At the cellular level, trazodone inhibits multiple cardiac ion channels, including hERG (IKr), IKs, INa, and ICa, in a concentration-dependent manner, thereby prolonging action potential duration and inducing early after-depolarizations, which may precipitate QT prolongation and ventricular arrhythmias [16]. This evidence concerns the gene KCNH2 and Ventricular arrhythmia.