A 46-year-old man, with nonischemic dilated cardiomyopathy and left bundle branch block, underwent implantation of a cardiac resynchronization therapy (CRT) defibrillator as primary prevention. The left ventricular (LV) lead was positioned percutaneously on a LV mediolateral segment. The device was programmed in DDDR mode at 50 to 150 beats/min, atrioventricular delay of 120 ms, and right ventricle to left ventricle pacing delay of −20 ms. Three weeks later, the patient was admitted with 64 episodes of torsade de pointes (A, B), many of which were being sustained and requiring electrical cardioversion. (EGM = electrocardiogram.) There were no metabolic or electrolyte abnormalities, the LV lead was not dislodged, and the LV pacing threshold was within normal values (1V/0.5 ms) with no evidence of loss of capture. Marked prolongation of the corrected JT (JTc) interval (C) compared with pre-device implantation recordings (D) was observed (527 ms vs. 382 ms; normal <350 ms), as well as narrowing of the QRS complex (120 ms vs. 180 ms). (cQT = corrected QT interval.) Medical therapy was ineffective, but upon CRT discontinuation, the arrhythmias completely disappeared. No subsequent attempts to adjust the CRT parameters were made. Biventricular pacing may exceptionally induce torsade de pointes by increasing transmural dispersion of repolarization, a mechanism similar to the long-QT syndrome. Baseline prolongation of transmural dispersion of repolarization, as with our patient, constitutes a risk factor for this type of uncommon presentation in CRT device recipients.