This editorial refers to ‘Expression of skeletal muscle sodium channel (Nav1.4) or connexin32 prevents reperfusion arrhythmias in murine heart’ by E.P. Anyukhovsky et al. , doi:10.1093/cvr/cvq284. Circulating cardiac excitation was first described by George R. Mines in his seminal publication ‘On dynamic equilibrium in the heart’.1 Mines recognized the importance of his finding and suggested that circulating excitation may be responsible for ‘some cases of paroxysmal tachycardia as observed clinically’, and directly defined the optimal circumstances for circular excitation: ‘The circumstances under which the phenomenon made its appearance were such as to produce the favourable conditions of slow conduction and short refractory period'. During acute myocardial ischaemia, [K+]o is increased which leads to a reduced membrane potential and partial inactivation of the cardiac Na+ current (Nav1.5). Secondly, ischaemia leads to intracellular acidification,2 which in turn leads …