as having nonvagal AF (Group II); the remaining seven patients were excluded from analysis because of incomplete data. Results: The patients in Group I were significantly younger and more likely to have paroxysmal lone AF, as compared to those in Group II. There was no significant difference in left atrial size and left ventricular function in the two groups. The mean SAPW was significantly shorter in Group I when compared to Group II (118 ± 5 ms vs 149 ± 39 ms, P < 0.001). Whereas all patients in Group I had a normal SAPW, 79% of patients in Group II had an abnormal SAPW (P < 0.001). A normal SAPW was significantly predictive of vagal AF independent of other co-variables. Conclusions: (1) Patients with vagal AF are younger, and invariably have paroxysmal lone AF. (2) SAPW is normal and significantly shorter in vagal AF when compared to patients with nonvagal AF. (3) This suggests that those in the vagal AF population have normal intraatrial conduction, which has implications for AF ablation in these patients.

The purpose of this study was to verify the spatial distribution of myocardial repolarization heterogeneity using a newly developed 187-channel signal-averaged vector-projected ECG (187-ch SAVP-ECG). We constructed corrected recovery time (RTc) and Tpeak-end (corrected Tp-e) dispersion maps using a 187-ch SAVP-ECG based on vector-projection theory using a Mason-Likar lead system. We compared the spatial distribution and quantitative values of dispersion maps by 187-ch SAVP-ECG with those by 64-ch magnetocardiography (MCG) in 27 normal controls (control) and 16 patients (12 myocardial infarction (MI), and 4 dilated cardiomyopathy (DCM)). The wave pattern of the 187-ch SAVP-ECG in the representative cases was similar to those in 64-ch MCG. Spatial distribution increased RTc and corrected Tp-e dispersion maps defined by 187-ch SAVP-ECG were in agreement with those by 64-ch MCG. The value of RTc dispersion in MI was higher than that in control (41 +/- 21 ms in MI versus 30 +/- 12 ms in control, P0.05). The value of corrected Tp-e dispersion in DCM was higher than that in control (58 +/- 12 ms in DCM versus 30 +/- 13 ms in control, P0.001). There was a good correlation between RTc and corrected Tp-e dispersion values determined by 187-ch SAVP-ECG and 64-ch MCG modalities (y = 0.46x + 18, r = 0.62, P = 0.02 for RTc dispersion; y = 0.52x + 15, r = 0.63, P = 0.01 for corrected Tp-e dispersion). RTc and corrected Tp-e dispersion maps by 187-ch SAVP-ECG based on vector-projection theory can evaluate the spatial distribution of myocardial repolarization heterogeneity.

The role of P-wave signal-averaged electrocardiography (P-SAECG) in the prediction of atrial fibrillation (AF) attacks has been validated in various disease states. In the present study, we aimed to investigate the effect of hemodialysis (HD) on P-SAECG parameters and to determine the related risk factors that might affect those parameters. Ninety-one HD patients and 68 controls were included. Hemoglobin levels, serum electrolytes, arterial pH, and interdialytic weight changes were assessed. P-wave duration (PWD) and late potentials of P wave (root-mean-square voltage for the last 20 ms of the signal-averaged P wave [LP20]) were determined by P-SAECG. Pre- and postdialysis PWDs were significantly increased in HD patients than in controls (both P

The mechanism of reentrant tachycardia was established nearly a century ago, but the relationships between myocardial infarction and predisposition to sudden death were not unravelled until much later. In the latter half of the twentieth century many studies sought to ascertain what variables were predictive of death following myocardial infarction. Approximately one half of all deaths during the year following myocardial infarction are sudden and due to ventricular tachycardia (VT) or ventricular fibrillation (VF). We aimed to utilise non-invasive signal-averaging, along with programmed electrical stimulation of the heart, to determine whether one could predict spontaneous ventricular tachycardia and sudden death late after myocardial infarction. The sensitivity of ventricular electrical instablility (inducible ventricular tachycardia or fibrillation) as a predictor of instantaneous death or spontaneous VT was 86%, and the specificity was 83%. When other variables (delayed ventricular activation at signal-averaging, ejection fraction at gated heart pool scan, ventricular ectopic activity at ambulatory monitoring and exercise testing) were taken into account, inducible VT at electrophysiological study was the single best predictor of spontaneous VT and sudden cardiac death after myocardial infarction. The Westmead studies of Uther et al. in the decade or so from 1980 established programmed stimulation as the best predictor of sudden death after myocardial infarction. Subsequent studies by others have demonstrated a survival advantage of defibrillator implantation in patients with low ejection fraction (and inducible ventricular tachycardia) after myocardial infarction.