The epicardial border zone (EBZ) of canine infarcts has increased anisotropy because of transverse conduction slowing. It remains unknown whether changes in gap junctional conductance (G_j) accompany the increased anisotropy. Ventricular cell pairs were isolated from EBZ and normal hearts (NZ). Dual patch clamp was used to quantify G_j. At a transjunctional voltage (V_j) of +10 mV, side-to-side G_j of EBZ pairs (9.2±3.4 nS, n=16) was reduced compared with NZ side-to-side G_j (109.4±23.6 nS, n=14, P<0.001). G_j of end-to-end coupled cells was not reduced in EBZ. Steady-state G_j of both NZ and EBZ showed voltage dependence, described by a two-way Boltzmann function. Half-maximal activation voltage in EBZ was shifted to higher V_j in positive and negative directions. Immunoconfocal planimetry and quantification showed no change in connexin43 per unit cell volume or surface area in EBZ. Decreased side-to-side coupling occurs in EBZ myocytes, independent of reduced connexin43 expression, and is hypothesized to contribute to increased anisotropy and reentrant arrhythmias.