Atrial fibrillation (AF) is the commonest cardiac arrhythmia. Congestive heart failure is a major risk factor for the development of AF. Using a sheep model of heart failure we sought to establish the effects of heart failure on atrial excitation contraction coupling and intracellular Ca handling. Induction of heart failure by right ventricular tachypacing (210bpm) was performed in sheep aged approximately 18 months with untreated age-matched animals as controls. Animals were anaesthetised with isoflurane (1-3% in oxygen) and perioperative analgesia provided (meloxicam, 0.5mg/kg). All experiments were performed at 37°C, on freshly isolated single cardiac myocytes obtained from the left atrium, using the perforated patch voltage clamp technique. Fluo-5F was used to measure intracellular calcium. Data are presented as mean ± SEM. Statistical significance was determined using a students t-test. Heart failure in the atria resulted in cellular hypertrophy (60.5 ± 2.2 pF vs 143.5 ± 10.5 pF, n=43-76, p<0.001). Peak ICa,L was reduced in heart failure atrial myocytes (2.3 ± 0.2 pA/pF vs 1.3 ± 0.1 pA/pF, n=31-39, p<0.001). This was associated with a reduction in the amplitude of the systolic Ca transient (365.0 ± 36.1 nmol/l vs 240.4 ± 39.0 nmol/l, n=25-28, p<0.05). The rate of decay of the systolic Ca transient was reduced (8.4 ± 0.5 s-1 vs 5.7 ± 0.7 s-1, n=18-24, p<0.01). This is explained by a reduction in SERCA dependent Ca removal rate (7.4 ± 0.6 s-1 vs 3.8 ± 0.9 s-1, n=7-19, p<0.01). Interestingly, despite a reduction in SERCA function SR Ca content was increased (226.6 ± 14.0 μmol/l vs 287.6 ± 17.9 μmol/l, n=22-27, p<0.01). In conclusion, heart failure in sheep produces significant alterations to atrial EC coupling in particular a reduced peak ICa,L, which is a hallmark of AF. This together with the increased SR Ca content provides a likely substrate for arrhythmias to occur. Further work is required to determine the mechanism behind the increased SR Ca content despite a reduced SERCA function.