It was traditionally admitted that junctional tachycardia was based on an intranodal reentry pathway. However, lesions created at a distance from the atrioventricular node by surgery or other physical means (fulguration or radiofrequency energy ablation) demonstrated that the reentry circuit could use the slow and fast atrial pathways. This study performed in 6 human hearts less than 1 hour after death was undertaken to perform enzyme histochemical analysis of the atrial pre-nodal region. The specimens were rapidly frozen in liquid nitrogen and sliced with a cryostat. After localisation of the different regions by routine staining methods, histochemical reactions were performed using the semi-permeable membrane method for weakly bound enzyme. Ten enzymes were studied covering the principal metabolic pathways. Though routine histological stain did not show any particular structures, the enzyme histochemical reactions showed a band of myocardium following the septal insertion of the tricuspid valve, joining the orifice of the coronary sinus to the posterior part of the compact atrioventricular node. This zone of myocardium had an enzymatic make-up similar to that of the sinus node. An analogous structure was also observed above the insertion of the anterior mitral leaflet. These two regions could constitute the trajectory of the slow conduction pathways.