Ventricular arrhythmias responsible for sudden cardiac death (SCD) have a considerable share in heart failure (HF) mortality and may be related to myocardial ischemia, scar, or fibrosis, neurohumoral activation, worsening congestion, electrolyte abnormalities, proarrhythmic drugs, calcium overload, and genetic susceptibility. Myocardial scar or fibrosis serves as the arrhythmogenic substrate of reentry, the commonest mechanism of sustained monomorphic ventricular tachycardia (VT), which occasionally may degenerate into ventricular fibrillation (VF). However, other mechanisms (abnormal automaticity and triggered activity) may also lead to polymorphic VT and VF. With the possible exception of rapid nonsustained VT (NSVT), asymptomatic complex ventricular arrhythmias, including frequent/multifocal premature ventricular complexes (PVCs) and runs of NSVT, may not predict SCD in HF patients, as these arrhythmias may be a nonspecific manifestation of decompensation. Survivors of malignant ventricular arrhythmias (VT/VF) should be offered an implantable cardioverter defibrillator (ICD) or cardiac resynchronization therapy defibrillator (CRT-D), as appropriate, for secondary prevention of SCD. Patients with potentially malignant ventricular arrhythmias (PVCs/NSVT) may selectively receive ICD/CRT-D for primary prevention if left ventricular ejection fraction is <35% or get further stratified with an electrophysiology study or cardiac magnetic resonance imaging. Catheter ablation is reserved for suspected PVC-induced cardiomyopathy or frequently recurring/incessant VT or electrical storm.