Previous studies have demonstrated that the slope of the function relating the action potential duration (APD) and the diastolic interval (DI), known as the APD restitution curve, plays an important role in the initiation and maintenance of ventricular fibrillation (VF). Since the APD restitution slope critically depends on the kinetics of the L-type Ca²⁺ current, we hypothesized that manipulation of the subunit composition of these channels may represent a powerful strategy to control cardiac arrhythmias. We studied the kinetic properties of the L-type Ca²⁺ channel (Ca_v1.2) co-expressed with the ₂subunit alone (_1c+₂) or in combination with _2a, _2b or ₃ subunits (1C+2+) using Ca²⁺ as the charge carrier. We then incorporated the kinetic properties observed experimentally into the L-type Ca²⁺ current of a mathematical model of the cardiac action potential to demonstrate that the APD restitution slope can be selectively controlled by altering the subunit composition of the Ca²⁺ channel. Assuming that _2b most closely resembles the native cardiac L-type Ca current, the absence of , as well as the co-expression of _2a, were found to flatten restitution slope and stabilize spiral waves. These results imply that subunit modification of L-type Ca²⁺ channels can potentially be used as an antifibrillatory strategy.