Non‐technical summary Diseases, genetic defects, or ionic imbalances can alter the normal electrical activity of cardiac myocytes causing an anomalous heart rhythm, which can degenerate to ventricular fibrillation (VF) and sudden cardiac death. Well‐recognized triggers for VF are aberrations of the cardiac action potential, known as early afterdepolarizations (EADs). In this study, combining mathematical modelling and experimental electrophysiology in real‐time (dynamic clamp), we investigated the dependence of EADs on the biophysical properties of the L‐type Ca²⁺ current (I_Ca,L) and identified modifications of I_Ca,L properties which effectively suppress EAD. We found that minimal changes in the voltage dependence of activation or inactivation of I_Ca,L can dramatically reduce the occurrence of EADs in cardiac myocytes exposed to different EAD‐inducing conditions. This work assigns a critical role to the L‐type Ca²⁺ channel biophysical properties for EADs formation and identifies the L‐type Ca²⁺ channel as a promising therapeutic target to suppress EADs and their arrhythmogenic effects.