Efficient pumping of the heart requires simultaneous contraction of all cardiac muscle cells. The necessary coordination is obtained by transmission of ‘‘action potentials:’’ periodic changes in transmembrane voltage which, in muscle cells, trigger the calcium influx needed for contraction. In cardiac muscle, they also cause an electric current flow to neighboring cells through intercellular connections. This current causes an action potential in each neighbor, leading to rapid activation of the whole heart. Normally the initial activation comes from a specialized region called the sinus node, at a regular pace adapted to the needs of the body. Ventricular tachycardia (VT) is a potentially fatal disturbance of this mechanism, characterized by a very fast heart rate and an abnormal activation pattern. VT can be caused by an ‘‘ectopic focus,’’ a small area of tissue that starts activating itself and its neighbors on its own account. A far more common cause, however, are scars due to infarction, cardiomyopathy, or surgery. These can embed a maze of small surviving muscle fibers through which activation may proceed during a substantial part of a heartbeat before it reaches the healthy myocardium again. The activation may then round the scar and re-enter the narrow pathway (see Fig. 1). Continuous reentry in this fashion results in re-entrant VT. Treatment options for VT include pharmacological suppression, implantation of a cardioverter-defibrillator (ICD), surgical resection of the arrhythmogenic area, and catheter ablation. None of these methods is perfect. Pharmacological treatment often fails [7]. An ICD can reliably terminate VT but does not prevent it from recurring; frequent ICD shocks can cause significant morbidity [7]. Surgical treatment is limited by its invasiveness and relatively high morbidity and mortality. Catheter ablation is only minimally invasive and, if successful, can provide a definitive cure. It is presently considered as a first-choice treatment for focal VT in patients with structurally normal hearts, and as a secondary treatment in patients who are experiencing too many ICD discharges. Procedures to find a suitable ablation site include ‘‘pace mapping’’ and ‘‘activation sequence mapping.’’ In pace mapping, the heart is stimulated from the catheter tip, resulting in an electrocardiogram (ECG) that mimics the ECG that would be obtained if the VT originated at the catheter tip location. Comparison with an ECG recorded during VT provides an estimate of the origin relative to the catheter tip. After displacing the catheter and stimulating again, a new ECG is made. This procedure is repeated until the two ECGs match, and allows for the localization of the ‘‘exit site,’’ where the abnormal activation reaches the healthy myocardium. Patients with more than one VT circuit can have several exit sites. In activation sequence mapping, the VT is induced, and the activation pattern is assessed by recording signals at many locations with one or two catheters. The goal is to find the earliest activated site. This is a time-consuming procedure, during which the patient has to be kept in VT. To gain time, the exit site found by pace mapping can be used as a starting point [3]. M. Potse (&) Research Center, Sacre-Coeur hospital, Montreal, QC, Canada e-mail: mark@potse.nl