Single sodium channel currents were recorded by patch clamp technique in isolated guinea-pig ventricular myocytes, and action potentials of papillary muscle and ECG were conventionally measured. Sea anemone toxin (ATXII), a high affinity toxin to sodium channel, was used to change the sodium channel dynamics. Changes in the duration of action potentials and the QT interval of ECG depending on the channel modes were studied in order to provide hints to an understanding of pathogenesis of the long QT syndrome (a genetic disease). With the binding of ATXII to the sodium channel, the occurrence frequency and the open time constant of the "long opening" mode of single Na channels increased significantly, whereas the action potential durations, APD50 and APD90, were prolonged by 23% and 27% respectively. Following application of ATXII, on the other hand, the QT interval and the QTc, a rectified QT interval, increased by 18.6% and 18.9% respectively. The results suggest that the dynamics or modes of Na channel play an important role in determining the action potential duration and the QT interval of ECG. The dynamical changes in Na channels induced by genetic mutation may be partially responsible for the long QT syndrome.