Electrocardiographic localization of the site of origin of ventricular tachycardia in patients with prior myocardial infarction

Abstract

The utility of the 12 lead electrocardiogram (ECG) in identifying the site of origin of sustained ventricular tachycardia in patients with previous myocardial infarction was studied. A new mapping grid, based on biplanar fluoroscopic imaging of the heart, was utilized for the definition of left ventricular endocardial sites. On the basis of QRS configurations resulting from left ventricular endocardial pacing at disparate sites in 22 patients (Group I), ECG features that were specific for particular sites were identified and used to construct an algorithm. Apical and basal sites were differentiated by the QRS configuration in leads V4 and aVR, anterior and inferior sites by that in leads II, III and V6 and septal and lateral sites were differentiated using leads I, aVL and V1. The algorithm was used to predict the site of earliest endocardial activation during 44 episodes of sustained ventricular tachycardia in a second group of 42 patients (Group II) in a blinded fashion. Anterior sites were correctly predicted in 83% of cases, inferior sites in 84%, septal sites in 90% and lateral sites in 82% of cases. Apical and basal sites were each correctly predicted in 70% of cases, whereas intermediate sites were less well predicted (29 to 55%) on the basis of QRS configuration. Precise localization of the site of origin of ventricular tachycardia (in all three planes) was achieved in 17 cases (39%), and in 16 cases (36%) the site of origin was immediately adjacent to the predicted site. Prediction of the site of origin of ventricular tachycardia from the 12 lead ECG may serve as a useful, time-saving adjunct to, but not a substitute for, activation sequence mapping during ventricular tachycardia.

An algorithm for topical electrocardiographic diagnosis of ventricular arrhythmias in children

“…впервые создали ал-горитм топической диагностики левожелудочковых аритмий у взрослых пациентов с ишемической бо-лезнью сердца [15]. Затем L. Jadonath и соавт.…”

Localization of breakthrough site of canine monomorphic ventricular tachycardia by pacemapping. A vectorial approach.

“…It is not known whether pacemapping may be a useful and valuable technique in such patients because few reports have rigorously addressed the accuracy of pacemapping in human VT. [6][7][8]28 The accuracy of pacemapping conducted in a canine model as described in this study cannot be extrapolated to human VT. Orthogonal surface ECG leads can be readily recorded in the electrophysiology laboratory during clinical VT and pacemapping. However, obviously our hypothesis cannot be tested for human VT using the same technique in the electrophysiology laboratory because neither epicardial recordings nor a great number of simultaneous LV endocardial recordings are feasible.…”

Twelve-Lead ECG of Ventricular Tachycardia in Structural Heart Disease

“…On the basis of the assumption that pacing at the VT endocardial exit site may generate a QRS morphology identical to the VT morphology, Kuchar et al 5 proposed a different algorithm for localizing the VT SoO. They used ventricular pacemapping as surrogate for a VT exit site.…”

“…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.…”