Signal-averaged electrocardiogram in Ebstein's anomaly

Tede, Nikola; Shivkumar, Kalyanam; Perloff, Joseph K.; Middlekauff, Holly R.; Fishbein, Michael C.; Child, John S.; Laks, Hillel

doi:10.1016/j.amjcard.2003.10.058

Cited by 25 publications

(9 citation statements)

References 22 publications

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“…56 In unoperated patients, signal-averaged ECGs almost universally identify late potentials corresponding to delayed conduction across atrialized right ventricle. 59 In the absence of ventricular preexcitation, the QRS axis is generally normal although occasionally leftward. 60 Q waves are noted in lead V 1 in about 50% of patients and may extend as far as lead V 4 .…”

Section: Ebstein's Anomalymentioning

confidence: 99%

Clinical Use of Electrocardiography in Adults With Congenital Heart Disease

Khairy

Marelli

2007

Circulation

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Section: Ebstein's Anomalymentioning

confidence: 99%

Clinical Use of Electrocardiography in Adults With Congenital Heart Disease

Khairy

Marelli

2007

Circulation

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“…8 Several histopathologic studies on EA demonstrated that the atrialized portion of the RV becomes disproportionately dilated and has extensive fibrosis with reduced numbers of myocytes. 19,20 In addition, the abnormal signal observed during endocardial mapping of the aRV was related to the bizarre configuration of the widened QRS complexes on surface ECG. 21,22 They also showed that the aRV was particularly irritable and, therefore, could serve as a substrate for ventricular fibrillation.…”

Section: Fqrs Complexes and Risk Of Ventricular Tachyarrhythmiasmentioning

confidence: 99%

Fragmented QRS Complex in Adult Patients With Ebstein Anomaly and Its Association With Arrhythmic Risk and the Severity of the Anomaly

Park

Chung

et al. 2013

Circ: Arrhythmia and Electrophysiology

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Background-Fragmented QRS complex (fQRS) on 12-lead ECG, a marker of myocardial scar, is a predictor of arrhythmic events in patients with ischemic and nonischemic cardiomyopathy. We investigated whether the presence of fQRS is associated with the severity of the anomaly and with increased arrhythmic events in adult patients with Ebstein anomaly (EA). Methods and Results-In 51 consecutive adult patients with EA (median age, 37 years; 18 males), the severity index of EA calculated from echocardiographic data and clinical arrhythmic events were analyzed. The extent of fQRS in each patient was measured by counting the number of ECG leads showing fQRS. There were 35 (68.6%) patients with fQRS (fQRS group) and 16 (31.4%) patients without fQRS (non-fQRS group). fQRS was observed more frequently in the inferior (n=26) and precordial (n=25) leads versus the lateral leads (n=5). The patients in the fQRS group had a worse functional class, greater cardiothoracic ratios, more severe tricuspid regurgitation, larger atrialized right ventricular areas, higher EA severity scores, and more frequent arrhythmic events compared with those in the non-fQRS group. The atrialized right ventricular area showed a positive correlation with the fQRS extent (r=0.51; P<0.001). In multivariable Cox regression models, the presence of fQRS was independently associated with arrhythmic events (P=0.036). Conclusions-Fragmented

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“…The previously mentioned histopathology of the atrialized portion of the right ventricle is compatible with reduced cell‐to‐cell connections, disordered fiber orientation, and increased electrical impedance, all of which mitigate normal conduction. Second, Tede et al demonstrated late potentials by signal averaged ECGs in 23 patients with Ebstein's anomaly, which they hypothesized to be caused by slow conduction in the atrialized right ventricle 1 . In a separate subset of their patients undergoing surgical intervention, histologic sections from this region showed clusters of myocytes within a fibrous matrix.…”

Section: Editorial Commentmentioning

confidence: 99%

“…Hence, there is some distance between the annulus and leaflet coaptation plane, giving rise to the “atrialized portion” of the right ventricle. Histologically, this portion of the right ventricle shows fibrosis and decreased numbers of myocytes 1,2 . Insufficient apoptosis during right ventricular development is the currently favored mechanism to explain Ebstein's anomaly.…”

Section: Editorial Commentmentioning

confidence: 99%