T-tubules are extensive tubular invaginations of the sarcolemma mostly located at the Z-line in cardiomyocytes. With membrane staining the t-tubules are seen to form a regular striation pattern with a sarcomere distance between the transverse lines. However, the tubules are highly interconnected and wrap around the myofibrils. Here they come in close contact with the junctional part of the sarcoplasmic reticulum (SR) to form dyads where calcium induced calcium release occurs. In these specialized regions, L-type calcium channels and Na,Ca-exchangers in the t-tubule membrane, and ryanodine receptors of the SR are closely clustered. Hence efficient transmission of the action potential in the t-tubular system will provide a rapid calcium release that is synchronized throughout the cardiac cell with a short lag of a few ms (1). In failing hearts the t-tubules become disorganized and some longitudinal tubules start to appear. This reshaping of the t-tubular system contributes to dyssynchronous calcium release because a larger fraction of ryanodine receptors will be outside the dyads and calcium will have to diffuse a longer distance to activate them (1, 2). Thus, time to peak of the calcium transient becomes longer, and contraction slower. However, t-tubule disorganization can only explain part of the dyssynchrony. In failing hearts, the basic calcium release “quantum” – the spark – is altered. About 20% of sparks have a markedly slower rise time and some are quite prolonged. This variability in spark kinetics contributes to dyssynchrony of the calcium transient (3). The reason for this variability seems to be that in some dyads the ryanodine receptors become rearranged. Dyssynchrony can be partly offset by increased SR calcium content and/or increased ryanodine receptor sensitivity to calcium (2). Prolongation of the action potential in failing hearts could also contribute to dyssynchronous calcium release, but this effect seems to be offset by increased sensitivity of the ryanodine receptors (4). If the SR function is dramatically decreased by removing the calcium-pump (SERCA2) in a conditional, cardiac specific knock-out mouse model, calcium for contraction is provided across the sarcolemma (5). In these hearts t-tubules proliferate and grow longitudinally in the cell. Dyads are formed at the A-band midway between the Z-lines (6). Interestingly, in these new dyads L-type calcium channels seem to be absent, whereas Na,Ca-exchangers are found opposite the ryanodine receptors. Thus, we believe that calcium entry via Na,Ca-exchange can trigger calcium release, indicating that the growth of new longitudinal T-tubules is compensatory. Thus, existing data show that T-tubules are highly plastic structures that can grow, shrink or become disorganized in the adult cardiac cells. This has important functional consequences for the formation of dyads and the efficiency and synchrony of calcium release throughout the cell.