The conventional prediction of drug-induced arrhythmia has been conducted by testing effects of candidate drugs on the rapidly activating delayed rectifier K⁺ current (I_Kr) because block of I_Kr may prolong action potential duration and cause arrhythmia. However, it turned out that a number of potentially useful drug candidates without the side effect were excluded in this approach. One of the reasons why this approach for arrhythmia risk prediction is not so accurate is that the occurrences of early afterdepolarization (EAD) can be different even under the same prolonged action potential duration. In the present study, we examined how various drug effects on properties of L-type Ca²⁺ channel can account for the different EAD occurrences in under the same prolonged action potential duration. By using O'Hara Rudy model, the de facto standard Human ventricular model, we examined simulated effects of various properties of L-type Ca²⁺ channel blockers on EAD. We found that the different EAD occurrences can be accounted for by the voltage dependent drug effects on L-type Ca²⁺ channel. These results suggest that the risk in drug-induced arrhythmia should be predicted not only by checking block of I_Kr and prolongation of action potential duration but also checking voltage dependent drug effects on L-type Ca²⁺ channel.