We have shown that the gene SCN10A encoding the sodium channel Na_v1.8 is a susceptibility factor for heart block and serious ventricular arrhythmia. Since Na_v1.8 is known to be present in nerve fibres that mediate pain, it may be related to both cardiac pain and dysrhythmia. The localisation of Na_v1.8 and other key nociceptive ion channels, including Na_v1.7, Na_v1.9, capsaicin receptor TRPV1, and purinergic receptor P2X₃, have not been reported in human heart. The aim of this study was to determine the distribution of Na_v1.8, related sodium and other sensory channels in human cardiac tissue, and correlate their density with sympathetic nerves, regenerating nerves (GAP-43), and vascularity. Human heart atrial appendage tissues (n = 13) were collected during surgery for valve disease. Tissues were investigated by immunohistology using specific antibodies to Na_v1.8 and other markers. Na_v1.8 immunoreactivity was detected in nerve fibres and fascicles in the myocardium, often closely associated with small capillaries. Na_v1.8 nerve fibres per mm² correlated significantly with vascular markers. Na_v1.8-immunoreactivity was present also in cardiomyocytes with a similar distribution pattern to that seen with connexins, the specialised gap junction proteins of myocardial intercalated discs. Na_v1.5-immunoreactivity was detected in cardiomyocytes but not in nerve fibres. Na_v1.7, Na_v1.9, TRPV1, P2X₃/P2X₂, and GAP43 positive nerve fibres were relatively sparse, whereas sympathetic innervation and connexin43 were abundant. We conclude that sodium channel Na_v1.8 is present in sensory nerves and cardiomyocytes of human heart. Na_v1.8 and other pain channels provide new targets for the understanding and treatment of cardiac pain and dysrhythmia.