This editorial refers to ‘The heart rate of ventricular tachycardia following an old myocardial infarction is inversely related to the size of scarring’ by L. Woie et al., on page 864. The underlying mechanism of most ventricular tachycardias (VTs) after myocardial infarction (MI) is reentry involving areas of ventricular scar. Dense fibrous scars alone cannot cause arrhythmias; however, when surrounded by bundles of surviving myocytes in the peri-infarction zone, an arrhythmogenic substrate may arise. Areas of dense fibrosis intersperse with surviving myocardial bundles and form regions of conduction block that define reentry circuit borders. The presence of fibrosis between these surviving bundles prolongs the pathway for impulse propagation, creating slow conduction through the scar.1 The complex structure of these scars is likely to determine reentrant circuit characteristics and thereby VT characteristics.2 Late gadolinium-enhancement cardiac magnetic resonance (LGE-CMR) has increasingly been used to visualize the three-dimensional (3D) geometry of myocardial fibrosis and has become the gold standard for detection of non-transmural scars because of its superior spatial resolution.3 Woie et al .4 have addressed an interesting question of whether myocardial scar characteristics as visualized and defined by LGE-CMR correlate with VT characteristics, specifically with the VT cycle length (VTCL). They hypothesized that the rate of spontaneous VTs is related to the size of the post-infarction scar or its border zone. They studied 24 patients with remote MI and indication for implantation of an internal cardioverter-defibrillator for primary or secondary prevention who underwent LGE-CMR for quantification of left ventricular (LV) volumes, function, size of core infarct, and size of the infarct border zone prior to device implantation. Patients were followed every 3 months during the first year after implantation. Twenty out of 24 patients had VTs with a median VTCL of 325 ms (range 239–438 ms). None of …