A case of a 38-year-old male patient is reported. Left ventricular assist device was implanted because of end stage heart failure. In the early postoperative period, electrical storm with rapid ventricular tachycardia (VTs) occurred that was refractory to medical therapy. Emergency VT ablation was performed successfully. VT frequently occurs after LVAD implantation and radiofrequency ablation can be an effective therapeutic option. We report a case of a 38-year-old male patient, who suffered an extensive anterior ST-segment elevation myocardial infarction in 2002 treated with thrombolysis. LAD PCI (2005), amiodarone-induced hyperthyreosis (2007) and primary prophylactic ICD implantation (2008) are the most relevant findings in his past medical history. Since then he required several hospitalizations for worsening heart failure symptoms. In May 2013, he was admitted due to rapid VT causing hemodynamic instability requiring two appropriate ICD shocks. Heart transplantation was considered as an option but it was contraindicated because of high pulmonary vascular resistance refractory to vasodilator therapy. Left ventricular assist device (LVAD, HeartMate II) implantation was performed as ‘‘destination therapy’’. In the early postoperative period (5 days after implantation) electrical storm occurred requiring multiple ICD shocks. Shock therapy of ICD was deactivated and multiple external electric cardioversions were needed despite the intravenous administration of high dose antiarrhythmic drugs (amiodarone, procainamide and beta blocker). Due to drug refractory electrical storm radiofrequency ablation of the incessant VT was decided in the early postoperative period. Procedure was performed under uninterrupted anticoagulation, respecting the high thromboembolic risk of the assist device. We decided to use transaortic retrograde approach only. During the electrophysiological study sustained monomorphic VT was inducible (cycle length: 330 ms, superior axis, right bundle branch block morphology). During ongoing arrhythmia, rapid electroanatomic mapping (CARTO3, Biosense Webster) was performed which found that the site of earliest activation is at the inferoseptal region of the left ventricle, in the intrinsic myocardial scar near to the junction of the inflow cannula. The exit point was also identified at the same site with entrainment mapping. Then 5 radiofrequency ablations were applied (total ablation time 790 s, energy 40 W, temperature 43 C) using 3.5 mm irrigated tip catheter (Thermocool, D curve, Biosense Webster). We would like to highlight that the ablation site was near to the inflow cannula but we kept some distance from the device to avoid damaging of the surgical sutures. The VT stopped immediately and was no longer inducible even with 2 ventricular extrastimuli at 330 ms drive. No complications were observed during or in relation to the ablation procedure (total procedure time: 45 min, fluoroscopy time: 8 min). After the procedure, patient was free of sustained VT episodes during the 12-month follow-up period. VT is frequently observed in patients after LVAD implantation, but very limited data are available regarding VT ablation in the early postoperative period. Until now publications usually dealt with VTs originating near the cannula, but there are scarce data about VTs arising from the intrinsic scar [1–5]. Managing VT in these difficult N. Szegedi G. Szeplaki B. Merkely L. Geller (&) Heart and Vascular Center, Semmelweis University, Varosmajor street 68, Budapest 1122, Hungary e-mail: laszlo.geller@gmail.com