Mammalian ventricular myocytes are characterised by the presence of an extensive transverse (t-) tubule network which is responsible for the synchronous rise of intracellular Ca²⁺ concentration ([Ca²⁺]_i) during systole. Disruption to the ventricular t-tubule network occurs in various cardiac pathologies and leads to heterogeneous changes of [Ca²⁺]_i which are thought to contribute to the reduced contractility and increased susceptibility to arrhythmias of the diseased ventricle. Here we review evidence that, despite the long-held dogma of atrial cells having no or very few t-tubules, there is indeed an extensive and functionally significant t-tubule network present in atrial myocytes of large mammals including human. Moreover, the atrial t-tubule network is highly plastic in nature and undergoes far more extensive remodelling in heart disease than is the case in the ventricle with profound consequences for the resulting systolic Ca²⁺ transient. In addition to considering the functional role of the t-tubule network in the healthy and diseased atria we also provide an overview of recent data concerning the putative factors controlling the formation of t-tubules and conclude by posing some important questions that currently remain to be addressed and whether or not targeting t-tubules offers potential novel therapeutic possibilities for heart disease. This article is part of a Special Issue entitled “Calcium Signaling in Heart”.