Heart failure is a disorder with diverse aetiology and increasing prevalence. 50% of deaths related to this condition are due to sudden ventricular arrhythmias. Although the changes in cellular Ca2+ regulation that occur in failing hearts are now more recognized and better understood than in the past, the links between such alterations and the occurrence of arrhythmias remain uncertain. Ca2+ waves are thought to underlie some forms of ventricular tachyarrhythmia and are considered to be associated with increased spontaneous sarcoplasmic reticulum (SR) Ca2+release for a given SR Ca2+ content. The spontaneous release events appear to result from a change in (1) the control of cytoplasmic [Ca2+] by the SR Ca2+ATPase (SERCA2a) and the sarcolemmal Na+/Ca2+ exchange (NCX) and (2) certain regulatory elements of the SR Ca2+ release channel (the ryanodine receptor – RyR2). There is also complex interplay between intracellular Na+ and Ca2+ regulation, so altered levels of intracellular Na+ concentration ([Na+]i) could be expected to have profound effects on the Ca2+ transient and, via NCX, the membrane potential and consequently arrhythmogenesis. The experiments that will be described focus (1) on the changes that may take place to the regulation of [Na+]i in heart failure and (2) provide evidence that suggests sub-sarcolemmal [Na+] has an important role to play in the initiation and propagation of potentially arrhythmogenic SR Ca2+ release events. The former were conducted on a well characterised model of cardiac hypertrophy and heart failure in the guinea-pig induced by constriction of the ascending aorta (AC). Voltage clamp experiments were used to assess Na+/K+ ATPase current in ventricular myocytes enzymatically isolated from 30, 60 and 150 days sham and AC hearts. The size of the current recorded in cells isolated from hearts 30 days after AC is not different from cells isolated from sham operated hearts. However, the size of the current recorded from cells isolated from hearts 60 and 150 days after AC is reduced by about half compared with sham operated hearts. These data indicate that there are alterations to the regulation of [Na+]i in the failing heart. The latter experiments were conducted on ventricular myocytes isolated from normal healthy rat hearts. The main finding was that reducing Na+ current (either pharmacologically or by voltage clamping the cells at different holding potentials) decreases the frequency of Ca2+ sparks and the frequency and velocity of Ca2+ waves. Together these findings suggest that changes to intracellular [Na+] maybe a reason for the increased predisposition of the failing heart to arrhythmia.