Transverse (t)-tubules are membrane invaginations that enable close coupling of surface L-type calcium channels and ryanodine receptors of the sarcoendoplasmic reticulum to facilitate triggered calcium release throughout the cell. In diseases such as heart failure (HF) there is disruption to the t-tubule network that contributes to dysynchronous calcium release and thus contractile dysfunction. Compared to the ventricle, atrial t-tubule remodelling in HF is more extensive with an 81% reduction in t-tubule density reported in the HF sheep atria (1). Despite the importance of atrial t-tubules, little is currently known about triggered calcium release in the atria and if this is altered in HF. Sheep were anaesthetised with isoflurane (2-4% v/v in oxygen) and implanted with a pacemaker and pacing lead for induction of HF by ventricular pacing at 210 bpm. Meloxicam (0.5 mg/kg) and Enrofloxacin (5 mg/kg) were provided perioperatively for analgesia and antibiosis. Control and HF sheep were euthanased with 200 mg/kg intravenous pentobarbitone and cells isolated from the left atrial appendage. Perforated patch clamp experiments were performed in Fluo-3 loaded cells using a confocal microscope to assess spatial calcium release. T-tubules were simultaneously imaged in patched cells using Wheat Germ Agglutinin Alexa Fluor 647. Data is presented as mean ± SEM for 14-16 cells from 5-6 animals, compared using t-test or two way repeated measures ANOVA where appropriate. Global calcium transient amplitude was reduced by 60.4±7.9% in HF (p<0.001), with the transient also 62.8±7.5% slower to rise compared to control (p<0.001). In control cells, triggered calcium release occurred at discrete sites on the surface and throughout the cell corresponding to t-tubule locations. In HF, calcium release was primarily triggered at the surface with release in the centre comparatively more reliant on propagation. The loss of t-tubules in HF contributed to increased dysynchrony of calcium release with calcium transients reduced in amplitude by 23.2±17.6% and 25.43±15.1% slower to rise in the cell centre vs surface (p<0.001). No spatial differences were observed in control cells. The loss of t-tubules in HF contributes to reduced central calcium release in the atria. Our data indicates that triggered release occurs in discrete locations on the surface and in the centre of atrial cells, with less central release in HF likely to be associated with reduced t-tubule density.