A 59-year-old male was admitted to our hospital with heart failure (HF) exacerbation and sustained monomorphic ventricular tachycardia (SMVT) episodes. The patient was known to have had severe non-ischemic left ventricular (LV) dysfunction for the past four years. His history was also remarkable for diabetes mellitus, hypertension, and gastric banding. The patient had documentation of LV ejection fraction (EF) of 20%, diffuse hypokinesis and LV end systolic and diastolic volumes (LVESV/LVEDV): 134/172 ml. His coronary catheterization demonstrated non-significant coronary artery disease and he had a normal cardiac biopsy. Over those years the patient was hospitalized frequently due to worsening HF symptoms and was graded as New York Heart Association (NYHA) functional class III. His baseline ECG showed normal sinus rhythm with QRS duration of 92 ms. Recurrent 24h-Holter monitoring showed >40% (>50,000) PVCs with a morphology of intermediate right bundle (RS in V1) and right-inferior axis, with multiple episodes of SMVT. Tachycardia-induced cardiomyopathy was suspected.Sixteen months prior to current hospital admission the patient had underwent an electrophysiology study (in another medical center) in order to map and ablate the arrhythmia; endocardial, aortic cusps and coronary sinus (CS) mapping of PVCs using a 4F CARDIMA catheter for the CS and CARTO 3-D mapping system were employed. Earliest activation was located to the middle part of the great cardiac vein (anterior interventricular branching) with 12/12 pace mapping, 50 ms prior to QRS. The operator was unable to pass an ablation catheter forward to distal CS and the procedure was discontinued. A few months later the patient underwent another ablation attempt: an epicardial catheter was located opposite to the earliest point of the CARDIMA CS catheter. RF ablation at that area abolished the PVCs, but PVCs resumed after a few hours. Several months later the patient was referred for a third procedure. Conscious sedation caused temporary disappearance of PVCs and no inducibility of VT. Pace mapping was not perfect and the procedure was discontinued. The patient refused further attempts.He was treated with maximal tolerated doses of sotalol, quinidine and then was fully loaded with amiodarone (each antiarrhytmic drug at a time) along with beta blockers. Despite those antiarrhythmic drugs (several months each), the patient had recurrent hospitalizations for HF exacerbations and SMVT episodes. The patient had an indication for ICD implantation for secondary prevention and although the patient had narrow QRS, we decided to implant a CRT-D because we anticipated a need for overdrive RV pacing in a patient with an upfront severe LV dysfunction and an expected further LV function deterioration. Furthermore, the final decision was to implant two LV leads at different locations, aiming for a stronger possible antiarrhythmic effect -as proposed in the discussion section. The patient gave his written informed consent to the procedure. A transvenous biventricular ICD (PRO...