This symposium talk aims to give an overview of the role played by the cardiac sodium channel in the decline in function of the heart as it begins to fail.  The following summary will provide some background for the talk. In adapting to disease and loss of tissue the heart shows great phenotypic plasticity that involves changes to its structure, composition and electrophysiology.  In parallel, global cardiovascular adaptations occur involving stimulation of the sympathetic nervous system,  release of natriuretic peptides and activation of the renin-angiotensin-aldosterone pathway.  These adaptations provide compensation for the initial decline in cardiac function but, for reasons not understood, do not provide continued benefit in the longer term.  The heart begins to fail in its task to produce sufficient cardiac output to meet the body’s requirements for oxygen and nutrients.  Heart failure is a chronic and progressive condition with very poor prognosis.   Approximately 60% of people diagnosed with heart failure are dead within five years and, although exact percentages depend on the type of failure, up to half of those will die from disturbances of rhythm. At the cellular level compensation responses involve a spectrum of changes to structure,  electrophysiology and Ca2+ homeostasis.   There is an increase in late Na+ current and a decrease in Na+/K+ ATPase current. The cardiac myocytes gain Na+ and this alters the balance of Ca2+ flux mediated by the Na+/Ca2+ exchange that limits early contractile impairment.   Action potential duration prolongs as a result of the increase in late Na+ current and changes in the expression and function of other ion channels and transporters, notably those carrying K+.    Cytosolic Na+ perturbations can disturb Ca2+-dependent energy metabolism and reactive oxygen production in mitochondria reducing energy supply. The normal spatial arrangements of Ca2+-handling proteins are essential for efficient excitation–contraction (EC) coupling and the stability of this amplification mechanism. There is a reduction in T-tubule density in myocytes from failing hearts leading to an increased spatial separation of the junctional SR from the T-tubule membrane.  These structural changes are thought to underlie temporal delays in EC coupling and an increase in spontaneous Ca2+-release events (Ca2+ sparks).  It is likely that these structural and electrophysiological responses occur at the expense of (1) increasing the likelihood of arrhythmogenesis, (2) activating hypertrophic and apoptotic signalling pathways and (3) decreasing the efficiency of EC coupling.  The combination of action potential prolongation, altered Na+ regulation, inconsistent Ca2+ release from SR and a less stable ventricular membrane potential provides a setting for triggered arrhythmias initiated either by early or delayed afterdepolarizations.  The cardiac sodium channel plays an important role in the passage of the heart from function to dysfunction.