In particular, the activation of the NLRP3 inflammasome exacerbates cardiac sympathetic hyperactivity by promoting the release of the proinflammatory cytokine IL-1β, and this inflammatory-neural interaction results in altered electrophysiological properties of the heart, such as prolongation of the action potential duration and shortening of the effective refractory period, which increases the risk of ventricular arrhythmias (117, 118). This evidence concerns the gene NLRP3 and Ventricular arrhythmia.