Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease.

Miller, John M.; Marchlinski, F E; Buxton, Alfred E.; Josephson, Mark E.

doi:10.1161/01.cir.77.4.759

Cited by 186 publications

(95 citation statements)

References 23 publications

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“…Ventricular tachycardia was then induced, and the twelve lead ECG recordings of induced VT were analyzed to regionalize the site of origin. 11 The VT mapping techniques included activation mapping, entrainment mapping, and pace-mapping. All mapping techniques were always performed in combination as clinically indicated.…”

Section: Mappingmentioning

confidence: 99%

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Characterization of Endocardial Electrophysiological Substrate in Patients With Nonischemic Cardiomyopathy and Monomorphic Ventricular Tachycardia

2003

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Background-Although catheter mapping has been used to define the endocardial electrogram characteristics in patients with ventricular tachycardia (VT) and coronary disease, characterization of the electrophysiological substrate in patients with VT and nonischemic cardiomyopathy is limited. Methods and Results-Left ventricular endocardial electroanatomical mapping was performed in 19 patients with nonischemic cardiomyopathy and monomorphic VT with an average of 178Ϯ83 sites per chamber mapped. Abnormal bipolar electrogram was defined as endocardial voltage signal amplitude of Ͻ1.8 mV. The extent and location of abnormal endocardium was estimated by measuring areas of abnormal electrogram recordings from 3D voltage maps. The origin of VT was approximated by identifying sites of entrainment with concealed fusion or early presystolic activity and/or by pace mapping. Abnormal electrograms were recorded over a 41Ϯ28 cm 2 area that represented 20Ϯ12% of total endocardial surface. The majority of patients (14/19 patients) had only a modest area (Ͻ25%) of endocardial abnormality. All patients had abnormal low-voltage endocardial areas located near the ventricular base in the perivalvular region. There were 3Ϯ1 VT morphologies per patient. The majority (88%) of the 57 mapped VTs originated from the ventricular base, corresponding to regions with abnormal endocardial electrograms. Conclusions-Electroanatomical

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Section: Mappingmentioning

confidence: 99%

“…The site of origin of the VT was then determined by the site of pace-mapping with the paced QRS morphology mimicking that of VT on the 12 lead ECG. 11,14,15 To further characterize the VT substrate, selective epicardial recordings were performed via coronary sinus and epicardial veins in 3 patients.…”

Section: Mappingmentioning

confidence: 99%

Characterization of Endocardial Electrophysiological Substrate in Patients With Nonischemic Cardiomyopathy and Monomorphic Ventricular Tachycardia

2003

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“…When the location of these Q waves matches that of negative QRS complexes during tachycardia it also suggests VT [38].…”

Section: Electrocardiographic Manifestationsmentioning

confidence: 93%

Sustained ventricular tachycardia in structural heart disease

Hadid

2015

Cardiol J

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“…The SoO of a scar-related re-entrant VT has been differently defined as (1) the VT exit site, from which the normal myocardium is rapidly activated, which corresponds to the scar border and coincides with the QRS onset on the surface ECG [4][5][6][7] ; (2) the re-entry circuit exit site from which the activation wavefront emerges from the critical slow conducting VT isthmus, which may not necessarily correspond to the scar border and may precede the activation of the rapidly conducting myocardium with only little effect on the 12-lead ECG; or (3) the target site for ablation, usually defined as the critical slow conducting VT isthmus, which is activated during diastole, thereby not contributing to the surface ECG at all. 8 The 12-lead ECG morphology of a scar-related re-entrant VT depends mainly on the VT exit site, or the site(s) or the area(s) from which the normal myocardium is activated.…”

Section: Vt Soomentioning

confidence: 99%

“…In the pioneering work of Miller et al, 4 the VT SoO was defined as the earliest recorded activity on the second half of the diastole during endocardial VT activation mapping. All 182 mapped VTs from 102 patients with single previous myocardial infarction (MI) had 1 endocardial site activated at least 40 ms before the QRS onset.…”

Section: Soo As Exit Sitementioning

confidence: 99%

Twelve-Lead ECG of Ventricular Tachycardia in Structural Heart Disease

Riva

Watanabe

Zeppenfeld

2015

Circ: Arrhythmia and Electrophysiology

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951I n patients with structural heart disease (SHD), defined by the presence of myocardial scarring either on cardiac imaging or electroanatomical mapping, catheter ablation is increasingly used for the treatment of ventricular tachycardia (VT).With more detailed knowledge of potential substrates and anatomic structures involved in VT, not only the endocardium of the left ventricle (LV) and right ventricle (RV) but also more complex structures like the aortic root, the cardiac veins, or the epicardium have become areas of interest for ablation.Preprocedural analysis of the clinically documented VT 12-lead ECG is often used to predict the VT site of origin (SoO), and it is considered to be an important tool for planning the ablation, to estimate the probability of success, and to recognize potential procedural limitations and related risks. These factors may have important implications not only for patient advice and decision making but also for the selection of a center capable to perform the expected procedure.Because the majority of inducible VTs in patients with SHD are not hemodynamically tolerated, 1,2 a detailed analysis of the VT 12-lead ECG of each induced VT may also be helpful. Combining the ECG with information of the scar size and distribution obtained from electroanatomical mapping during sinus rhythm or from preprocedural imaging may direct mapping to the area of interest with the potential of increasing procedural success and to reduce procedural duration.In this review, we will focus on the reported evidence for the value of the 12-lead VT ECG as a mapping tool in patients with scar-related VT and discuss its potential implications when combined with scar information from electroanatomical mapping or imaging. VT SoOThe mechanism of the majority of VTs in patients with structurally normal hearts is focal, and the 12-lead ECG can be helpful to predict its SoO because rapid activation of the normal myocardium from a focal source results in typical QRS patterns. 3As a general rule, VTs originating from the structurally normal LV have a right bundle branch block (RBBB) morphology (defined as predominant R in lead V1) and VTs from the normal RV have a left bundle branch block (LBBB) morphology (defined as predominant S in lead V1). The precordial transition for RBBB VTs (first lead with a predominant S) changes from positive concordant for VTs originating from the base of the LV to progressively earlier transition in V2-V4 as the VT origin moves toward the apex of the ventricle. For LBBB VTs, VTs originating from the basoseptal area of the RV have an early transition (first lead with a predominant R), and the transition becomes progressively later as the VT origin moves toward the ventricular free wall. With regard to the frontal plane axis, VTs originating from the superior aspect of the ventricles show an inferior axis (predominant R in aVF), VTs from the inferior aspect of the ventricles show a superior axis (predominant S in aVF), LV free wall VTs have typically a right axis (with a dominant S in I...

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Relationship between the 12-lead electrocardiogram during ventricular tachycardia and endocardial site of origin in patients with coronary artery disease.

Cited by 186 publications

References 23 publications

Characterization of Endocardial Electrophysiological Substrate in Patients With Nonischemic Cardiomyopathy and Monomorphic Ventricular Tachycardia

Characterization of Endocardial Electrophysiological Substrate in Patients With Nonischemic Cardiomyopathy and Monomorphic Ventricular Tachycardia

Sustained ventricular tachycardia in structural heart disease

Twelve-Lead ECG of Ventricular Tachycardia in Structural Heart Disease

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