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Signal-averaged ECG (signal-averaged + ecg)
Selected AbstractsThe Full Stomach Test as a Novel Diagnostic Technique for Identifying Patients at Risk of Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 6 2006F.A.C.C., Ph.D., TAKANORI IKEDA M.D. Introduction: Autonomic modulation, particularly high vagal tone, plays an important role in the occurrence of ventricular tachyarrhythmias in the Brugada syndrome. Food intake modulates vagal activity. We assessed the usefulness of a novel diagnostic technique, the "full stomach test," for identifying a high-risk group in patients with a Brugada-type electrocardiogram (ECG). Methods and Results: In 35 patients with a Brugada-type ECG, we assessed 12-lead ECGs before and after a large meal, a pilsicainide pharmacological test, spontaneous ST-segment change, late potentials by signal-averaged ECG, microvolt T-wave alternans, and four other ECG parameters. These patients were divided into two groups (i.e., high-risk group [n = 17] and indeterminate risk group [n = 18]). The full stomach test was defined as positive when augmentation of characteristic ECG abnormalities was observed after meals. Thirteen patients had a prior history of life-threatening events such as aborted sudden death and syncope, with a total of 30 episodes. These episodes had a circadian pattern, at night and after meals. The full stomach test was positive in 17 of the study patients (49%). A positive test outcome was characterized by a higher incidence of a history of life-threatening events than a negative test outcome (P = 0.015, odds ratio = 7.1). In comparison between the two groups, the incidence (82%) of positive outcomes in the high-risk group was significantly higher than that (17%) in the indeterminate risk group (P = 0.0002). Conclusions: Characteristic ECG changes diagnostic of Brugada syndrome are augmented by a large meal. These data are associated with a history of life-threatening events in Brugada syndrome. [source] Assessment of Markers for Identifying Patients at Risk for Life-Threatening Arrhythmic Events in Brugada SyndromeJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2005YOUICHI AJIRO M.D. Introduction: Risk stratification for life-threatening arrhythmic events in Brugada syndrome is not yet established. The aim of the present study was to examine the usefulness of various markers in predicting life-threatening arrhythmic events in the Brugada syndrome. Methods and Results: Forty-six patients with Brugada-type ECGs were categorized into the symptomatic (n = 28) and asymptomatic (n = 18) groups. Statistical analyses were performed with respect to the usefulness of the following markers: SCN5A mutation, pharmacologic challenge, ventricular fibrillation (VF) inducibility by programmed electrical stimulation, and late potential (LP) by signal-averaged ECG (SAECG). Comparison between the two groups revealed a significant difference only in LP positivity (92.6% vs 47.1%, P = 0.0004). The symptomatic group had significantly lower RMS40, longer LAS40, and longer fQRSd compared with the asymptomatic group. A significant difference was noted, especially RMS40. The positive predictive value, negative predictive value, and predictive accuracy when setting a cutoff value of 15 ,V were 92.0%, 78.9%, and 86.4%, respectively. Furthermore, patients with an RMS40 value <15 ,V (n = 25) showed significantly higher rates of VF recurrence compared with patients with an RMS40 value , 15 ,V (n = 19, P = 0.047). Conclusion: Regarding risk stratification for identifying high-risk patients in Brugada syndrome, only LP by SAECG was shown to be useful, suggesting the importance of RMS40 in predicting the history of life-threatening arrhythmic events and the recurrence of VF. [source] Relatively Benign Clinical Course in Asymptomatic Patients with Brugada-Type Electrocardiogram Without Family History of Sudden DeathJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 1 2001SHIHO TAKENAKA M.D. Asymptomatic Brugada-Type ECG.Introduction: The incidence of sudden death or ventricular fibrillation (VF) in asymptomatic Brugada syndrome patients with a family history of sudden death is reported to be very high. However, there are few reports on the prognosis of asymptomatic Brugada syndrome patients without a family history of sudden death. Methods and Results: Eleven patients (all male; mean age 40.5 ± 9.6 years, range 26 to 56) with asymptomatic Brugada-type ECG who had no family history of sudden death were evaluated. The degrees of ST segment elevation and conduction delay on signal-averaged ECG (SAECG) before and after pilsicainide were evaluated in all 11 patients. VF inducibility by ventricular electrical stimulation also was evaluated in 8 of 11 patients. Patients were followed for a period of 9 to 84 months (mean 42.5 ± 21.6). The J point level was increased (V1 :0.19 ± 0.09 mV to 0.36 ± 0.23 mV; V2: 0.31 ± 0.12 mV to 0.67 ± 0.35 mV) by pilsicainide. Conduction delay was increased (total QRS: 112.2 ± 6.3 msec to 131 7 ± 6.3 msec; under 40 , V: 42.0 ± 8.5 msec to 52.7 ± 12.7 msec; last 40 msec: 17.4 ± 5.9 , V to 10.4 ± 6.1 , V) on SAECG by pilsicainide. VF was induced in only 1 of 8 patients. None of the patients had syncope or sudden death during a mean follow-up of 42.5 ± 21.6 months. Conclusion: This study suggests that asymptomatic patients with Brugada-type ECG who have no family history of sudden death have a relatively benign clinical course. [source] Ventricular Dyssynchrony and Risk Markers of Ventricular Arrhythmias in Nonischemic Dilated Cardiomyopathy:PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003A Study with Phase Analysis of Angioscintigraphy FAUCHIER, L.,et al.: Ventricular Dyssynchrony and Risk Markers of Ventricular Arrhythmias in Nonischemic Dilated Cardiomyopathy: A Study with Phase Analysis of Angioscintigraphy.Biventricular pacing is a new form of treatment for patients with dilated cardiomyopathy and ventricular dyssynchrony. Limited information is available regarding the relationship between ventricular dyssynchrony and risk markers of ventricular arrhythmias in idiopathic dilated cardiomyopathy (IDC). In 103 patients with IDC, Fourier phase analysis of both ventricles was performed from equilibrium radionuclide angiography (ERNA). The difference between the mean phase of the LV and RV was a measure of interventricular dyssynchrony, and the standard deviations of the mean phases in each ventricle measured intraventricular dyssynchrony. There were no significant differences in inter- and intraventricular dyssynchrony between patients with versus without histories of sustained VT or VF, nonsustained VT, abnormal signal-averaged ECG, or induced sustained monomorphic VT. Dyssynchrony was not related to decreased heart rate variability (HRV). LV and interventricular dyssynchrony were weakly related to QT duration and QT dispersion. During a follow-up of27 ± 23 months, 21 patients had major adverse cardiac events (MACE), including 7 cardiac deaths, 11 progression of heart failure leading to cardiac transplantation, and 3 sustained VT/VF. The only independent predictors of MACE were an increased standard deviation of LV mean phase (P = 0.003), a decreased HRV (standard deviation of normal-to-normal intervals, P = 0.004), and histories of previous VT/VF (P = 0.03) or nonsustained VT (P = 0.04). In conclusion, left intraventricular dyssynchrony evaluated with ERNA was an independent predictor of MACE in IDC and was not related to usual risk markers of ventricular arrhythmias. This may have implications for resynchronization therapy and/or the use of implantable cardioverter defibrillators in IDC. (PACE 2003; 26[Pt. II]:352,356) [source] Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial InfarctionPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 5 2001PAULUS KIRCHHOF KIRCHHOF P., et al.: Prolonged QRS Duration Increases QT Dispersion But Does Not Relate to Arrhythmias in Survivors of Acute Myocardial Infarction. QT dispersion has been suggested and disputed as a risk marker for ventricular arrhythmias after myocardial infarction. Delayed ventricular activation after myocardial infarction may affect arrhythmic risk and QT intervals. This study determined if delayed activation as assessed by (1) QRS duration in the 12-lead ECG and by (2) late potentials in the signal-averaged ECG affects QT dispersion and its ability to assess arrhythmic risk after myocardial infarction. QT duration, JT duration, QT dispersion, and JT dispersion were compared to QRS duration in the 12-lead ECG and to late potentials in the signal-averaged ECG recorded in 724 patients 2,3 weeks after myocardial infarction. Prolonged QRS duration (> 110 ms) and high QRS dispersion increased QT and JT dispersion by 12%,15% (P < 0.05). Presence of late potentials, in contrast, did not change QT dispersion. Only the presence of late potentials (n = 113) was related to arrhythmic events during 6-month follow-up. QT dispersion, JT dispersion, QRS duration, and QRS dispersion were equal in patients with (n = 29) and without arrhythmic events (QT disp 80 ± 7 vs 78 ± 1 ms, JT disp 80 ± 6 vs 79 ± 2 ms, mean ± SEM, P > 0.2). In conclusion, prolonged QRS duration increases QT dispersion irrespective of arrhythmic events in survivors of myocardial infarction. Presence of late potentials, in contrast, relates to arrhythmic events but does not affect QT dispersion. Therefore, QT dispersion may not be an adequate parameter to assess arrhythmic risk in survivors of myocardial infarction. [source] Electrocardiographic Alterations during Hyperinsulinemic Hypoglycemia in Healthy SubjectsANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2008Tomi Laitinen M.D. Background: We evaluated the arrhythmogenic potential of hypoglycemia by studying electrocardiographic (ECG) changes in response to hyperinsulinemic hypoglycemia and associated sympathoadrenal counterregulatory responses in healthy subjects. Methods: The study population consisted of 18 subjects, aged 30,40 years. Five-minute ECG recordings and blood samplings were performed at baseline and during the euglycemic and hypoglycemic hyperinsulinemic clamp studies. PR, QT, and QTc intervals of electrocardiogram and ECG morphology were assessed from signal-averaged ECG. Results: Although cardiac beat interval remained unchanged, PR interval decreased (P < 0.01) and QTc interval (P < 0.001) increased in response to hyperinsulinemic hypoglycemia. Concomitant morphological alterations consisted of slight increases in R-wave amplitude and area (P < 0.01 for both), significant decreases in T-wave amplitude and area (P < 0.001 for both), and moderate ST depression (P < 0.001). Counterregulatory norepinephrine response correlated with amplification of the R wave (r =,0.620, P < 0.05) and epinephrine response correlated with flattening of the T wave (r =,0.508, P < 0.05). Conclusions: Hyperinsulinemic hypoglycemia with consequent sympathetic humoral activation is associated with several ECG alterations in atrioventricular conduction, ventricular depolarization, and ventricular repolarization. Such alterations in cardiac electrical function may be of importance in provoking severe arrhythmias and "dead-in-bed" syndrome in diabetic patients with unrecognized hypoglycemic episodes. [source] Lack of Impact of Myocardial Ischemia on the Signal-Averaged ECG Assessment by Time-Domain AnalysisANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2002Michael A. E. Schneider M.D. Background: Late potentials represent an arrhythmogenic substrate in chronically infarcted myocardium. It is hypothesized that acute transient ischemia enhances anisotropic electrical ventricular activation and facilitates reentry mechanisms. Study aim was the prospective assessment of the impact of dipyridamole-induced myocardial ischemia on the signal-averaged ECG. Methods: Dipyridamole stress thallium-201 SPECT imaging was utilized to avoid noise contamination of the signal-averaged ECG from exercise and to document evidence and localization of myocardial ischemia or persistent perfusion defects in 68 patients with suspected coronary artery disease. Before and during dipyridamole-induced vasodilatation serial signal-averaged ECG was performed to evaluate the influence of transient ischemia on the occurrence of late potentials. Results: There was a significant difference between heart rate at rest and heart rate under dipyridamole influence in patients with inducible ischemia (70 ± 13 vs. 87 ± 13; P < 0.0001) in contrast to patients without dipyridamole-induced ischemia (74 ± 20 vs. 80 ± 16; n.s.). The number of averaged beats and achieved noise level was comparable between both groups. Thirty-three of 68 patients (49%) revealed dipyridamole-induced ischemia; however, no changes of the SAECG parameters, such as QRS, RMS, LAS at 25,250 and 40,250 Hz bandpass filtering in the leads X, Y, Z and vector magnitude, respectively, were observed as a result of ischemia. Conclusion: These results suggest that transient myocardial ischemia does not affect the signal-averaged ECG. Clinically, the signal-averaged ECG analysis seems not to be helpful in identifying patients with silent ischemia. A.N.E. 2002;7(3):191,197 [source] Randomized Study of Early Intravenous Esmolol Versus Oral Beta-Blockers in Preventing Post-CABG Atrial Fibrillation in High Risk Patients Identified by Signal-Averaged ECG: Results of a Pilot StudyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2002Nomeda Balcetyte-Harris M.D. Background: Patients with prolonged signal-averaged ECG have four times higher risk for development of atrial fibrillation (AF) after coronary artery bypass surgery (CABG). Incidence of AF is reduced, but not eliminated by prophylaxis with beta-blockers. The limitations of prophylaxis with oral beta-blockers may be related to the delayed effect of oral therapy. We performed a pilot study of the efficacy of early intravenous esmolol and an oral beta-blocker regimen for prevention of postoperative AF. Methods: Fifty patients referred for CABG and considered to be at high risk for postoperative AF on the basis of prolonged signal-averaged ECG P wave duration > 140 ms were randomized to receive either a 24-hour infusion of esmolol 6,18 hours after CABG, at an average dose 67 ± 7 ,/kg/min, followed by oral beta-blockers versus oral beta-blockers only beginning on postoperative day 1. Results: Seven of 27 patients (26%) in the esmolol group and 6 of 23 patients (26%) in the oral beta-blocker group developed postoperative AF, P = NS. The mean time of onset of AF (2.7 ± 0.5 vs 2.7 ± 0.3 postoperative day, P = NS) and the median duration of AF (10 [2192] vs 7 [1.16] hours, P = NS) were similar between the two groups. Eleven (41%) patients treated with esmolol developed adverse events (hypotension: 8, bradycardia requiring temporary pacing: 2, left ventricular failure:1 patient) as compared to only one patient (4%) in the beta-blocker group who developed hypotension, P = 0.006. Conclusions: This randomized controlled pilot study suggests that intravenous esmolol is less well tolerated and offers no advantages to standard beta-blocker in preventing AF after CABG. A.N.E. 2002;7(2):86,91 [source] | ||||||||||