Fig. 7. Computational modeling of cardiac action potentials of epicardial, midmyocardial, and endocardial myocytes using the Luo-Rudy dynamic model. (  A ) Simulation of ventricular action potentials under standard conditions (control) and with 50% inhibition of I^Kr. Action potential prolongation was larger in endocardial (20 ms or approximately 9%) than in epicardial myocytes (13 ms or approximately 7%). In midmyocardial cells, repolarization did not occur within one stimulation interval, and early afterdepolarizations developed. (  B ) Simulation of control action potentials and with 50% inhibition of I^Krand 40% inhibition of I^CaL. While the action potential duration in midmyocardial cells was prolonged by 28 ms (approximately 10%), such a combined channel block abolished the prolongation of the action potential duration in endocardial and epicardial cells. No early afterdepolarizations developed. All simulations were performed with a basic cycle length of 1,000 ms for 500 cycles at body temperature.