Ventricular tachycardia (VT) ablations are one of the emerging frontiers in clinical electrophysiology. Multiple clinical trials have extended the indications for life-saving defibrillator therapy to an increasing number of patients. Apart from those with previous life-threatening arrhythmias (secondary prevention), a large number of patients with a structurally abnormal heart benefit from placement of an ICD without previous episodes of ventricular tachycardia or fibrillation (primary prevention).

A large number of those patients present in the follow-up period with frequent and appropriate defibrillator shocks for ventricular arrhythmias. Indeed, VT storm (≥3 shocks per 24 hours) has been observed in ~4.5% of patients with primary and up to 40% of patients with secondary prevention. While pharmacological therapy is usually the first line therapy in this patient population, its long-term usage is often limited by efficacy and side effects, making VT ablation the next appropriate step. Moreover, at least two multi-center trials have also demonstrated a significant decrease of future ICD shocks with “prophylactic” VT ablation at the time of ICD implantation in patients with ischemic heart disease.

Therefore, a clinical need exists to make VT ablations faster, safer and more efficient to meet the growing clinical need.

However, procedure times frequently still surpass 5 hours, and a recurrence rate of 50+% in long-term follow-up is common. If structural heart disease is present, VT ablations target myocardial scar, which is the substrate for most reentrant VTs. In cases in which the ventricular arrhythmias are hemodynamically stable, standard entrainment criteria are used to determine the electrical circuit within the scar. Ablation within the critical pathway or at the exit site of the VT often results in acute elimination of the arrhythmia. However, up to 90% of VTs are either non-sustained or hemodynamically unstable and require a substrate-guided approach. In this case, the amplitude of bipolar voltage recordings is used to classify a location point as healthy myocardium, scar or border zone (“voltage mapping”). Using a clinical mapping system, up to several hundred of those mapping points are combined to build a voltage map of the heart. It provides information about the anatomic location and extent of the scar and border zone. An ablation catheter is used to pace within the scar and along its border zone trying to match the 12-lead morphology of the VT (“pace mapping”). An identical morphology of the pace map and VT suggests a location close to the VT exit site from the scar and ablation lesions at that site have a good chance to eliminate the VT.

However, voltage mapping has several important limitations. Low voltage recordings can represent true myocardial scar, but can also be the result of poor catheter contact with the cardiac muscle. Voltage mapping can take >1-2 hours and prolong the procedure times. This also limits the average spatial resolution of voltage maps, and small areas of scar between two mapping points may be overlooked. Importantly, a single endocardial voltage recording is a poor surrogate of a complex intramural scar with variable degrees of scar transmurality or patchy myocardial fibrosis. Therefore, a detailed assessment of myocardial scar using a different approach than voltage mapping alone has the potential of providing helpful information and improve VT ablations.