Electrophysiological remodeling of ion channels in heart failure causes action potential prolongation and plays a role in arrhythmia mechanism. The importance of down-regulation of potassium currents is well-known, but a role for Na current (I_Na) in heart failure is less well established. We studied I_Na in heart failure ventricular cells from a canine pacing model of heart failure and also from explanted failing human hearts. Peak I_Na density was significantly decreased by 39% and 57% in the dog model and in human heart failure, respectively. The kinetics of peak I_Na were not different in heart failure. Late I_Na was measured 750 ms after the initial depolarization as the saxitoxin (STX)-sensitive current and also as the current remaining after contaminating currents were blocked. Late I_Na as a percentage of the peak I_Na was significantly increased in both conditions. In dogs, STX sensitive late I_Na was 0.5 ± 0.1% n = 16 cells from eight normal hearts and 3.4 ± 1.4% n = 12 cells from seven failing hearts; in humans, it was 0.2 ± 0.1% n = 4 cells from two normal hearts and 2.4 ± 0.5% n = 10 cells from three human failing hearts (–40 mV). Quantitative measures of mRNA including RNase protection assays and real time quantitative PCR in the dog model showed no differences for different α subunit isoforms (NaV1.1, 1.3, 1.5) and for the β1 and β2 subunits. This suggests neither α subunit isoform switching nor altered β subunit expression is a mechanism for increased late I_Na. We conclude that a peak I_Na is decreased, and non-inactivating late I_Na is increased in heart failure and this may contribute to action potential prolongation and the generation of arrhythmia.