The basis of this review is the underlying hypothesis that the QRS morphology on 12-lead ECG is, to a great extent, determined by the site from which a focal ventricular tachycardia (VT) arises or from which a reentrant circuit exits the central isthmus to activate the “normal” myocardium. The ability to localize or, at the very least, regionalize “the sites of origin” of VTs enables the electrophysiologist to concentrate mapping to a specific region. Several factors limit the ability of the QRS patterns to localize VT origin, including (1) presence and size of infarction, (2) degree of intramyocardial fibrosis, (3) shape of the heart (e.g., aneurysm) and its position within the chest cavity, (4) site and mechanism of VT within an infarct or scarred area, (5) influence of nonuniform anisotropy in affecting propagation from the site of the tachycardia, (6) effects of acute ischemia, antiarrhythmic drugs, or metabolic abnormalities on conduction, (7) integrity of the His-Purkinje system, (8) presence of increased myocardial mass, and (9) presence of structural abnormalities unrelated to tachycardia origin or mechanisms.
