Contrast-enhanced CMR imaging of ventricular tachycardia isthmus sites to guide ablation: an approach in evolution.

SEE PAGE 774 T he mechanism of ventricular tachycardia (VT) in patients with structural heart disease is primarily scar-related reentry (1). Although any disease process that results in the formation of myocardial scar can predispose to reentrant VT, the best characterized substrate is post-myocardial infarction VT. After myocardial infarction, ventricular tissue can be classified into 3 types: normal myocardium, dense scar, and the intervening border zone (BZ). In the BZ, myocardial fibrils are interspersed between electrically inert fibrotic tissue causing electrical conduction to take a circuitous path and, together with abnormal myocyte cell-to-cell coupling, causes slow conduction, a necessary component for reentrant VT (2). Electrical conduction through these myocardial channels can exit the scar and depolarize normal myocardium resulting in 12-lead electrocardiogram morphology of the VT that is dependent on the location of this exit site. Myocardial channels are identified during VT ablation on the basis of their abnormal conduction properties, which yield fractionated and late potentials and are incorporated in the ablation strategy based on observations that they are strongly associated with VT isthmus sites (3). Additionally, pacing from within the BZ may identify a potential VT isthmus site when the paced 12-lead QRS morphology matches the VT. Although late potentials and good pacemapping sites may denote potential VT isthmus sites, their participation in any VT can only be proven by entrainment maneuvers performed