New onset atrial fibrillation (AF) is increased ~2 fold in severe heart failure (HF). Alternans, a beat-to-beat oscillation in the atrial action potential (AP) and/or Ca transient, has been implicated in the promotion of AF. Atrial alternans aetiology is not fully understood and it remains unknown if susceptibility to alternans is increased in the HF atria. Atrial contraction is driven by intracellular Ca cycling in response to membrane depolarisation. The cellular AP and Ca transient are directly linked via the L-type Ca current and the Na/Ca exchanger such that alteration in one can result in alternation of the other. Therefore, alternans often occurs in both the AP and Ca transient irrespective of causality. We investigated whether cellular alternans occurred more readily in HF and how remodelling of electrical or Ca handling parameters in HF exacerbated mechanisms driving alternans. HF was induced in sheep by rapid ventricular pacing, via a pacemaker, with the pacing lead implanted in the endocardial apex of the right ventricle using a minimally invasive transvenous approach under fluoroscopic guidance. Surgical plane anaesthesia was maintained under isoflurane (3-5%) mixed with of oxygen (4.5-6 L.min-1). Left atrial myocytes were isolated from control and HF animals. Fluo-5F loaded atrial myocytes were incrementally paced at physiological rates (1-3Hz) under current clamp control. The lowest frequency at which alternans was detectable was deemed the alternans threshold. In HF vs. control a greater proportion of cells were seen to alternate (91% vs.72.4%) and the threshold for Ca2+ alternans (1.7 ± 0.1 Hz vs.2.2 ± 0.1 Hz) and AP alternans (1.6 ± 0.1 Hz vs. 2.2 ± 0.1 Hz) were decreased (p<0.05). Increased alternans susceptibility in HF was associated with a longer AP duration at 1Hz (APD90; 414 ± 110 ms vs. 345 ± 120 ms; p<0.05). The longer HF AP was unable to rate adapt as effectively as the control AP, quantified by the steepness of a restitution curve through an S1S2 protocol (Gradient of curve; 1.3 ± 0.3 vs. 0.4 ± 0.1; p<0.05). We hypothesised that the long HF AP, that was less able to rate adapt, would be less likely to fully repolarise between stimulations suggesting alternans may arise via the Na current. Hyperpolarisation of the membrane potential to increase Na channel recovery from inactivation, increased repolarisation speed by ≈107 ms (APD85; 312 ± 38 ms vs. 205 ± 22 ms; p<0.05) and terminated alternans in every HF cell (n=4). Our data shows that alternans occurs more readily in HF atrial cells, potentially providing a mechanism for increased prevalence of AF in HF.