Cardiac voltage-gated Na+ channels underlie membrane depolarization during the upstroke of the action potential (AP). These channels also exhibit a late, slowly-inactivating component of current (late INa) that may be enhanced under pathological conditions such as heart failure, and may therefore promote AP prolongation and increase the likelihood of arrhythmia. Ca2+/calmodulin-dependent protein kinase II (CaMKII) functionally modifies Na+ channels, however it remains unclear if the CaMKII-dependent changes in late INa are a major contributor to cellular arrhythmias such as early after depolarizations (EADs). In this study we develop a model of INa, including CaMKII-dependent effects, based on experimental measurements. The Na+ channel model is incorporated into a computational model of the whole myocyte which describes excitation-contraction coupling via stochastic simulation of individual Ca2+ release sites. Simulations suggest that relatively small augmentation of late INa is sufficient to significantly prolong APs and lead to the appearance of EADs.