Life-threatening ventricular arrhythmias (VAs) pose a significant challenge in clinical management due to their impact on mortality, particularly the risk of sudden cardiac death, which remains a concern despite the use of only partially effective anti-arrhythmic drugs and repeated catheterablation. There is also a need for more precise risk stratification tools for implantable cardioverter defibrillators (ICD). Sustained ventricular tachycardia (VT) most commonly occurs in patients with a history of myocardial infarction (MI) or non ischemic cardiomyopathy characterized by fibrotic ventricular scars, which can be identified as areas of late gadolinium enhancement (LGE) through cardiac magnetic resonance or as low-voltage areas via three-dimensional electroanatomic mapping. Both the presence and extent of cardiac fibrosis are linked to ventricular arrhythmogenesis and the risk of sudden death. Fibrosis contributes to VAs for several reasons; primarily, it causes structural remodelling that alters the myocardial architecture and promotes reentry circuits. On this regard, increasing evidence highlights the role of inflammation mediated by the NLR family pyrin domain containing 3 (NLRP3) inflammasome as a key factor in scar development, cardiac electrical instability, and disease progression. Secondly, systemic and local sympathetic hyperactivity significantly contribute to electrical instability. The interplay between inflammation, cardiac fibrosis and sympathetic hyperactivity has been neglected for a long time. However, a deep insight in the pathogenesis of VAs is warranted in order to develop new and tailored pharmacological strategies. Therefore, the NLRP3 inflammasome pathway, autonomic imbalance, and early stage of myocardial fibrosis may represent promising therapeutic targets for mitigating adverse ventricular remodeling and the burden of VAs. On this basis of multiple evidence, inflammation plays a role of trigger in a hypothetical Coumel's triangle of arrhythmogenesis for the pathogenesis of VAs, where the ventricular substrate is represented by cardiac fibrosis, and the favoring modulating factor is provided by sympathetic hyperactivity.