Electrophysiologic substrate underlying postinfarction ventricular tachycardia: characterization and role in catheter ablation.

The electrophysiologic substrate underlying the development of ventricular tachycardia (VT) in patients with prior infarction has been studied in depth. An increased understanding of its composition and role in the maintenance of reentrant VT has led to the development of substrate modification approaches to ablation of unmappable VT. The area of low bipolar voltage that corresponds to the subendocardial projection of the scar as well as specific potential targets within it have been defined. These targets are selected because they may be involved in forming, or are in close proximity to, critical diastolic isthmuses during VT. The targets include sites of good pacemaps in the border zone, corridors of relatively preserved voltage within dense scar, regions between electrically unexcitable scar, isolated potentials, very late potentials, and regions with good pacemaps which display long stimulus to QRS delays. Ablation strategies have been designed based on these targets, mostly incorporating linear lesions to transect putative isthmus sites. This review examines the role that the electrophysiologic substrate plays in the mechanism of scar-related VT and how this substrate is mapped, defined, and ablated.