It has been persuasively shown in the last two decades that the development of heart failure is closely linked to distinct alterations in Ca(2+) cycling. A crucial point in this respect is an increased spontaneous release of Ca(2+) out of the sarcoplasmic reticulum during diastole via ryanodine receptors type 2 (RyR2). The consequence is a compromised sarcoplasmic reticulum Ca(2+) storage capacity, which impairs systolic contractility and possibly diastolic cardiac function due to Ca(2+) overload. Additionally, leaky RyR2 are more and more regarded to potently induce proarrhythmic triggers. Elimination of spontaneously released Ca(2+) via RyR2 in diastole can cause a transient sarcolemmal inward current and hence delayed after depolarisations as substrate for cardiac arrhythmias. In this article, the pathological role and consequences of the SR Ca(2+)-leak and its regulation are reviewed with a main focus on protein kinase A and Ca(2+)-calmodulin-dependent kinase II. We summarise clinical consequences of "leaky RyR2" as well as possible therapeutic strategies in order to correct RyR2 dysfunction and discuss the significance of the available data.