T-tubules are deep invaginations of the cellular surface membrane containing a host of ion channels known to be important in excitation contraction coupling in the heart. While an important functional role for ventricular t-tubules has been well defined it has been generally assumed that the atria lacks these important structures. More recently our lab and others have demonstrated the existence of t-tubules in the atria of a number of large mammalian species including human. In cells where t-tubules are absent (small mammalian atrial myocytes) triggered release of Ca2+, responsible for initiating cellular contraction, occurs only at the cell periphery. The presence of atrial t-tubules is associated with triggered Ca2+ release in the cell interior. Ventricular t-tubules are decreased in heart failure, playing an important role in the pathophysiology of the disease. Using a sheep rapid paced model of heart failure (instrumented under anaesthesia with 1-4% isoflurane and analgesia provided by 0.25mg/kg meloxicam) we have shown atrial t-tubules to be virtually absent at the point of heart failure. Loss of atrial t-tubules in heart failure is associated with a reduction in the L-type Ca2+ current, the loss of triggered Ca2+ release in the cell interior and, significantly, a decrease in Ca2+ transient amplitude. It is therefore important to understand if t-tubules can be restored to the failing atria in order to restore function. Following termination of rapid pacing sheep were allowed to recover from heart failure. Recovery was associated with the restoration of atrial t-tubules although these structures were extremely disordered. Preliminary data however suggests despite this disorder recovery of t-tubules may restore functional properties to the atria. Thus atrial t-tubules are not only important in normal excitation contraction coupling but also play a significant role in the pathophysiology of disease.