Previously, we have shown abnormalities in V̇_max and in the recovery of V̇_max in myocytes dispersed from the epicardial border zone (EBZ) of the 5-day infarcted canine heart (myocytes from the EBZ [IZs]). Thus, we sought to determine the characteristics of the whole-cell Na⁺ current (I_Na) in IZs and compare them with the I_Na of cells from noninfarcted hearts (myocytes from noninfarcted epicardium [NZs]). I_Na was recorded using patch-clamp techniques under conditions that eliminated contaminating currents and controlled I_Na for measurement (19°C, 5 mmol/L [Na⁺]_o). Peak I_Na density (at −25 mV) was significantly reduced in IZs (4.9±0.44 pA/pF, n=36) versus NZs (12.8±0.55 pA/pF, n=54; P<.001), yet the half-maximal activation voltage (V_0.5), time course of decay, and time to peak I_Na were no different. However, in IZs, V_0.5 of the availability curve (I/I_max curve) was shifted significantly in the hyperpolarizing direction (−80.2±0.48 mV in NZs [n=45] versus −83.9±0.59 mV in IZs [n=27], P<.01). Inactivation of I_Na directly from a depolarized prepotential (−60 mV) was significantly accelerated in IZs versus NZs (fast and slow time constants [τ₁ and τ₂, respectively] were as follows: NZs [n=28], τ₁=71.5±5.6 ms and τ₂=243.7±17.1 ms; IZs [n=21], τ₁=36.3±2.4 ms and τ₂=153±11.3 ms; P<.001). Recovery of I_Na from inactivation was dependent on the holding potential (V_H) in both cell types but was significantly slower in IZs. At V_H=−90 mV, I_Na recovery had a lag in 18 (82%) of 22 IZs (with a 17.6±1.5-ms lag) versus 2 (9%) of 22 NZs (with 5.9- and 8.7-ms lags); at V_H=−100 mV, τ₁=60.9±2.6 ms and τ₂=352.8±28.1 ms in NZs (n=41) versus τ₁=76.3±4.8 ms and τ₂=464.4±47.2 ms in IZs (n=26) (P<.002 and P<.03, respectively); at V_H=−110 mV, τ₁=33.4±1.8 ms and τ₂=293.5±33.6 ms in NZs (n=21) versus τ₁=44.3±2.9 ms and τ₂=388.4±38 ms in IZs (n=18) (P<.002 and P<.07, respectively). In sum, I_Na is reduced, and its kinetics are altered in IZs. These changes may underlie the altered excitability and postrepolarization refractoriness of the ventricular fibers of the EBZ, thus contributing to reentrant arrhythmias in the infarcted heart.